Search Criteria: Research Area is "Neurobiology Research: Alzheimer's Disease"

New Strains Awaiting Transfer from the Donor
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JAX® Mice Strains

Stock
Number
Strain Name
 
Strain Description
Standard Supply
002052 B6.129P2-Apoetm1Unc/J
Level 2
Mice homozygous for the Apoetm1Unc mutation show a marked increase in total plasma cholesterol levels that are unaffected by age or sex. Fatty streaks in the proximal aorta are found at 3 months of age. The lesions increase with age and progress to lesions with less lipid but more elongated cells, typical of a more advanced stage of pre-atherosclerotic lesion. Moderately increased triglyceride levels have been reported in mice with this mutation on a mixed C57BL/6 x 129 genetic background. Aged apoE-deficient mice (>17 months) have been shown to develop xanthomatous lesions in the brain consisting mostly of crystalline cholesterol clefts, lipid globules, and foam cells. Smaller xanthomas were seen in the choroid plexus and ventral fornix. Additional studies indicate that apoE-deficient mice have altered responses to stress, impaired spatial learning and memory, altered long term potentiation, and synaptic damage.
002609 B6.129P2-Nos2tm1Lau/J
Level 4
Mice homozygous for the Nos2tm1Lau targeted mutation resemble wildtype mice in appearance and histology. Homozygotes are viable and fertile. Unlike Nos1 and Nos3, Nos2 is synthesized de novo in response to a variety of inflammatory stimuli. Induction of Nos2 results in the production of large amounts of nitric oxide (NO) over prolonged periods of time. Excessive NO production has been shown to be beneficial through its antitumor and antimicrobial activities. It is also thought to cause tissue damage and contribute to pathology in a variety of inflammatory conditions including rheumatoid arthritis, inflammatory bowel disease, cardiac allograft rejection, hepatoxicity, myocardial ischemia-reperfusion and septic shock. NO has been demonstrated to play a role in the regulation of blood pressure and hemodynamics. In an LPS-induced model of septic shock, Nos2tm1Lau homozygotes had virtually no serum NO response, but were .....
For more information please see the full phenotype on the strain data sheet
016198 129S6.Cg-Tg(Camk2a-tTA)1Mmay/JlwsJ
Repository- Live
Transgenic mice expressing the tetracycline-controlled transactivator protein (tTA) under regulatory control of the forebrain-specific calcium-calmodulin-dependent kinase II (Camk2a) promoter are viable and fertile. When hemizygotes are mated to a second strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE; tetO), expression of the target gene can be blocked by administration of the tetracycline analog, doxycycline (dox). These mice are a "Tet-Off" tool that allow the inducible expression of genes in forebrain neurons, and may be useful in studying brain disorders such as Alzheimer's disease, Parkinson's disease, or other neurodegenerative diseases.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally .....
For more information please see the full phenotype on the strain data sheet

004714 B6.129-Bace1tm1Pcw/J
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Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of brain tissue. Primary cultures of cortical neurons isolated from homozygotes aged embryonic day 16.5 do not secrete amyloid beta peptides (Aβ1-40/42 or Aβ11-40/42) or beta C-terminal fragments (βCTFs). When transfected with a recombinant adenovirus expressing the mutant humanized Beta amyloid precursor protein (APP), hAPPSwe, cultured embryonic cortical neurons do not secrete detectable levels of Aβ1-40/42 or Aβ11-40/42 peptides. This mutant mouse strain may be useful in studies of Alzheimer's disease.
022401 B6.129-Cdk5r1tm2.1Lht/J
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The Cdk5r1, cyclin-dependent kinase 5, regulatory subunit 1 (p35) gene encodes the p35 protein, which when cleaved by calpain results in a truncated p25 protein. The p25 protein is an activator of cyclin-dependent kinase 5, and as a complex with CDK5 causes hyperphosphorylation of tau and neurofilament proteins, as well as neuronal cell death. These Δp35 KI mice express a mutant calpain cleavage-resistant p35 protein in which six amino acid residues adjacent to the calpain-cleavage site (Δ93 -98) were deleted with a leucine replacing the alanine. In mice homozygous for the mutation, expression levels for the mutant protein are similar to wildtype levels. Calpain cleavage of p35 and formation of the p25 truncated protein is abolished in homozygotes while other native CDK5R1 protein activity is unaltered. Homozygotes are viable and fertile, and exhibit impaired memory extinction. While hippocampal long-term potentiation (LTP) is the same as wildtype controls, hipp .....
For more information please see the full phenotype on the strain data sheet
005582 B6.129P-Cx3cr1tm1Litt/J
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Mice that are homozygous for the CX3CR1-GFP targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. RT-PCR analysis of lymphoid tissue from homozygotes detects mutant gene product (mRNA) and no wild type gene product (mRNA). Flow cytometric analysis of peripheral blood cells identified a subset of green fluorescent cells not observed in wild type mice. Enhanced Green Fluorescent Protein (EGFP), but not the endogenous gene, is expressed in monocytes, dendritic cells, NK cells, and brain microglia, mimicking endogenous gene expression. The same subset of peripheral blood cells isolated from heterozygote mice express detectable levels of EGFP. Immunohistochemical analysis of spleen and peripheral nerve tissue from homozygotes does not detect EGFP. These CX3CR1-GFP mutant mice may be useful in studies of leukocyte migration and trafficking, as well as for transplantation studies.

Of note, CX3CR1-GFP mice are also avail .....
For more information please see the full phenotype on the strain data sheet

023726 B6.129P2-C1qatm1.1Tenn/J
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These mice contain four mutations (A13, P14, N16, P20) in the complement component 1, q subcomponent, alpha polypeptide (C1qa) gene, designed to mimic the corresponding sequence from human A chain (E13, A14, R16, R20). C1q, a macromolecule composed of 6 each of A, B, and C chains, is a component of the classical complement pathway (CCP) which can be activated by immune complexes (via interaction with multiple C1q globular domains) as well as molecules containing specifically spaced negative charges. Excessive or unregulated complement activation can contribute to the pathogenesis of diseases such as Alzheimer's disease. Mice lack arginine residues in the C1q A chain N-terminal collagen-like region, present in humans which are present in humans and thought to enable CCP activation by some non immune complex activators. These mice contain mutations that facilitate binding of molecules like beta-amyloid fibrils (fAβ) to C1q. While these mice did not show any differences in .....
For more information please see the full phenotype on the strain data sheet
002213 B6.129S4-Ngfrtm1Jae/J
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Mice homozygous for the Ngfrtm1Jae mutation are viable and fertile. They display a decreased cutaneous innervation by calcitonin gene-related peptide- and substance P-immunoreactive sensory fibers. Because of this decreased innervation they develop ulcers on their toes by four months of age. The toes become inflamed and progressively infected. There is also reduced sensitivity to heat in the extremities of these mice. Pineal glands lack sympathetic innervation and innervation to sweat glands on foot pads is either reduced or absent. Deficits in the peripheral nervous system were examined by looking at cellular responses of p75-deficient dorsal root ganglion (DRG) and superior cervical ganglion (SCG) neurons to different neurotrophins. p75-deficient DRG and SCG neurons displayed a two- to three-fold decreased sensitivity to NGF at embryonic day 15 and postnatal day three, respectively. These ages coincide with the peak of naturally occurring cell death. p75-deficient .....
For more information please see the full phenotype on the strain data sheet
004133 B6.129S7-Apptm1Dbo/J
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At birth, mice homozygous for the targeted allele are viable, and do not display any gross physical or behavioral abnormalities. No App gene product (mRNA or protein) is detected. Body weight is 15-20% less than that observed in wildtype age-matched control mice. By 14 weeks of age the mice exhibit evidence of reactive gliosis. Neurological evaluation reveals significantly reduced forelimb grip strength and decreased locomotor activity. This mutant strain offers a model useful in studies related to Alzheimer's disease.
007251 B6.129X1-Mapttm1Hnd/J
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Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by RT-PCR analysis of total brain RNA, Western blot analysis of total brain homogenates or immunostraining of coronal brain sections. Hippocampal neurons from homozygous embryos, in primary culture, have delayed axonal extension and shorter total dendritic length when compared to wildtype controls. Mitochondria in the primary culture cells cluster at the distal end of axons. The frequency and velocity of mitochondrial anterograde movements is increased.

This mutant mouse strain may be useful in studies of neuronal development, axonogenesis, and organelle movement.

007083 B6.Cg-Cav1tm1Mls/J
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Mice that are homozygous for the targeted mutation are viable, fertile and do not display any gross physical abnormalities. Mutant mice exhibit exercise intolerance when challenged and are slightly hyperphagic. No gene product (protein) is detected by Western blot analysis in adipose, lung and heart tissues or in cultured mouse embryonic fibroblasts (MEFs). A decrease in the level of co-expressed caveolin-2 protein is immunodetected. At age 4-5 months, mutant mice are often smaller than their wildtype littermates. By one year of age, mutant mice weigh 5 to 7 grams less than wildtype, and are resistant to diet-induced obesity. Progressive adipose pathology results in reduced white adipose tissue with abnormally small adipocytes and enlarged, hyperplastic brown adipose tissue. Homozygotes display lipid metabolism and uptake disruption with elevated serum triglycerides and free fatty acid levels, and reduced leptin levels. Isolated aortic tissue segments have a diminished vasoconstriction .....
For more information please see the full phenotype on the strain data sheet
005491 B6.Cg-Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
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Mice that are homozygous for the targeted allele and hemizygous for the transgene are viable and fertile. Although no endogenous mouse MAPT is detected, all six isoforms (including both 3R and 4R forms) of human MAPT are expressed. Hyperphosphorylated MAPT is detected in cell bodies and dendrites by three months of age. Paired helical filaments of aggregated insoluble MAPT can be isolated from brain tissue as early as two months of age. These mutant mice may be useful in studies examining the relationship between human MAPT and Alzheimer's disease pathogenesis

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

005866 B6.Cg-Tg(APP695)3Dbo Tg(PSEN1dE9)S9Dbo/Mmjax
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Double transgenic mice are viable and fertile. At 6 months of age, double-transgenic mice show visible amyloid plaque deposition but are indistinguishable from nontransgenic animals in all cognitive measures. By 18 months, amyloid deposits were much higher in APPswe/PS1dE9 mice with statistically significant but mild decreases in cholinergic markers (cortex and hippocampus) and somatostatin levels (cortex). Performance of older double-transgenic mice is impaired in all cognitive tasks, and deficits in episodic-like memory tasks correlate with total amyloid-beta peptide loads in the brain. Mutant mice, hemizygous for each transgene, and on the C57BL/6J background (N6), have altered EEG (decreased cortical theta activity and increased beta and gamma activity). EEG differences are detected as early as 7 month of age (Wang et al. Brain Res 2002).
008730 B6.Cg-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax
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Hemizygous mice are viable and fertile. These 5XFAD transgenic mice overexpress both mutant human APP(695) with the Swedish (K670N, M671L), Florida (I716V), and London (V717I) Familial Alzheimer's Disease (FAD) mutations and human PS1 harboring two FAD mutations, M146L and L286V. Expression of both transgenes is regulated by neural-specific elements of the mouse Thy1 promoter to drive overexpression in the brain. Mice from this founder line have high APP expression correlating with high burden and accelerated accumulation of the 42 amino acid species of beta-amyloid (Aβ-42). 5XFAD mice generate Aβ-42 almost exclusively and rapidly accumulate massive cerebral levels. On the B6SJL F1 genetic background (see MMRRC stock 34840), intraneuronal Abeta;-42 accumulation is observed starting at 1.5 months of age, just prior to amyloid deposition and gliosis, which begins at two months of age. On a congenic C57BL/6 .....
For more information please see the full phenotype on the strain data sheet
005864 B6.Cg-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax
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Double transgenic mice express a chimeric mouse/human amyloid precursor protein (Mo/HuAPP695swe) and a mutant human presenilin 1 (PS1-dE9) both directed to CNS neurons. Both mutations are associated with early-onset Alzheimer's disease. The “humanized” Mo/HuAPP695swe transgene allows the mice to secrete a human A-beta peptide. Both the transgenic peptide and holoprotein can be detected by antibodies specific for human sequence within this region (Signet Laboratories' monoclonal 6E10 antibody). The included Swedish mutations (K595N/M596L) elevate the amount of A-beta produced from the transgene by favoring processing through the beta-secretase pathway. This “humanized” Mo/HuAPP695swe protein is immunodetected in whole brain protein homogenates. The transgenic mutant human presenilin protein (PS1-dE9), which in high levels displaces detectable endogenous mouse protein, is also immunodetected in whole brain protein homogenates. The donating investigator reports tra .....
For more information please see the full phenotype on the strain data sheet
016197 B6.Cg-Tg(CAG-OTC/CAT)4033Prab/J
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C57BL/6.mCAT mice (MCAT transgenic mice) have a CMV enhancer/chicken beta-actin promoter (CAG; from the pCAGGS vector) driving the expression of a human Catalase (CAT) gene in mitochondria. Hemizygous MCAT mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Catalase is a an enzyme, normally expressed in peroxisomes, that reduces hydrogen peroxide (H2O2) to water and molecular oxygen, mitigating the potential for H2O2 to cause damage to molecules. Mitochondrial catalase expression in MCAT mice results in a 5.5-month increase in median life span for both males and females. Catalase activity is elevated in heart, skeletal muscle, and brain. Cardiac mitochondria have 50 times higher catalase activity than in wild-type littermates leading to a delay in cardiac pathology. They also display improved cardiac performance with age, reducing their susceptibility to c .....
For more information please see the full phenotype on the strain data sheet
007004 B6.Cg-Tg(Camk2a-tTA)1Mmay/DboJ
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Transgenic mice expressing the tetracycline-controlled transactivator protein (tTA) under regulatory control of the forebrain-specific calcium-calmodulin-dependent kinase II (Camk2a) promoter are viable and fertile. When hemizygotes are mated to a second strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE; tetO), expression of the target gene can be blocked by administration of the tetracycline analog, doxycycline (dox). These mice are a "Tet-Off" tool that allow the inducible expression of genes in forebrain neurons, and may be useful in studying brain disorders such as Alzheimer's disease (when used in conjunction with Stock No. 005706, Stock No. 007049, Stock No. 007051, Stock No. 007052), Parkinson's .....
For more information please see the full phenotype on the strain data sheet
004631 B6.Cg-Tg(GFAP-APOE_i4)1Hol Apoetm1Unc/J
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These transgenic mice express the human apolipoprotein E4 isoform (APOE4) under the direction of the human glial fibrillary acidic protein (GFAP) promoter and do not express endogenous mouse apolipoprotein E (APOE). The transgenic isoform expression pattern follows the endogenous mouse APOE and GFAP expression patterns in the brain. Human APOE4 is immunodetectable in glia and neuropil in developing and adult mutant mice. Cultured astrocytes from transgenic mice secrete APOE4 in lipoproteins that are similar in size to high-density (HDL) plasma lipoproteins. Detergent-soluble APOE4 protein levels in hemizygous mice forebrain tissue and in adult human cortex tissue are similar. Mice that are hemizygous or homozygous for the transgenic insert and homozygous for the targeted allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain represents a model that may be useful in studies examining the function of APOE4 in t .....
For more information please see the full phenotype on the strain data sheet
006293 B6.Cg-Tg(PDGFB-APPSwInd)20Lms/2Mmjax
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These transgenic mice express a mutant form of the human amyloid protein precursor bearing both the Swedish (K670N/M671L) and the Indiana (V717F) mutations (APPSwInd). Expression of the transgenic insert is directed by the human platelet-derived growth factor beta polypeptide (PDGFB) promoter. Hemizygotes express immunodetectable transgene product in cerebral neurons, with the highest level of expression occurring in the neocortex and hippocampus. Enzyme-linked immunosorbent assay (ELISA) analysis reveals approximate total amyloid beta peptides and 42 amino acid length amyloid beta peptides in neocortical and hippocampal tissue from mutant mice. At five to seven months of age diffuse amyloid beta peptides deposition in the dendate gyrus and neocortex forms. Amyloid deposition is progressive with all transgenic mice exhibiting plaques by age eight to 10 months. Pups born of carrier females have shown an increased mortality rate in our colonies. The Donating Researcher has .....
For more information please see the full phenotype on the strain data sheet
008596 B6.Cg-Tg(Prnp-Abca1)EHol/J
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These transgenic mice express the mouse Abca1 (ATP-binding cassette, sub-family A (ABC1), member 1) gene under the control of the mouse Prnp (prion protein) promoter.

These founder line E mice have a 6-fold increase in expression of ABCA1 in the cortex over wild-type levels. Trangene expression is high in total brain tissue, kidney, testis and muscle as detected by Western blot analysis. Transgenic mice exhibit reduced apoE levels: 40% of wild-type levels in the hippocampus, approximately half of wild-type levels in cerebrospinal fluid (CSF). The apoE protein that is overexpressed has altered biochemical properties and is not as soluble as that found in controls. Lipoprotein particles from the CSF that contain apoE protein are larger in size than wild-type, indicating that the transgenic apoE particles are more lipidated.

Male transgenic mice have atropied testes, defective spermatogenesis and are infertile. The strain can be maintained by mating hemizygous femal .....
For more information please see the full phenotype on the strain data sheet

005999 B6.Cg-Tg(SBE/TK-luc)7Twc/J
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Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express luciferase in response to activation of the Smad2/3-dependent signaling pathway. Cultured primary astrocytes isolated from transgenic mice exhibited luciferase activity when stimulated with TGF-beta. Higher treatment levels of activin and nodal elicited similar luciferase activity. Lipopolysaccharide (LPS) challenge results in strong bioluminescence emissions from the intestinal region and brain. Mechanical injury to the neocortex results in an increase of bioluminescence in 2 hours, which peaks at 4 hours and returns to baseline approximately 48 hours after the injury. Biochemical assays for luciferase activity correlated with noninvasive bioluminescence imaging analysis. The strain was backcrossed to the albino C57BL/6J-Tyrc-2J/J strain for 2 generations to facilitate bioluminescence imaging. .....
For more information please see the full phenotype on the strain data sheet
004807 B6;129-Psen1tm1Mpm Tg(APPSwe,tauP301L)1Lfa/Mmjax
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Mice homozygous for all three mutant alleles (3xTg-AD; homozygous for the Psen1 mutation and homozygous for the co-injected APPSwe and tauP301L transgenes (Tg(APPSwe,tauP301L)1Lfa)) are viable, fertile and display no initial gross physical or behavioral abnormalities. Translation of the overexpressed transgenes appears to be restricted to the central nervous system, notably in Alzheimer's disease-relevant areas including the hippocampus and cerebral cortex. The initial characterization of this mouse line indicated a progressive increase in amyloid beta peptide deposition, with intracellular immunoreactivity being detected in some brain regions as early as 3-4 months. Synaptic transmission and long-term potentiation are demonstrably impaired in mice 6 months of age. Between 12-15 months aggregates of conformationally altered and hyperphosphorylated tau are detected in the hippocampus. This mutant mouse exhibits plaque and tangle pathology associated with synaptic dysfunction, tra .....
For more information please see the full phenotype on the strain data sheet
002596 B6;129P2-Nos2tm1Lau/J
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Mice homozygous for the Nos2tm1Lau targeted mutation resemble wildtype mice in appearance and histology. Homozygotes are viable and fertile. Unlike Nos1 and Nos3, Nos2 is synthesized de novo in response to a variety of inflammatory stimuli. Induction of Nos2 results in the production of large amounts of nitric oxide (NO) over prolonged periods of time. Excessive NO production has been shown to be beneficial through its antitumor and antimicrobial activities. It is also thought to cause tissue damage and contribute to pathology in a variety of inflammatory conditions including rheumatoid arthritis, inflammatory bowel disease, cardiac allograft rejection, hepatoxicity, myocardial ischemia-reperfusion and septic shock. NO has been demonstrated to play a role in the regulation of blood pressure and hemodynamics. In an LPS-induced model of septic shock, Nos2tm1Lau homozygotes had virtually no serum NO response, but were .....
For more information please see the full phenotype on the strain data sheet
006410 B6;129S6-Chattm2(cre)Lowl/J
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Mice that are homozygous for the ChAT-IRES-Cre knockin are viable and fertile. An "IRES-Cre" sequence is inserted downstream of the stop codon such that cre expression is controlled by the endogenous Chat gene promoter. Chat gene expression, however, is unaffected. Cre recombinase activity is reported in all cholinergic neurons. These mice may be useful for "Cre-lox" technology applications in neurobiology, including studies of motor function, learning and memory, Alzheimer's disease, and Down syndrome, and in obesity and diabetes research.

View cre expression characterization.

005993 B6;129S6-Pcsk9tm1Jdh/J
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Homozygous mice are viable and fertile with no behavioral abnormalities. No expression of the endogenous RNA or protein is observed in liver. Homozygotes have reduced plasma cholesterol levels; apolipoprotein B (apoB)-containing low-density liproprotein (LDL) is nearly undetectable and apolipoprotein E (apoE)-containing high density liproprotein (HDL) levels are reduced 30%. Homozygotes show increased hepatic LDL-receptor (LDLR) protein (but not RNA) expression. Homogygous mice also have accelerated clearance of circulating cholesterol. Lovastatin addition to the diet of homozygous mice results in further increased hepatic LDLR and LDL clearance from the blood. Heterozygous mice have intermediate plasma cholesterol and LDL clearance. This mouse may be useful in studies of lipid homeostasis, cholesterol metabolism, apolipoprotein function, and statin treatment for hypercholesterolemia.
012604 B6;129S7-Lrp1tm2Her/J
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These LRPflox/flox mutant mice possess a floxed Neo cassette and a single loxP sites downstream of exon 2 of the targeted low-density lipoprotein (LDL) receptor-related protein (LRP) 1 gene, Lrp1. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, the resulting offspring will have exons 1 and 2 deleted in the cre-expressing tissue, resulting in inactivation of Lrp1 gene function. This strain may be useful for studying physiological role of LRP in the uptake of cholesterol-rich lipoproteins from circulation and in maintenance of plasma lipid homeostasis.
008169 B6;C3-Tg(Prnp-MAPT*P301S)PS19Vle/J
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These PS19 transgenic mice (P301S Tg mice) express the P301S mutant form of human microtubule-associated protein tau (MAPT), under the direction of the mouse prion protein, Prnp, promoter. The expression of the mutant human MAPT is five-fold higher than the expression of the endogenous mouse MAPT protein. Hyperphosphorylated, insoluble mutant human MAPT protein in the brain accumulates with age causing decreased microtubule binding. At three months of age, transgenic mice exhibit clasping and limb retraction when lifted by the tail, which progresses to limb weakness. By 10 months of age the mice exhibit a hunched back and paralysis, followed by inability to feed. Transgenic mice have a median lifespan of approximately nine months with approximately 80% dying by 12 months. Histological analysis reveals neuron degeneration in hippocampus and ventricular dilatation (brain atrophy) by eight months of age, although significant neuron degeneration in the hippocampus occurs at .....
For more information please see the full phenotype on the strain data sheet
000231 B6;C3Fe a/a-Csf1op/J
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Mice homozygous for the osteopetrosis spontaneous mutation (Csf1op) are viable and exhibit osteopetrosis. The osteoclasts are the primary cell type affected in homozygous mutant mice. This results in a generalized macrophage deficiency, monocytopenia, and defective bone remodeling. Homozygous mutant mice also have abnormal calcium regulation, impaired dental growth and female mice fail to lactate. Total leukocyte counts are reduced and marrow cells are decreased to one-tenth of normal control mice. Homozygous mutant mice have a deficient microglia and macrophage response, and therefore may be useful tools to study the role of glia in neurological disease if mated to transgenic models of neurodegenerative disease.
004462 B6C3-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax
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Double transgenic mice express a chimeric mouse/human amyloid precursor protein (Mo/HuAPP695swe) and a mutant human presenilin 1 (PS1-dE9) both directed to CNS neurons. Both mutations are associated with early-onset Alzheimer's disease. The "humanized" Mo/HuAPP695swe transgene allows the mice to secrete a human A-beta peptide. Both the transgenic peptide and holoprotein can be detected by antibodies specific for human sequence within this region (Signet Laboratories' monoclonal 6E10 antibody). The included Swedish mutations (K595N/M596L) elevate the amount of A-beta produced from the transgene by favoring processing through the beta-secretase pathway. This "humanized" Mo/HuAPP695swe protein is immunodetected in whole brain protein homogenates. The transgenic mutant human presenilin protein (PS1-dE9), which in high levels displaces detectable endogenous mouse protein, is also immunodetected in whole brain protein homogenates. The donating investigator reports that transgenic mice develo .....
For more information please see the full phenotype on the strain data sheet
024025 B6N(Cg)-Psen1tm1.1(KOMP)Vlcg/J
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This strain was generated by the Knockout Mouse Phenotyping Program (KOMP2) at The Jackson Laboratory using embryonic stem cells provided by the International Knockout Mouse Consortium. The Psen1 (presenilin 1) gene encodes an enzyme that regulates amyloid precursor protein (APP) processing and cleavage of Notch receptors. Mutations in Psen1 have been associated with the onset and progression of Alzheimer?s disease. A beta-galactosidase-containing cassette disrupts the Psen1 gene in this strain. Phenotype data is being generated by the JAX KOMP2 program and will be available to the public when complete from the International Mouse Phenotyping Consortium website. For additional information on this mutation, please see the Regeneron Velocigene w .....
For more information please see the full phenotype on the strain data sheet
018957 B6N.129S6(B6)-Chattm2(cre)Lowl/J
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To be more suitable for use with C57BL/6N-congenic Knockout Mouse Project (KOMP) strains with floxed alleles, The Jackson Laboratory Repository chose several Cre recombinase-expressing strains and backcrossed them onto the C57BL/6N genetic background using a marker-assisted, speed-congenic approach. This approach employed 148 single nucleotide polymorphism (SNP) markers that differ between the C57BL/6N and C57BL/6J substrains, covering all 19 chromosomes and the X chromosome. This analysis has determined that all SNP markers are now C57BL/6N allele-type (with the exception of 2 markers near the Chat locus on chromosome 14).

The parental line, C57BL/6;129S6 ChAT-IRES-Cre knockin mice, are available and described as Stock No. 006410. It should be noted that the phenotype of these C57BL/6NJ-congenic ChAT-IRES-Cre knockin mice (Stock No. 018957) could vary from that of the parental line from which it was derived. We may .....
For more information please see the full phenotype on the strain data sheet

006554 B6SJL-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax
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These 5XFAD transgenic mice overexpress both mutant human APP(695) with the Swedish (K670N, M671L), Florida (I716V), and London (V717I) Familial Alzheimer's Disease (FAD) mutations and human PS1 harboring two FAD mutations, M146L and L286V. Expression of both transgenes is regulated by neural-specific elements of the mouse Thy1 promoter to drive overexpression in the brain. Mice from this founder line have high APP expression correlating with high burden and accelerated accumulation of the 42 amino acid species of beta-amyloid (Abeta-42). 5XFAD mice generate Abeta-42 almost exclusively, rapidly accumulating massive cerebral levels. On the B6SJL F1 genetic background (see MMRRC stock 34840, intraneuronal Abeta-42 accumulation is observed starting at 1.5 months of age, just prior to amyloid deposition and gliosis, which begins at two months of age. On a congenic C57BL/6J genetic background (For more information please see the full phenotype on the strain data sheet
007027 C57BL/6-Tg(Thy1-APPSwDutIowa)BWevn/Mmjax
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These transgenic mice express neuronally derived human amyloid beta-precursor protein, APP gene, 770 isoform, containing the Swedish K670N/M671L, Dutch E693Q and Iowa D694N mutations, under the control of the mouse thymus cell antigen 1, theta, Thy1, promoter. Mice hemizygous for the transgenic insert exhibit expression of human amyloid beta precursor protein in the cortex, hippocampus and brain stem with lower expression detected in the cerebellum. At age three months hemizygotes show a progressive accumulation of insoluble amyloid beta 40 and 42 peptides in brain tissue. The levels of accumulation of amyloid beta peptides is 12 to 14 fold higher in brain microvessels than in whole forebrain tissue homogenates. Fibrillar microvascular accumulations of amyloid beta peptides begin at approximately six months of age. Diffuse plaque-like deposits of amyloid beta that are similar to the plaques observed in human patients with the Dutch and Iowa familial disorders are initiall .....
For more information please see the full phenotype on the strain data sheet
007677 CB6-Tg(Gad1-EGFP)G42Zjh/J
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Mice hemizygous for this GAD67-GFP transgene are viable and fertile. GAD67-GFP (line G42) mice selectively express enhanced green fluorescent protein (EGFP) in the calcium-binding protein parvalbumin (Pv)-expressing subclass of basket interneurons (soma, dendrites, and axons) and also in putative presynaptic boutons. Transgene expression (EGFP expression) is published as early as postnatal day 0 (P0) with high expression levels throughout postnatal development. EGFP expression remains restricted to ~50% of Pv-expressing interneurons in adulthood. The donating investigator additionally reports transgene expression as early as embryonic day 14 (E14). EGFP expression is not reported in other interneuron classes positive for somatostatin (SOM), cholecystokinin (CCK), calretinin (CR), and VIP. These GAD67-GFP (line G42) mice may be useful for fluorescent labeling of the Pv-expressing subset of GABAergic neurons, allowing reliable and efficient characterization of perisomatic innervation .....
For more information please see the full phenotype on the strain data sheet
007072 CByJ.129P2(B6)-Nos2tm1Lau/J
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Mice homozygous for the Nos2tm1Lau targeted mutation resemble wildtype mice in appearance and histology. Homozygotes are viable and fertile. Unlike Nos1 and Nos3, Nos2 is synthesized de novo in response to a variety of inflammatory stimuli. Induction of Nos2 results in the production of large amounts of nitric oxide (NO) over prolonged periods of time. Excessive NO production has been shown to be beneficial through its antitumor and antimicrobial activities. It is also thought to cause tissue damage and contribute to pathology in a variety of inflammatory conditions including rheumatoid arthritis, inflammatory bowel disease, cardiac allograft rejection, hepatoxicity, myocardial ischemia-reperfusion and septic shock. NO has been demonstrated to play a role in the regulation of blood pressure and hemodynamics. In an LPS-induced model of septic shock, Nos2tm1Lau homozygotes had virtually no serum NO response, but were .....
For more information please see the full phenotype on the strain data sheet
003718 FVB-Tg(GadGFP)45704Swn/J
Repository- Live
Mice homozygous for the TgN(GadGFP)45704Swn transgene express Enhanced Green Fluorescent Protein (EGFP) under the control of the mouse Gad1 (GAD67) gene promoter. Homozygous mice exhibit no apparent physical or behavioral defects. Transgene expression occurs in a specific subpopulation of hippocampal and cortical GABAergic interneurons that express somatostatin. This subset of interneurons has been shown to be prone to injury during epilepsy, ischemia, and Alzheimer's disease. These transgenic mice are useful for the morphological identification and study of these interneurons in both living and fixed brain tissue.

Of note, this strain is one of many fluorescent GABAergic neuron strains, each with unique labeling characteristics (see Stock No. 006334 and Stock No. 006340).

015815 FVB-Tg(tetO-MAPT*P301L)#Kha/JlwsJ
Repository- Live
The tetO-MAPT*P301L transgene contains a tetracycline operator (tetO) driving expression of the human four-repeat microtubule-associated protein tau (MAPT) gene. The transgene also contains the frontotemporal dementia-associated P301L mutation sequences (tauP310L) and untranslated sequence from the mouse prion protein gene (Prnp) driving transgene expression in the brain. Homozygous mice are not viable. When mated to a mutant strain expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), expression of tauP301L protein may be regulated with the tetracycline analog doxycycline (dox) in the double mutant offspring.

When bred to mice expressing tTa under regulatory control of the forebrain-specific calcium-calmodulin-dependent kinase II (Camk2a) promoter (see Stock No. 003010), bitransgenic mice expressing a .....
For more information please see the full phenotype on the strain data sheet

006143 FVB/N-Tg(Thy1-cre)1Vln/J
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Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre activity is observed in nearly all neurons in cortex and hippocampus. When bred with any mouse containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in postnatal, neuron-specific deletion of the flanked genome. These mice may be useful in studies of the nervous system, including Alzheimer's disease.

View cre expression characterization.

004585 STOCK Cav1tm1Mls/J
Repository- Live
Mice that are homozygous for the targeted mutation are viable, fertile and do not display any gross physical abnormalities. Mutant mice exhibit exercise intolerance when challenged and are slightly hyperphagic. No gene product (protein) is detected by Western blot analysis in adipose, lung and heart tissues or in cultured mouse embryonic fibroblasts (MEFs). A decrease in the level of co-expressed caveolin-2 protein is immunodetected. At age 4-5 months, mutant mice are often smaller than their wildtype littermates. By one year of age, mutant mice weigh 5 to 7 grams less than wildtype, and are resistant to diet-induced obesity. Progressive adipose pathology results in reduced white adipose tissue with abnormally small adipocytes and enlarged, hyperplastic brown adipose tissue. Homozygotes display lipid metabolism and uptake disruption with elevated serum triglycerides and free fatty acid levels, and reduced leptin levels. Isolated aortic tissue segments have a diminished vasoconstriction .....
For more information please see the full phenotype on the strain data sheet
004779 STOCK Mapttm1(EGFP)Klt/J
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Mice that are homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. A knock-in of the EGFP coding sequence into the first exon disrupts expression of the Mapt gene and produces a cytoplasmic EGFP fused to the first 31 amino acids. No gene product (isoform proteins) is detected in whole brain lysates by Western blot analysis. EGFP signal is detected beginning at 9.0 days post coitum in the trigeminal ganglion and by 10.75 days post coitum fluorescent signal is detected throughout the developing central nervous system. EGFP expression persists to adult and closely patterns the expression of neuron specific beta-tubulin III, as detected by the TuJ1 antibody. The expression of cytoplasmic EGFP in the central nervous system of this mutant allows for non-invasive visualization of elongating nerve axons.
012307 B6.129-Apoetm3(APOE*4)Mae Ldlrtm1(LDLR)Mae/J
Under Development - Now Accepting Orders
Apoe4 Ldlrh mice harbor two humanized knock-in mutations; the human APOE*4 replacement allele (Apoetm3(APOE*4)Mae) and the human LDLR replacement allele (Ldlrtm1(LDLR)Mae). Unless noted otherwise, the phenotypes below are for mice maintained on regular chow (~5% fat; <0.1% cholesterol).

The human APOE*4 replacement allele (Apoe4 or E4) expresses the human apoE4 isoform in place of the endogenous apoE protein. Under direction of the endogenous mouse apoE promoter/regulatory regions, human apoE4 expression is observed at physiological levels in the same temporal and spatial pattern observed in humans. Mice homozygous for human APOE*4 (Apoe4/4) are viable and fertile with normal plasma lipid and lipoprotein profiles. Apoe4/4 show mild retinal changes with aging. When maintained on high fat/cholesterol diet mirroring that consumed by humans, Apoe4/ .....
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018623 B6N(Cg)-Dnajb6tm1.1(KOMP)Vlcg/J
Under Development - Now Accepting Orders
This strain was generated by the Knockout Mouse Phenotyping Program (KOMP2) at The Jackson Laboratory using embryonic stem cells provided by the International Knockout Mouse Consortium. The Dnajb6 (DnaJ (Hsp40) homolog, subfamily B, member 6) gene encodes a molecular chaperone protein which has been shown to suppress aggregation and toxicity of aggregation-prone proteins. A beta-galactosidase-containing cassette disrupts the Dnajb6 gene in this strain. Phenotype data is being generated by the JAX KOMP2 program and will be available to the public when complete from the International Mouse Phenotyping Consortium website. For additional information on this mutation, please see the Regeneron Velocigene website.
019460 C57BL/6-Tg(DYRK1A)36Wjs/J
Under Development - Now Accepting Orders
The DYRK1A (dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 1a) gene is located in the "Down Syndrome critical region" of human chromosome 21. It is ubiquitously expressed in both fetal and adult tissues of humans and rodents, with strongest expression in the heart and brain. Expression of DYRK1A protein is increased in the brains of human patients with Down Syndrome and Alzheimer's Disease. Interacting with a number of biological pathways, the full function of this gene is still being elucidated.

These hemizygous mice carry a single copy of a bacterial artificial chromosome (BAC) clone that contains the complete human DYRK1A genomic fragment, including the endogenous promoter. No other genes are included in the BAC. Protein expression is elevated 1.5-2 fold.

Hemizygotes show a significant impairment in hippocampal-dependent memory tasks as well as alterations in two forms of synaptic plasticity. Proliferation of embryonic neuronal cells is i .....
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024990 STOCK Mecp2tm1.1Jtc/SchvJ
Under Development - Now Accepting Orders
The early truncating MeCP2R168X nonsense point mutation in the methyl-CpG binding domain of MeCP2 is one of the most common MeCP2 mutations associated with Rett syndrome (RTT). The largely truncated R168X protein retains the capacity to bind methylated DNA and carries a partial nuclear localization signal, but lacks the transcriptional repression domain for interaction with co-repressors. MeCP2R168X mice are a model of RTT; exhibiting respiratory, neuromuscular and behavioral abnormalities similar, but not identical, to that of Mecp2 null mice. The phenotype is described in detail below. These mice also underscore the importance of including Mecp2 mutant females in preclinical studies.

MeCP2R168X mice on a mixed genetic background of ~87-93% C57BL/6J and ~13-6% 129S6/SvEvTac (B6J;129S6.MeCP2R168X) are Stock No. 024990. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved t .....
For more information please see the full phenotype on the strain data sheet

024064 STOCK Ppp3catm1Jse/J
Under Development - Now Accepting Orders
Ppp3ca (protein phosphatase 3, catalytic subunit, alpha isoform) is a calcium- and calmodulin-dependent serine/threonine protein phosphatase. It is an important signaling molecule in T cells, neurons, the heart, and kidneys.

The catalytic domain of Ppp3ca has been disrupted in this knockout allele. Although the composition and distribution of T cell subsets is normal in homozygous knockout mice, and in vitro responses to mitogenic stimulation are similar to those of wildtype, the animals generate defective antigen-specific T cell responses in vivo.

Hyperphosphorylated tau, the major component of the helical filaments of Alzheimer's disease, accumulates in the brains of homozygous animals. This accumulation occurs particularly in the mossy fibers of the hippocampus, which contain the highest level of calcineurin in the brains of wildtype mice. The mossy fibers exhibit abnormalities in their cytoskeleton and a lower neurofilament/microtubule ratio .....
For more information please see the full phenotype on the strain data sheet

024854 STOCK Tg(Camk2a-tTA)1Mmay Tg(tetO-MAPT*P301L)#Kha/J
Under Development - Now Accepting Orders
Transgenic mice expressing the tetracycline-controlled transactivator protein (tTA) under regulatory control of the forebrain-specific calcium-calmodulin-dependent kinase II (Camk2a) promoter were crossed with tetO-MAPT*P301L transgenic mice containing a tetracycline operator (tetO) driving expression of the human four-repeat microtubule-associated protein tau (MAPT) gene. The resulting rTg(tauP301L)4510 bitransgenic mice expressing approximately 13 units of transgene exhibit age-independent behavioral and pathological abnormalities, as well as age-dependent functional and structural abnormalities, associated with the progression of Alzheimer's disease. After treatment with dox, neuronal death ceases and the ability to acquire and retain new spatial memories is restored. Learning and memory tests performed on rTg4510 mice indicate impairments in the hippocampus and amygdala dysfunction. In addition, significant tau burden is observed in the amygdala. The behavio .....
For more information please see the full phenotype on the strain data sheet
005987 129-Achetm1Loc/J
Cryopreserved - Ready for recovery
Homozygous mice have 25% fetal mortality. Those born have retarded growth, fine motor tremors, unusual posture and gait, no righting reflex, malformed pinna, and sealed eyelids. These mice die emaciated and dehydrated by 3 weeks of age. Enriched diets for the nursing female and pups allow homozygous mice to survive to adulthood. Males exhibit no breeding behavior. Homozygous females can become pregnant when bred to heterozygous or wildtype males, but both female and pups do not survive. Acetylcholinesterase (AChE) activity is completely abrogated in serum and tissue from homozygous mice, and approximately half in heterozygotes. Many symptoms of organophosphate poisoning are observed in homozygous mice, including pulsating paws, body tremor, abnormal gait, pinpoint pupils, muscle weakness, and early death following seizure. When restrained, a white mucus forms on the eyes and seizures may occur. Mice also have several developmental delays, low body mass, decreased pain response, sexual .....
For more information please see the full phenotype on the strain data sheet
012938 129-Prnptm2Edin/J
Cryopreserved - Ready for recovery
In this strain, exon 3 of the prion protein (Prnp) gene is replaced with a neomycin resistance (neo) cassette abolishing gene function. Mice homozygous for the Prnp1 allele are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Brains from homozygotes show impaired mitochondrial morphology, altered antioxidant enzyme activity, hypercorticism, and exhibit reduced SOD activity accompanied by increased signs of oxidative stress. These mice may be useful for studying the effect of prion proteins on neurodegeneration.
018925 129S(B6)-Vps26atm1Cos/J
Cryopreserved - Ready for recovery
Exon 2 of the vacuolar protein sorting 26 homolog A (Vps26a) gene was replaced with a neo cassette, abolishing gene function. Vps26a gene product, Hβ58, is expressed in the hippocampal formation as part of a large multimeric complex called the retromer complex. This complex is involved in protein trafficking from endosomes to the trans-Golgi network. Homozygotes display delayed development beginning at E7.5 and embryonic arrest at about E9.5. Heterozygous mice are viable and fertile, and develop hippocampal-dependent memory and synaptic dysfunction associated with elevations concentrations of Aβ peptide.
006409 129S1.129(Cg)-Tg(APPSw)40Btla/Mmjax
Cryopreserved - Ready for recovery
These R1.40 transgenic mice express all mRNA and protein isoforms of the human amyloid beta (A4) precursor protein APP containing the Familial Alzheimer's Disease (FAD) Swedish mutation K670N/M671L. Transgene expression (mRNA and full-length protein) is 2 to 3 fold the wild-type mouse App expression level in the hemizygous state in brain tissue as revealed by RT-PCR and Western Blot analysis. Transgene expression pattern mimics wild-type mouse gene expression patterns. 3 to 4 month old transgenic mice, maintained on a C57BL/6J background, exhibit spontaneous seizure-like events (abnormal spiking) in EEG readings, without abnormal behavior and are more susceptible to kainic acid induced seizures (Vogt et al. Neurobiol Aging 2009). These R1.40 transgenic mice may be useful in studying the pathogenesis of Familial Alzheimer's Disease and possible therapeutic treatments.

Of note, this is one of two 129S1/SvImJ congenic R1.40 transgenic strains (129S1-R1.40) segr .....
For more information please see the full phenotype on the strain data sheet

008077 129S1/Sv-Bchetm1Loc/J
Cryopreserved - Ready for recovery
Mice homozygous for this BChE mutant allele are viable and fertile with no reported spontaneous abnormalities. All tissues and plasma from homozygous mice are devoid of BChE activity. As BChE (butyrylcholinesterase) is a bioscavenger molecule protecting acetylcholinesterase (AChE) activity against nerve agents and organophosphates, homozygous BChE-deficiency leads to impaired protection from toxic compounds. These BChE mutant mice are a model for human butyrylcholinesterase deficiency and may be useful for studying metabolic effects of organophosphorus toxicants or nerve agents, neurotransmitter function, and anti-Alzheimer's drug therapies.

Of note, the donating investigator has multiple strains available that may be useful for testing toxic compounds, including the AChE-deficient (Stock No. 005987), G117H BChE transgenic (Stock No. 007577), and BChE-deficient (see Stock .....
For more information please see the full phenotype on the strain data sheet

014556 129S6/SvEv-Apoetm4Mae/J
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The Apoetm4Mae mutant allele was created using the same targeting vector used to generate the Apoetm1Unc mutant allele. Both alleles are functionally identical; replacing part of exon 3 and intron 3 with a neomycin resistance cassette and abolishing apoE expression. Mice homozygous for the apoE mutation (apoE-deficient mice) are viable and fertile, with defective lipoprotein metabolism. Compared to wildtype mice, apoE-deficient mice exhibit increased plasma cholesterol and triglyceride levels, along with spontaneous development of atherosclerotic plaques in the aortic root and aortic arch. Several strain-specific differences are reported between apoE-deficient mice coisogenic on a 129S6/SvEv genetic background (129S6-apoE-/-) and apoE-deficient mice congenic on a C57BL/6 genetic background (B6-apoE-/- ; see Stock No. 002052). Compared to B6-apoE-/- mice, 129S6-a .....
For more information please see the full phenotype on the strain data sheet
006555 A.129(B6)-Tg(APPSw)40Btla/Mmjax
Cryopreserved - Ready for recovery
These R1.40 transgenic mice express all mRNA and protein isoforms of the human amyloid beta (A4) precursor protein APP containing the Familial Alzheimer's Disease (FAD) Swedish mutation K670N/M671L. Transgene expression (mRNA and full-length protein) is 2 to 3 fold the endogenous mouse App expression level in the hemizygous state in brain tissue as revealed by RT-PCR and Western Blot analysis. Transgene expression pattern mimics endogenous mouse gene expression patterns. The donating investigator reports increased mortality in young homozygous animals (higher incidence in females). 3 to 4 month old transgenic mice, maintained on a C57BL/6J background, exhibit spontaneous seizure-like events (abnormal spiking) in EEG readings, without abnormal behavior and are more susceptible to kainic acid induced seizures (Vogt et al. Neurobiol Aging 2009). These R1.40 transgenic mice may be useful in studying the pathogenesis of Familial Alzheimer's Disease and possible therapeutic tr .....
For more information please see the full phenotype on the strain data sheet
018132 B6.129(Cg)-Itm2btm1Ldad/J
Cryopreserved - Ready for recovery
These BRI2f/f floxed mutant mice possess loxP sites flanking exon 2 of the targeted integral membrane protein 2B (Itm2b) gene. The accumulation of cleaved amyloid β-peptide (Aβ) precursor proteins (APP) form amyloid plaques in the brains of patients with familial dementias such as Alzheimers disease. BRI2 is a membrane protein which binds to APP. When over-expressed, BRI2 inhibits the accumulation of Aβ in vitro. Also, mutations in BRI2 are associated with familial British dementia (FBD) and familial Danish dementia (FDD). Homozygous BRI2f/f mice are viable and fertile. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 2 deleted in cre-expressing tissues, abolishing gene expression. BRI2 deficiency results in severe hippocampal memory deficits.
005708 B6.129-Apbb1tm1Quhu/J
Cryopreserved - Ready for recovery
Homozygous mice are viable and normal in size and display no physical or histopathologically demonstrable abnormalities. Homozygotes are fertile but poor breeders, while heterozygous mice have no breeding problems. The endogenous full-length 97 kDa protein (p97) is not expressed in brain tissue from homozygous mice. The 60 kDa (p60) N-terminal truncated isoform of the endogenous protein is expressed in mutant and wildtype brain tissue, with mutant mice exhibiting 4-5-fold greater levels. Homozygous null mice exhibit slower learning rates on both aversive and spatial memory tasks and severe impairments in spatial memory extinction during relearning. Heterozygotes have an intermediate phenotype, except with normal spatial memory extinction during relearning. Fibroblasts from null mice show diminished neprilysin activity and mRNA expression. This mouse may be useful in studies of Alzheimer's disease, beta-amyloid precursor protein metabolism, hippocampus-dependent learning and memory, cel .....
For more information please see the full phenotype on the strain data sheet
004098 B6.129-Klc1tm1Gsn/J
Cryopreserved - Ready for recovery
The donating investigator indicates that mice that are homozygous for the targeted allele on a C57BL/6 genetic background exhibit significant perinatal mortality (60%). Mortality seems not to be a factor on a mixed B6;129 background. Surviving mice are noticeably smaller than wildtype mice. Mice surviving to adulthood breed poorly, possibly due to less than adequate nurturing capabilities. Minor amounts of a functionless, truncated protein product can be detected. Motor defects are evident, as are alterations in intracellular localization of kinesin-I and COP-I components.
013536 B6.129-Mapk8ip1tm3.1Rjd/J
Cryopreserved - Ready for recovery
In this strain, codon 103 in exon 3 of the endogenous mitogen-activated protein kinase 8 interacting protein 1 (Mapk8ip1 or Jip1) gene was mutated from a Threonine (ACT) to an Alanine (GCC). Homozygous mice are viable, fertile, and normal in size. Jip1 is expressed in neurons, the β cells of pancreatic islets, lung, and kidney. The JIP group of scaffold proteins bind to c-Jun N-terminal kinase (JNK), mitogen-activated protein kinase (MAPK) kinase 7 (MKK7), and to members of the mixed lineage protein kinase (MLK) group, and is required for JNK activation. Phosphorylation of codon 103 is essential for JIP1 to activate JNK, which results in diet-induced obesity and insulin resistance. The loss of JIP1-mediated JNK activation in these JIP1TA mice results in increased insulin sensitivity and fat oxidation when fed a high fat diet (HFD). These mice also exhibit a decrease in hepatic glucose production, accumulation of hepatic lipids and trigly .....
For more information please see the full phenotype on the strain data sheet
004193 B6.129-Psen1tm1Mpm/J
Cryopreserved - Ready for recovery
The targeted allele (PS1M146VKI) causes a mutation of the mouse Psen1 gene that results in expression of a presenilin-1 protein with the human familial Alzheimer's disease-linked mutation PS1M146V. The neo cassette was deleted from the targeted allele (using a CMV-Cre transgenic line of mice). Published findings indicate that this alteration should not influence the level of expression of mutant PS1. Northern blot analysis and RT-PCR determined mRNA expression of the targeted mutant allele is normal. Homozygous PS1M146VKI mice produce only the mutant gene product. Mice that express this targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Neurodegeneration seen in wild-type mice caused by excitotoxin kainate treatment is increased and accelerated in this mutant strain. Cultured cells expressing the mutant protein exhibit perturbed neuronal calcium homeostasis. This mutant mouse strain represents a model that may b .....
For more information please see the full phenotype on the strain data sheet
003615 B6.129-Psen1tm1Shn/J
Cryopreserved - Ready for recovery
Presenilin-1 is the major gene responsible for early-onset familial Alzheimer's disease. Mice that are homozygous null for this gene die within minutes after being born. Externally, mice exhibit shortened tails that curve to the right, thickened necks, loose skin and hind limbs that curve towards the midline. Their weight is 15-20% that of wildtype. Gross skeletal malformations and central nervous system abnormalities are observed. Death presumably results from impaired respiratory mechanics due to ribcage deformities. Histological examination indicates that alveoli are marginally expanded. By embryonic day 9.5, there is a drastic reduction in neural progenitor cells. Later, the brain exhibits hemorrhages and symmetric cerebral cavitation. Cavitation occurs primarily in the ventrolateral region of the ventricular zone in the posterior portion of the brain.
005300 B6.129-Tg(APPSw)40Btla/Mmjax
Cryopreserved - Ready for recovery
These R1.40 transgenic mice express all mRNA and protein isoforms of the human amyloid beta (A4) precursor protein APP containing the Familial Alzheimer Disease (FAD) Swedish mutation K670N/M671L. Transgene expression (mRNA and full-length protein) is two to three fold the endogenous mouse App expression level in the hemizygous state in brain tissue as revealed by RT-PCR and Western Blot analysis. Transgene expression pattern mimics endogenous mouse gene expression patterns. Levels of the beta- secretase generated human APP derivative, C-terminal 13.5kDA fragment, are elevated in brain tissue. ELISA enzyme-linked immunosorbent assay (ELISA) analysis of brain homogenates show a significant increase in total amyloid-beta peptides and 42 amino acid length amyloid beta peptides. By 14 months of age, homozygous mice develop both parenchymal and vascular amyloid beta deposits, which first appear in the frontal cortex and then spread into the hippocampus. The donating investigat .....
For more information please see the full phenotype on the strain data sheet
005617 B6.129P-Psen2tm1Bdes/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by Northern or Western blot analysis. Alveolar wall thickening, fibrotic deposits, hemorahages in alveoli and airways are observed by histological analysis of lung tissue from homozygotes 3 months of age and older. This mutant mouse strain may be useful in studies of Alzheimer's disease.
007685 B6.129P2-Psen1tm1Vln/J
Cryopreserved - Ready for recovery
These mice possess loxP sites on either side of exon 7 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these "floxed" mice are bred to mice that express Cre recombinase, resulting offspring can have one of three resulting genotypes (only exon 7 deleted, only the neo selection cassette deleted, or both exon 7 and the neo selection cassette deleted) in the cre-expressing tissue(s). These PS1-floxed mice may be useful in generating conditional knockouts of Presenilin 1 for studying Alzheimer's Disease.

For example, when crossed to a strain expressing Cre recombinase in postnatal neurons (see Stock No. 006143), this mutant mouse strain may be useful in studies of amyloid plaque formation.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are .....
For more information please see the full phenotype on the strain data sheet

007999 B6.129P2-Sorl1Gt(Ex255)Byg/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the gene-trapped allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The gene trap contains the reporter gene beta-geo and has been inserted into exon 47. The donating investigator reports that one year old mutant mice exhibit a higher incidence of diffuse immunoreactive beta-amyloid deposits when compared to wildtype littermate controls. This mutant mouse strain may be useful in studies of Alzheimer's disease.
008087 B6.129S1-Bchetm1Loc/J
Cryopreserved - Ready for recovery
Mice homozygous for this BChE mutant allele are viable and fertile with no reported spontaneous abnormalities. All tissues and plasma from homozygous mice are devoid of BChE activity. As BChE (butyrylcholinesterase) is a bioscavenger molecule protecting acetylcholinesterase (AChE) activity against nerve agents and organophosphates, homozygous BChE-deficiency leads to impaired protection from toxic compounds. These BChE mutant mice are a model for human butyrylcholinesterase deficiency and may be useful for studying metabolic effects of organophosphorus toxicants or nerve agents, neurotransmitter function, and anti-Alzheimer's drug therapies.

Of note, the donating investigator has multiple strains available that may be useful for testing toxic compounds, including the AChE-deficient (Stock No. 005987), G117H BChE transgenic (Stock No. 007577), and BChE-deficient (see Stock .....
For more information please see the full phenotype on the strain data sheet

002509 B6.129S2-Plautm1Mlg/J
Cryopreserved - Ready for recovery
Homozygotes develop normally, have a normal life span, and are poor breeders. Pups often need fostering. Rectal prolapse of a non-infectious origin develops in 9% of homozygotes and/or extensive non-healing ulcerations occur at the eyelids and around the face. Small, focal fibrin deposits are occasionally seen in the intestines and in the sinusoids of the liver, and excessive fibrin deposits are seen in ulcerated skin or prolapsed rectum. Pulmonary clot lysis is comparable to that seen in normal wildtype siblings. Endotoxin induced venous thrombosis is increased over normal wildtype siblings. Fibrin dissolution by PLAU-deficient macrophages is greatly reduced but macrophage invasion into the peritoneal cavity after thioglycollate injection is unaffected. Homozygous knockout mice have increased levels of Abeta42 and Abeta40 in plasma. Brain Abeta levels are not significantly different than controls. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, .....
For more information please see the full phenotype on the strain data sheet
005301 B6.129S2-Tg(APP)8.9Btla/J
Cryopreserved - Ready for recovery
These transgenic mice express all mRNA and protein isoforms of the wild-type human amyloid beta (A4) precursor protein, APP. The transgene expression level is equivalent to the level of endogenous mouse amyloid beta (A4) precursor protein (in the homozygous state). The expression pattern of the various protein isoforms of human APP mimics endogenous mouse gene expression patterns. These mice serve as a model for dosage imbalance for APP that occurs in Down syndrome and also provide a unique model to examine the regulation of APP isoforms, APP processing and amyloid beta metabolism and regulation.
004163 B6.129S4-Cdk5r1tm1Lht/J
Cryopreserved - Ready for recovery
At birth, mice homozygous for this targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Cdk5r protein product is not immunodetectable in homozygote whole-brain lysates. Histological analysis of homozygotes reveals severe defects in the patterning of the cerebral cortex and other areas of the brain. The normal lamination pattern of cortical neurons is disrupted; axonal trajectories and dendritic structures are altered. Homozygous mice are more susceptible to mortality from chemically induced-seizures. Sporadic adult lethality is also observed, presumably resulting from spontaneous seizures, a consequence of the disrupted cytoarchitecture observed in the cortex. This mutant mouse strain represents a model that may be useful in studies related to the mechanisms of cortical lamination, epilepsy, Alzheimer's and other neurodegenerative diseases.
010959 B6.129S4-Grk5tm1Rjl/J
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Grk5 (G protein-coupled receptor kinase 5) targeted mutant mice exhibit supersensitivity (lost desensitization) of brain and lung airway M2 muscarinic receptors. Aged homozygotes develop amyloid-like plaques and exhibit some cognitive defects. Although the gene is normally expressed in heart and lymphocytes, cardiac M2 muscarinic receptor function and lymphocyte chemotaxis in response to SDF-1 are normal. Homozygotes are viable and present no gross anatomical differences nor striking behavioral abnormalities. Western blot analysis demonstrates a loss of expression in brain, lymphocytes, lung and heart.
010960 B6.129S4-Grk5tm2Rjl/J
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These mice possess loxP sites on either side of exons 7 and 8 of Grk5 (G protein-coupled receptor kinase 5). Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice with a cre recombinase gene, exons 7 and 8 of the targeted gene are deleted in the cre-expressing tissues in the offspring mice. The floxed allele appears to be fully functional and expresses normal levels of GRK5 protein.

When bred to B6.FVB-Tg(Myh6-cre)2182Mds/J mice (Stock No. 011038) expressing Cre recombinase in cardiac muscle cells, offspring exhibit protection from cardiac hypertrophy following transverse aortic constriction.

004825 B6.129S4-Psen1tm2Shn/J
Cryopreserved - Ready for recovery
These mice possess loxP sites on either side of exons 2 and 3 of the targeted gene. Mice that are homozygous for this allele are viable and fertile. Northern blot and RT-PCR analysis of brain tissue from homozygotes reveal gene product (mRNA) transcription levels and size are the same as wildtype. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 2 and 3 deleted in the cre-expressing tissues.
006406 B6.129S4-Tg(APPSwLon)96Btla/Mmjax
Cryopreserved - Ready for recovery
Mice hemizygous for this "K670N/M671L + V717I" mutant APP YAC transgene are viable and fertile. RT-PCR analysis shows hemizygous mice express the mutant human APP mRNA at levels similar to endogenous mouse in brain and peripheral tissues. Further, transcript levels of the most common alternative splice variants (encoding human APP-695, -751 and -770) parallel the endogenous mouse gene expression. The levels of total amyloid-beta and longer amyloid-beta peptides (species terminating at amino acids 42/43) are elevated compared to wild-type mice, but not to the extent as observed in a similar strain carrying only the APP (K670N/M671L) mutant transgene (B6.129-Tg(APPSw)40Btla/Mmjax). These mice may be useful in studies of the pathogenesis of Familial Alzheimer's Disease, specifically focusing on the importance of processing at the gamma-secretase site to elevate levels of amyloid-beta 1-42(43).
006469 B6.129S4-Tg(PSEN1H163R)G9Btla/J
Cryopreserved - Ready for recovery
Mice hemizygous for this "H163R mutant PSEN1 YAC" transgene are viable and fertile, while the donating investigator reports that homozygous mice are non-viable. Semi-quantitative RT-PCR of multiple tissues shows expression of H163R mutant human PSEN1 at levels comparable to that of wildtype mouse PSEN1 (50–70%). In contrast to other PSEN1 transgenic models, tissues from this strain express alternatively spliced human PSEN1 transcripts encoding PSEN1 protein (with or without the tetrapeptide VRSQ) and accumulated an 18-kDa PSEN1 C-terminal fragment as shown by western blots, thus expressing a wide spectrum of different human PSEN1 mRNAs and proteins. When crossed to other FAD transgenic strains (for example Stock No. 005300), this transgene is associated with elevated levels of the 42 amino acid form of amyloid-beta (1–42) in both brain and plasma. These mice may be useful in studying neurological disorders such as Familial Alzheimer’s Disease and Down syndrome.
012564 B6.129S5-Dhcr24tm1Lex/SbpaJ
Cryopreserved - Ready for recovery
Homozygous mice on the C57BL/6 genetic background die within the first postnatal day with features of lethal restrictive dermopathy; including taut, wrinkle-free, shiny skin, severe defects in epidermal maturation/epidermal barrier function (impaired epidermal development), and increased presence of hyperproliferative immature keratinocytes (defective keratinocyte differentiation). The increased transepidermal water loss/increased epidermal water content is associated with increased aquaporin-3 (AQP3) expression throughout the epidermis. Mice heterozygous for this allele are viable and fertile, with no overt phenotype. As the Dhcr24 protein functions to catalyze the last step of cholesterol biosynthesis (the conversion of desmosterol to cholesterol), homozygous disruption of this locus results in desmosterolosis: almost no cholesterol in plasma and tissues with ~99% of total sterols in the form of desmosterol. lacZ expression from the mutant allele is not characterized. <> .....
For more information please see the full phenotype on the strain data sheet
021145 B6.129S6-Bin1tm2Gcp/J
Cryopreserved - Ready for recovery
These Bin1flox mice possess loxP sites flanking exon 3 of the bridging integrator 1 (Bin1) gene. BIN1 is a nucleocytoplasmic adaptor protein, involved in phagocytosis, apoptosis, and synaptic vesicle endocytosis. BIN1 has been implicated in the development of cardiac defects and Alzheimer's disease and has been shown to attenuate many types of cancer. Homozygotes are viable and fertile. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 3 deleted in cre-expressing tissues. Widespread deletion results in perinatal lethality due to ventricular cardiomyopathy.

When crossed to B6129-Tg(Wap-cre)11738Mam/J mice (Stock No. 003552) expressing Cre recombinase in mammary gland tissues, no long term increase in breast cancer incidence was observed in either virgin or parous animals, however, initiation with the Ras-activating carcinogen DMBA .....
For more information please see the full phenotype on the strain data sheet

013535 B6.129S6-Mapk8ip1tm1Rjd/J
Cryopreserved - Ready for recovery
In this strain, a neomycin resistance cassette replaces exon 3 of the endogenous mitogen-activated protein kinase 8 interacting protein 1 (Mapk8ip1 or Jip1) gene. Homozygous mice are viable, fertile and normal in size. Jip1 is normally expressed in neurons, the β cells of pancreatic islets, lung, and kidney. JIP1 protein also accumulates in the perinuclear region of hippocampal neurons following exposure to stress. The JIP group of scaffold proteins bind to c-Jun N-terminal kinase (JNK), mitogen-activated protein kinase (MAPK) kinase 7 (MKK7), and to members of the mixed lineage protein kinase (MLK) group, and is required for stress induced activation of JNK in hippocampal neurons. The JNK signaling pathways are involved in the regulation of cellular proliferation, transformation, and apoptosis, and has been implicated in some neurodegenerative diseases, diabetes, and arthritis. JIP1 activation of JNK also leads to diet-induced obesity and insulin resistan .....
For more information please see the full phenotype on the strain data sheet
004142 B6.129S7-Aplp2tm1Dbo/J
Cryopreserved - Ready for recovery
Mice that are homozygous null for the Aplp2 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Aplp2 gene product (mRNA or protein) is detected. This strain may be useful in studies related to Alzheimer's Disease, especially if used in conjunction with other mutant mouse strains (see B6.129S7-Apptm1Dbo, Stock No. 004133).
005642 B6.Cg-Clutm1Jakh/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the targeted mutation are viable, fertile, normal in size, and do not display any behavioral abnormalities. No protein is detected in serum, liver, or brain and in situ hybridization shows no mRNA in heart. This mutant has been studied for different functions on different backgrounds. On the Swiss Black outbred background, aging homozygous mutant mice develop a progressive glomerulopathy characterized by deposition of tubulo-fibrillary immune complexes devoid of inflammation or necrosis. On the FVB/N background, homozygous null mice with chemically induced autoimmune myocarditis show severe and diffuse lesions with postinflammatory functional impairment. Induced skin carcinogenesis is more severe than wildtype. On the C57BL/6 background, homozygotes given a hypoxia-ischemia brain injury (modeling cerebral palsy) had 50% less brain injury compared to wild type. Conversely, mutants have less neuroprotective properties after permanent focal cerebral isc .....
For more information please see the full phenotype on the strain data sheet
018282 B6.Cg-Mapttm1(Mecp2)Jae/LimmJ
Cryopreserved - Ready for recovery
The Tau-MeCP2 knockin mutation places the mouse MeCP2 cDNA sequence into exon 1 of the tau gene, in-frame with the endogenous tau start codon. Under control of the endogenous tau promoter/enhancer sequences, expression of the Tau-MeCP2 fusion protein (containing the first 31 amino acids of tau fused to the MeCP2 protein) is high in lung and kidney, low in heart, and very low in liver and spleen. Endogenous tau expression is abolished in the Tau-MeCP2 knockin allele. The axonal localization signal of tau is located in the 3' UTR, and therefore is not part of the Tau-MeCP2 mRNA. The onset of fusion protein expression correlates closely with endogenous tau expression (first detectable at 10.5 days post coitum [dpc]). While the amount of Mecp2 RNA is similar to Tau-MeCP2 RNA in heterozygous Tau-MeCP2 mice embryos and adult brain, the fusion protein expression level is approximately two-to-four times more abundant; suggesting a difference in either translation efficiency of the trans .....
For more information please see the full phenotype on the strain data sheet
017326 B6.Cg-Mapttm1Hnd Tg(MAPT)1Gds/Mmjax
Cryopreserved - Ready for recovery
Homozygotes/Hemizygotes: Mice that are homozygous for the targeted mutation and hemizygous for the transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These double mutant mice produce normal human tau (MAPT), while no endogenous mouse tau (Mapt) is produced. The ht-PAC-N transgenic mouse expresses all 6 human tau isoforms by P24 with the 3 repeat (3R)-tau predominant to the 4 repeat (4R) -tau ratio. This strain serves as a control for human tau mutations associated with frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP 17). No gross or microscopic pathologic lesions were observed in these mice. This mutant mouse strain may be useful in studies of tau isoforms in neurodegenerative disease.

Heterozygote: Not evaluated.

015852 B6.Cg-Mapttm1Hnd Tg(MAPT*S305S)4Gds/Mmjax
Cryopreserved - Ready for recovery
Homozygotes/Hemizygotes: Mice that are homozygous for the targeted mutation and hemizygous for the transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These double mutant mice produce mutated human tau (MAPT), while no endogenous mouse tau (Mapt) is produced. The ht-PAC-305S transgenic mouse expresses all 6 human tau isoforms with a 3 repeat (3R)-tau to 4 repeat (4R) -tau ratio of approximately 80% 4R-tau to 20% 3R-tau rather than the expected human ratio of 1:1. S305S is associated with frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP 17) and is believed to increase exon 10 inclusion during splicing by strengthening the weak exon 10 5' splice site. No gross or microscopic pathologic lesions were observed in these mice. This mutant mouse strain may be useful in studies of tau isoforms in neurodegenerative disease.

Heterozygote: Not evaluated.

017459 B6.Cg-Mapttm1Hnd Tg(MAPT*)1Gds/Mmjax
Cryopreserved - Ready for recovery
Homozygotes/Hemizygotes: Mice that are homozygous for the targeted mutation and hemizygous for the transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These double mutant mice produce mutated human tau (MAPT), while no endogenous mouse tau (Mapt) is produced. The ht-PAC-E10+14 transgenic mouse expresses all 6 human tau isoforms, however, the predominant isoform is changed from 3 repeat (3R) to 4 repeat (4R). E10+14 is associated with frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP 17) and is believed to increase exon 10 inclusion during splicing by weakening an intron splicing silencer. No gross or microscopic pathologic lesions were observed in these mice. This mutant mouse strain may be useful in studies of tau isoforms in neurodegenerative disease.
017545 B6.Cg-Mapttm1Hnd Tg(MAPT*V337M)1Gds/Mmjax
Cryopreserved - Ready for recovery
Homozygotes/Hemizygotes: Mice that are homozygous for the targeted mutation and hemizygous for the transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These double mutant mice produce mutated human tau (MAPT), while no endogenous mouse tau (Mapt) is produced. The ht-PAC-377M transgenic mouse expresses all 6 human tau isoforms with 3 repeat (3R)-tau as the predominant isoform and 4 repeat (4R) -tau as the second most abundant isoform. Mutations in MAPT are associated with frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP 17). Unlike several of the other ht-PAC mutations, 377M does not influence exon 10 expression. Unpublished data suggests that these mice have behavioral deficits and oxidative damage in the brain. This mutant mouse strain may be useful in studies of tau isoforms in neurodegenerative disease.
017797 B6.Cg-Mapttm1Hnd Tg(Thy1-MAPT*)3608Gds/Mmjax
Cryopreserved - Ready for recovery
These double mutant mice produce human tau (MAPT) truncated at amino acid E391 and no endogenous mouse tau (Mapt). The low expressing E391-3608 transgenic mouse expresses the most abundant tau isoform found in the adult human brain, 4R1N, at 2.6 fold higher than normal endogenous mouse tau. Proteolytic cleavage of tau at the C-terminus is associated with neurofibrillary tangles and abnormal neurites in Alzheimer Disease. The E391 mutant tau exhibits the pathologic phenotype - conformational change or hyperphosphorylation - in the superficial granule cells, cingulate gyrus, amygdala, and entorhinal cortex and to a lesser extent in the CA1 neuronal soma and apical dendrites. E391-3608 mice exhibit irregularly shaped pyramidal neurons with thickened dendrites in the cortex, and atypical dystrophic neurites in the cingulate gyrus. Despite the existence of "pretangle" tau pathology, mice do not develop late-stage neurofibrillary tangles. This mutant mouse strain may be usefu .....
For more information please see the full phenotype on the strain data sheet
017798 B6.Cg-Mapttm1Hnd Tg(Thy1-MAPT*)3610Gds/Mmjax
Cryopreserved - Ready for recovery
These double mutant mice produce human tau (MAPT) truncated at amino acid E391 and no endogenous mouse tau (Mapt). The high expressing E391-3610 transgenic mouse expresses the most abundant tau isoform found in the adult human brain, 4R1N, at 2.6 fold higher than normal endogenous mouse tau. Proteolytic cleavage of tau at the C-terminus is associated with neurofibrillary tangles and abnormal neurites in Alzheimer Disease. The E391 mutant tau exhibits the pathologic phenotype - conformational change or hyperphosphorylation - in the inner dentate molecular layer, CA1 neuronal soma and apical dendrites and cingulate gyrus neuropil. Despite the existence of "pretangle" tau pathology, mice do not develop late-stage neurofibrillary tangles. This mutant mouse strain may be useful in studies of tau in neurodegenerative disease.
009126 B6.Cg-Nos2tm1Lau Tg(Thy1-APPSwDutIowa)BWevn/Mmjax
Cryopreserved - Ready for recovery
These APPSwDI/NOS2 bigenic mice harbor the APPSwDI transgene and a targeted "null" mutation of the nitric oxide synthase 2 (Nos2) locus. Expression of the APPSwDI transgene (a neuronally derived human amyloid beta-precursor protein [APP or AβPP] 770 isoform containing three Alzheimer's disease-associated mutations [Swedish K670N/M671L, Dutch E693Q and Iowa D694N] all under the control of the mouse thymus cell antigen 1, theta [Thy1] promoter) produces amyloid-beta (Aβ) peptides that cannot be transported out of the brain across the cerebrovascular interface and results in Aβ peptide accumulation at the blood vessels (see C57BL/6-Tg(Thy1-APPSwDutIowa)BWevn/Mmjax). The Nos2 mutation results in loss of inducible NOS (iNOS) expression which alters physiological functions related to disease and injury (see B6.129P2-Nos2tm1Lau/J). Homozygous bigenic mice (APPSwDI/NOS2-/-) progress from Abeta; production and amyloid depos .....
For more information please see the full phenotype on the strain data sheet
004684 B6.Cg-chtl Nos2tm1Lau/GrsrJ
Cryopreserved - Ready for recovery
This mutant has an overall lighter coat, tail and ears than a black +/+ control. Both males and females breed and it is maintained as a homozygous stock.
007575 B6.Cg-Tg(CAG-Ngb,-EGFP)1Dgrn/J
Cryopreserved - Ready for recovery
These transgenic mice express mouse neuroglobin and Enhanced Green Fluorescent Protein under the direction of the chicken beta actin promoter coupled with the cytomegalovirus (CMV) distal enhancer. Western blot analysis detects increased NGB protein in heart brain of homozygotes. Transgenic mice have NGB-overexpressing neurons, astrocytes and endothelial cells in the cerebral cortex. The donating investigator reports that fluorescence is detected in all tissues. Experimentally induced ischemia in transgenic mice results in cerebral infarct volume reduction of approximately 30% and myocardial infarct volume reduction of approximately 25% when compared to wild-type. Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of cerebral (CNS) and myocardial ischemia and stroke.

In an attempt to offer alleles on well-characterized or multiple genetic .....
For more information please see the full phenotype on the strain data sheet

005855 B6.Cg-Tg(Camk2a-Prkaca)426Tabe/J
Cryopreserved - Ready for recovery
Mice hemizygous for the transgene are viable and fertile with no gross anatomical abnormalities or structural lesions within the hippocampus or other regions. Transgene expression is observed in hippocampus (CA1, CA3, and dentate gyrus), neocortex, olfactory bulb, striatum, and amygdala. Transgenic mice have a 50% reduction in basal cAMP-dependent protein kinase A (PKA or PRKACA) activity, defective protein synthesis-dependent late phase of long-term potentiation, and reduced place cell stability in hippocampus. Mice have defective long-term, but not short-term, memory in hippocampus-based spatial and non-spatial tasks. This parallels the phenotype observed in mice treated with inhibitors of PKA or inhibitors of protein synthesis. Functional magnetic resonance imaging reveals reduced CA1 hippocampal signal. Transgenic mice are more sensitive to ethanol-induced sedation. Mice expressing this transgene may be useful in a wide variety of memory studies, including Alzheimer's disease, hipp .....
For more information please see the full phenotype on the strain data sheet
004996 B6.Cg-Tg(DBH-Gal)1923Stei/J
Cryopreserved - Ready for recovery
These transgenic mice overexpress the mouse galanin protein under the direction of the human dopamine beta-hydroxylase promoter. Mice that are homozygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. In situ hybridization analysis of brain detects a 5-fold increase in galanin mRNA levels in the locus coeruleus region. Radioimmunoassay reveals a 2-fold increase in gene product peptide level in the forebrain. An increase of galanin-like immunoreactive staining and fiber density is also detected. The number of basal forebrain cholinergic neurons is decreased. Transgenic mice have impaired learning and memory as assessed by the Morris spatial navigational test and the social transmission of food preference test. Resistance to seizures induced by perforant path stimulation or administration of kainic acid is increased. Mutant mice exhibit increased afterdischarge (AD) induction threshold and diminished glutamate release after .....
For more information please see the full phenotype on the strain data sheet
004632 B6.Cg-Tg(GFAP-APOE_i2)14Hol Apoetm1Unc/J
Cryopreserved - Ready for recovery
These transgenic mice express the human apolipoprotein E2 isoform (APOE2) under the direction of the human glial fibrillary acidic protein (GFAP) promoter and do not express endogenous mouse apolipoprotein E (APOE). The transgenic isoform expression pattern follows the endogenous mouse APOE and GFAP expression patterns in the brain. Human APOE2 is immunodetectable in glia and neuropil in developing and adult mutant mice. Cultured astrocytes from transgenic mice secrete APOE2 in lipoproteins that are similar in size to high-density (HDL) plasma lipoproteins. Detergent-soluble APOE2 protein levels in hemizygous mice forebrain tissue and in adult human cortex tissue are similar. Mice that are hemizygous or homozygous for the transgenic insert and homozygous for the targeted allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain represents a model that may be useful in studies examining the function of APOE2 in t .....
For more information please see the full phenotype on the strain data sheet
004633 B6.Cg-Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/J
Cryopreserved - Ready for recovery
These transgenic mice express the human apolipoprotein E3 isoform (APOE3) under the direction of the human glial fibrillary acidic protein (GFAP) promoter and do not express endogenous mouse apolipoprotein E (APOE). The transgenic isoform expression pattern follows the endogenous mouse APOE and GFAP expression patterns in the brain. Human APOE3 is immunodetectable in glia and neuropil in developing and adult mutant mice. Cultured astrocytes from transgenic mice secrete APOE3 in lipoproteins that are similar in size to high-density (HDL) plasma lipoproteins. Detergent-soluble APOE3 protein levels in hemizygous mice forebrain tissue and in adult human cortex tissue are similar. Mice that are hemizygous or homozygous for the transgenic insert and homozygous for the targeted allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain represents a model that may be useful in studies examining the function of APOE3 in t .....
For more information please see the full phenotype on the strain data sheet
007673 B6.Cg-Tg(Gad1-EGFP)3Gfng/J
Cryopreserved - Ready for recovery
Mice hemizygous for this GAD67-GFP transgene are viable and fertile. In the hippocampus, GAD67-GFP (line 3) mice selectively express enhanced green fluorescent protein (EGFP) in newborn dentate granule cells. At two weeks of age, EGFP is expressed in large numbers of dentate granule cells, and the number of EGFP-positive cells diminishes with age in a pattern consistent with the postnatal development of dentate granule cells/age-related reduction in adult neurogenesis in the dentate gyrus. The EGFP expression in newborn dentate granule cells begins within the first week of cell division and disappears as newborn neurons mature (about 4 weeks postmitotic), and EGFP positive dentate granule cells also express the newborn neuron markers PSA-NCAM and doublecortin. The bright labeling of newborn neurons with EGFP makes it possible to visualize the details of dendrites, which reach the outer edge of the molecular layer, and their axon terminals (mossy fiber boutons) in the CA3 region. In ad .....
For more information please see the full phenotype on the strain data sheet
008323 B6.Cg-Tg(Mc4r-MAPT/Sapphire)21Rck/J
Cryopreserved - Ready for recovery
These mice express a tau (MAPT)-sapphire green fluorescent protein (GFP) under the transcriptional control of the mouse melanocortin 4 receptor (Mc4r) promoter. Central nervous system distribution of GFP-producing cells is identical to that of Mc4r mRNA in wild-type mice and nearly all GFP-producing cells coexpress melanocortin 4 mRNA. This strain may be useful in studying the role of melanocortin signaling in the regulation of feeding behavior and autonomic homeostasis. Hemizygotes are viable and fertile and do not display any gross physical or behavioral abnormalities.
008321 B6.Cg-Tg(Npy-MAPT/Sapphire)1Rck/J
Cryopreserved - Ready for recovery
These mice express a tau (MAPT)-sapphire green fluorescent protein (GFP) under the transcriptional control of the mouse neuropeptide Y (Npy) promoter. Immunohistochemistry for NPY in colchicine-treated animals demonstrated ~95% colocalization of NPY with the GFP-expressing neurons in the hypothalamic arcuate nucleus. This strain has been useful in studying the role of neuropeptide Y and leptin in food intake. Hemizygotes are viable and fertile and do not display any gross physical or behavioral abnormalities.
004662 B6.Cg-Tg(PDGFB-APP)5Lms/J
Cryopreserved - Ready for recovery
These transgenic mice express a wildtype human amyloid protein precursor (APP) under the control of the human platelet-derived growth factor beta polypeptide (PDGFB) promoter. PCR primer modification was used to alter the sequence of the APPInd mutation to the wildtype sequence in this transgene. Hemizygotes express immunodetectable transgene product in cerebral neurons, with the highest level of expression occurring in the neocortex and hippocampus. Enzyme-linked immunosorbent assay (ELISA) analysis of neocortical and hippocampal tissue reveals approximate total amyloid beta peptides levels and 42 amino acid length amyloid beta peptides levels that are lower than levels found in the APP SwInd mutant line. No amyloid plaques are detected by immunohistochemistry at 8-10 months of age or at 24 months of age. Mutants display age dependent decrease in density of synaptophysin-immunoreactive presynaptic terminals indicative of neurodegeneration. This strain serves as the control for Stock N .....
For more information please see the full phenotype on the strain data sheet
018923 B6.Cg-Tg(PDGFB-MAPT*P301S)77Elan/J
Cryopreserved - Ready for recovery
These mice carry a transgene containing the human P301S mutant microtubule-associated protein tau, MAPT, under the direction of the human platelet-derived growth factor beta (PDGFB) promoter. The Donating Investigator reports that hemizygotes are viable and fertile and that there is no phenotype.
008324 B6.Cg-Tg(Pmch-MAPT/CFP)1Rck/J
Cryopreserved - Ready for recovery
These mice express a tau (MAPT)-cyan fluorescent protein (CFP) under the transcriptional control of the mouse pro-melanin-concentrating hormone (Pmch) promoter. Neurons expressing PMCH can be easily identified in the brain. Hemizygotes are viable and fertile and do not display any gross physical or behavioral abnormalities.
008322 B6.Cg-Tg(Pomc-MAPT/Topaz)1Rck/J
Cryopreserved - Ready for recovery
These mice express a tau (MAPT)-sapphire green fluorescent protein (GFP) under the transcriptional control of the mouse pro-opiomelanocortin-alpha (Pomc) promoter. Immunohistochemistry for POMC in colchicine-treated animals demonstrated greater than 99% colocalization of POMC with the GFP-expressing neurons in the hypothalamic arcuate nucleus. This strain has been useful in studying the role of Pomc and leptin in food intake and may be useful in further understanding the function of the associated neurons. Hemizygotes are viable and fertile and do not display any gross physical or behavioral abnormalities.
006006 B6.Cg-Tg(Prnp-APP)A-2Dbo/J
Cryopreserved - Ready for recovery
These transgenic mice express the human amyloid precursor protein (APP) under the control of the mouse prion protein promoter. Mice that are hemizygous for the transgene are viable and fertile. This mutant mouse strain may be useful in studies of Alzheimer's Disease.
006005 B6.Cg-Tg(Prnp-App/APPswe)E1-2Dbo/Mmjax
Cryopreserved - Ready for recovery
These transgenic mice express a chimeric mouse/human amyloid precursor protein (APPswe) under the control of the mouse prion protein promoter. Mice that are hemizygous for the transgene are viable and fertile. More than half of the female hemizygous mice do not survive past 15 months of age. This mutant mouse strain may be useful in studies of Alzheimer's Disease.
007180 B6.Cg-Tg(Prnp-ITM2B/APP695*40)1Emcg/J
Cryopreserved - Ready for recovery
Mice hemizygous for this BRI-Abeta40 transgene are viable and fertile with a normal lifespan and no obvious behavioral abnormalities. Transgenic BRI-Abeta mRNA is expressed in a pattern characteristic of the mouse prion protein promoter; with highest expression in the cerebellar granule cells and hippocampus, followed by the cortex, pons, thalamus, and midbrain. The BRI-Abeta40 fusion protein takes advantage of the BRI protein that is normally cleaved by furin or a furin-like protease near the COOH-terminus (releasing a soluble 23 amino acid peptide in the wildtype BRI protein). As Abeta1-40 is fused to the C terminus of the BRI protein at the furin cleavage site, cleavage releases Abeta into the lumen or extracellular space, resulting in efficient secretion of Abeta1-40. Therefore, these mice specifically express the Abeta1-40 isoform in the absence of human amyloid beta protein precursor (APP) overexpression. In contrast to the BRI-Abeta42 strain (Stock No. For more information please see the full phenotype on the strain data sheet
007182 B6.Cg-Tg(Prnp-ITM2B/APP695*42)A12Emcg/J
Cryopreserved - Ready for recovery
Mice hemizygous for this BRI-Abeta42 transgene are viable and fertile with a normal lifespan and no obvious behavioral abnormalities. Transgenic BRI-Abeta42 mRNA is expressed in a pattern characteristic of the mouse prion protein promoter; with highest expression in the cerebellar granule cells and hippocampus, followed by the cortex, pons, thalamus, and midbrain. The BRI-Abeta42 fusion protein takes advantage of the BRI protein that is normally cleaved by furin or a furin-like protease near the COOH-terminus (releasing a soluble 23 amino acid peptide in the wild-type BRI protein). As Abeta1-42 is fused to the C terminus of the BRI protein at the furin-like cleavage site, cleavage releases Abeta into the lumen or extracellular space, resulting in efficient secretion of Abeta1-42. Therefore, these mice specifically express the Abeta1-42 isoform in the absence of human amyloid beta protein precursor (APP) overexpression. In contrast to the BRI-Abeta40 strain (Stock No. For more information please see the full phenotype on the strain data sheet
012597 B6.Cg-Tg(Thy1-COL25A1)861Yfu/J
Cryopreserved - Ready for recovery
Mice hemizygous for the Thy1-COL25A1 allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Collagen XXV alpha 1 (COL25A1), also known as collagen-like Alzheimer's amyloid plaque component precursor, is a type II transmembrane protein expressed in neurons that colocalizes with Amyloid β (Aβ) in senile plaques in the brains of Alzheimer's patients. In the Thy1-COL25A1 mouse, overexpression of human COL25A1 is regulated by a murine Thy1.2 promoter (Thy1), which leads to expression in the cortex and the hippocampus. This overexpression results in accumulation of Aβ and increased levels of p35/p25 and β-site APP-cleaving enzyme 1 (BACE1), which may induce synaptic dysfunction leading to the behavioral changes associated with Alzheimer's Disease. COL25A1 precursor is expressed in cell membranes of cortical neurons, in 2 month old mice. At 6 months, COL25A1 precursor was expressed in t .....
For more information please see the full phenotype on the strain data sheet
007051 B6.Cg-Tg(tetO-APPSwInd)102Dbo/Mmjax
Cryopreserved - Ready for recovery
Hemizygotes for this tetO-APPswe/ind transgene are viable and fertile. These transgenic mice express a chimeric mouse/human amyloid precursor protein (APP695) bearing the Swedish (KM570/571NL) and Indiana (V617F) mutations associated with Alzheimer's disease (APP695swe/ind) under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the control of a tissue-specific promoter, APP695swe/ind expression in the appropriate tissues of the bitransgenic offspring can be regulated with the tetracycline analog doxycycline (dox). These tetO-APPswe/ind transgenic mice may be useful in studies of Alzheimer's disease and other neurodegenerative diseases.

For example, when bred to a strain expressing tTA in brain tissues (Tg(Camk2a-tTA)1Mmay), bi-transgenic offspring show 10-30 fold grea .....
For more information please see the full phenotype on the strain data sheet

007052 B6.Cg-Tg(tetO-APPSwInd)107Dbo/Mmjax
Cryopreserved - Ready for recovery
Hemizygotes for this tetO-APPswe/ind transgene are viable and fertile. These transgenic mice express a chimeric mouse/human amyloid precursor protein (APP695) bearing the Swedish (KM570/571NL) and Indiana (V617F) mutations associated with Alzheimer's disease (APP695swe/ind) under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of a tissue-specific promoter, APP695swe/ind expression in the target tissue of the bitransgenic offspring can be regulated with the tetracycline analog doxycycline (dox) in the resulting double mutant offspring. These tetO-APPswe/ind transgenic mice may be useful in studies of Alzheimer's disease and other neurodegenerative diseases.

For example, when bred to a strain expressing tTA in brain tissues (Tg(Camk2a-tTA)1Mmay), bi- .....
For more information please see the full phenotype on the strain data sheet

007049 B6.Cg-Tg(tetO-APPSwInd)885Dbo/Mmjax
Cryopreserved - Ready for recovery
Hemizygotes for this tetO-APPswe/ind transgene are viable and fertile. These transgenic mice express a chimeric mouse/human amyloid precursor protein (APP695) bearing the Swedish (KM570/571NL) and Indiana (V617F) mutations associated with Alzheimer's disease (APP695swe/ind) under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of a tissue-specific promoter, APP695swe/ind expression can be regulated in the appropriate tissue of the bitransgenic offspring with the tetracycline analog doxycycline (dox). These tetO-APPswe/ind transgenic mice may be useful in studies of Alzheimer's disease and other neurodegenerative diseases.

For example, when bred to a strain expressing tTA in brain tissues (Tg(Camk2a-tTA)1Mmay), bi-transgenic offspring show 10-30 fold .....
For more information please see the full phenotype on the strain data sheet

009337 B6.FVB-Tg(Prnp-RTN3)2Yanr/J
Cryopreserved - Ready for recovery
Mice hemizygous for the hRTN3 transgene are viable and fertile, with C-terminally myc-tagged human reticulon 3 (RTN3) expression directed to neurons by the mouse prion protein (PrP or Prnp) promoter. Transgenic mice (Tg-RTN3) from founder line 2 have approximately 1- to 2-fold greater RTN3 than wildtype mice, with highest expression levels in cerebral cortex, slightly less in the hippocampus, and lowest in the cerebellum. Overexpression of RTN3 leads to the development of RTN3 immunoreactive dystrophic neurite aggregation (a distinguishing pathological feature of Alzheimer's disease) with neither amyloid deposition nor paired helical filament tangles. The donating investigator reports that dystrophic neurite aggregation is apparent in the hippocampal CA1 region of Tg-RTN3 line 2 mice by ~12 months. This aggregation results in impaired spatial learning and memory, as well as impaired synaptic plasticity.
006394 B6;129-Apba2tm1Sud Apba3tm1Sud Apba1tm1Sud/J
Cryopreserved - Ready for recovery
Triple homozygous knock-in mice are viable and fertile and and do not display any gross physical or behavioral abnormalities. Expression of all three proteins is normal. When crossed with a cre deleter strain that eradicates protein expression, Apba1/Abcba2 (Apba1/2) double knockout and Apba1/2/3 triple knockout mice exhibit a high percentage of postnatal lethality (only ~20% of the mice survive). Apba1/2 mice are visually indistinguishable from their littermates and display no major alterations in breathing, movements or reaction to stimuli several hours after birth, but fail to nurse and die within 24 hours. Their brains are morphologically and structurally normal. Quantitation of 18 neuronal proteins fails to reveal significant changes. Surviving mice show reduced weight gain and exhibit movement dysfunction. Cultured neurons from triple knock-in neonates show impairments in presynaptic neurotransmitter release after treatment with lentiviral cre. Apba1/3 .....
For more information please see the full phenotype on the strain data sheet
008364 B6;129-Chattm1(cre/ERT)Nat/J
Cryopreserved - Ready for recovery
These targeted mutation mice carry a tamoxifen-inducible Cre cassette knocked into the 3' UTR of the gene. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating 4-hydroxytamoxifen-induced, Cre-mediated targeted deletions specifically in cholinergic neurons. Heterozygotes and homozygotes are normal in size, viability and fertility.
008476 B6;129-Ncstntm1Sud/J
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Floxed homozygous mice express intact nicastrin gene. They are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 3 deleted in the cre-expressing tissue(s). General deletion in all tissues results in E9.0 embryonic lethality. g-secretase activity is abolished in cells derived from homozygous cre-recombined mice. These mice are useful to study the role of g-secretase in various tissues in combination with tissue specific cre lines.
007605 B6;129P-Psen1tm1Vln/J
Cryopreserved - Ready for recovery
These mice possess loxP sites on either side of exon 7 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these "floxed" mice are bred to mice that express Cre recombinase, resulting offspring can have one of three resulting genotypes (only exon 7 deleted, only the neo selection cassette deleted, or both exon 7 and the neo selection cassette deleted) in the cre-expressing tissue(s). These PS1-floxed mice may be useful in generating conditional knockouts of Presenilin 1 for studying Alzheimer's Disease.

For example, when crossed to a strain expressing Cre recombinase in postnatal neurons (see Stock No. 006143), this mutant mouse strain may be useful in studies of amyloid plaque formation.

005618 B6;129P2-Bace2tm1Bdes/J
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Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Transcripts derived from the targeted locus do not contain exon 6. One of the enzyme's active sites is encoded by exon 6 so consequently, proteins generated from the targeted locus lack beta-secretase activity. This mutant mouse strain may be useful in studies of Alzheimer's disease.
008333 B6;129P2-Dldtm1Ptl/J
Cryopreserved - Ready for recovery
Mice heterozygous for the Dld (dihydrolipoamide dehydrogenase or E3 component) targeted mutation are viable and fertile. Heterozygous mice exhibit approximately half of wild-type enzymatic activity levels for E3 and all affected mitochondrial multienzyme complexes. Heterozygotes (on a C57BL/6;129P2 genetic background) exhibit increased vulnerability to treatments with MPTP (dopaminergic neurotoxin used to induce Parkinson's disease-like lesions), malonate (inhibitor of cellular respiration used to mimic Huntington's disease features), and 3-NP (mitochondrial toxin used to mimic Huntington's disease features). Homozygous mice exhibit normal development and metabolism during the preimplantation period, explained by the persistence of E3 enzyme from the oocyte. Homozygotes exhibit developmental delays shortly after implantation (7.5 to 8.5 days postcoitum (dpc)) and cease development within the subsequent two days. These Dld mutant mice may be useful to study early murine em .....
For more information please see the full phenotype on the strain data sheet
003822 B6;129S-Psen1tm1Shn/J
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Presenilin-1 is the major gene responsible for early-onset familial Alzheimer's disease. Mice that are homozygous null for this gene die within minutes after being born. Externally, mice exhibit shortened tails that curve to the right, thickened necks, loose skin and hind limbs that curve towards the midline. Their weight is 15-20% that of wildtype. Gross skeletal malformations and central nervous system abnormalities are observed. Death presumably results from impaired respiratory mechanics due to ribcage deformities. Histological examination indicates that alveoli are marginally expanded. By embryonic day 9.5, there is a drastic reduction in neural progenitor cells. Later, the brain exhibits hemorrhages and symmetric cerebral cavitation. Cavitation occurs primarily in the ventrolateral region of the ventricular zone in the posterior portion of the brain.
012639 B6;129S4-Mapttm3(HDAC2)Jae/J
Cryopreserved - Ready for recovery
Mice homozygous for the HDAC2OE allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Expression of Hdac2 from the microtubule-associated protein tau (Mapt) locus, results in neuron-specific overexpression of Hdac2. This overexpression results in a 2-3 fold expression of Hdac2, increased histone deacetylation, and impaired synaptic plasticity in the hippocampus leading to a negative function in regulating memory formation. This strain may be useful for studying the functional and structural synaptic changes and neuronal adaptive responses implicated in memory formation and storage.
012865 B6;129S6-Apbb1tm1Her/J
Cryopreserved - Ready for recovery
The FE65 knockout allele has a nuclear localized-lacZ replacing exon 2 of the Apbb1 gene. No protein expression is detected from the mutant locus, and the donating investigator reports that whether lacZ staining faithfully reflects FE65 expression has not been conclusively resolved. Homozygous (FE65-/-) mice are viable, fertile, and indistinguishable from wildtype littermates. Histological examination of adult brains shows no obvious neuroanatomical abnormalities. These FE65 mutant mice may be useful in studying brain development (neuronal positioning and establishment of axonal projections) and abnormal brain morphology (Cobblestone Lissencephaly, marginal zone heterotopias, and pial basement membrane integrity); as well as the function of FE65 family proteins in amyloid precursor protein (APP) processing, Alzheimer's disease, and neuronal protein trafficking.

For example, mice homozygous for both this FE65 knockout allele and the FE65L1 knockout allele (see S .....
For more information please see the full phenotype on the strain data sheet

012869 B6;129S6-Apbb2tm1Her/J
Cryopreserved - Ready for recovery
The FE65L1 knockout allele has a tau-lacZ fusion protein replacing exon 4 of the Apbb2 gene. No protein expression is detected from the mutant locus, and the donating investigator reports that whether lacZ staining faithfully reflects FE65L1 expression has not been conclusively resolved. Homozygous (FE65L1-/-) mice are viable, fertile, and indistinguishable from wildtype littermates. Histological examination of adult brains shows no obvious neuroanatomical abnormalities. These FE65L1 mutant mice may be useful in studying brain development (neuronal positioning and establishment of axonal projections) and abnormal brain morphology (Cobblestone Lissencephaly, marginal zone heterotopias, and pial basement membrane integrity); as well as the function of FE65 family proteins in amyloid precursor protein (APP) processing, Alzheimer's disease, and neuronal protein trafficking.

For example, mice homozygous for both this FE65L1 knockout allele and the FE65 knockout alle .....
For more information please see the full phenotype on the strain data sheet

017759 B6;129S7-Cyp46a1tm1Rus/J
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A tau-β-galactosidase (lacZ) fusion protein, followed by a neomycin (neo) resistance cassette, replaces the 3' end of exon 1 of the Cyp46a1 gene, abolishing gene function. Cyp46a1 encodes the enzyme cholesterol 24-hydroxylase which is expressed mainly in the brain, with low expression in liver. Cholesterol 24-hydroxylase is involved in cholesterol biosynthesis and turnover, and has also been implicated in the development of amyloid plaques in Alzheimer's disease. Homozygous mice are viable and fertile. In these mice, lacZ staining is evident in the spinal cord, midbrain, and hindbrain at E11.5, with expression decreasing between E11.5 and E13.5. LacZ staining is intensified between E11.5 and E13.5 in cells of the telencephalon, and the cerebral cortex. Beginning at E13.5, expression is restricted to dividing neurons in the neuroepithelium and post-mitotic neurons of the primordial plexiform layer of the telencephalon. These mice display a 4 .....
For more information please see the full phenotype on the strain data sheet
008636 B6;C-Tg(Prnp-APP695*/EYFP)49Gsn/J
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A mouse prion protein promoter drives expression of the human amyloid precursor protein 695 (APP695) carboxy terminus tagged with enhanced yellow fluorescent protein (EYFP) in this transgenic line. Expression in brain, spinal cord and sciatic nerve has been confirmed by Western blot. Primary hippocampal cultures express EYFP at low levels. Mice appear normal and have no observable abnormalities.
007002 B6;C3-Tg(Prnp-ITM2B/APP695*42)A12Emcg/Mmjax
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Mice hemizygous for this BRI-Abeta42 transgene are viable and fertile with a normal lifespan and no obvious behavioral abnormalities. Transgenic BRI-Abeta42 mRNA is expressed in a pattern characteristic of the mouse prion protein promoter; highest transgene expression levels are detected in the cerebellar granule cells and hippocampus, followed by the cortex, pons, thalamus, and midbrain. Wildtype BRI protein is cleaved by furin or a furin-like protease near the COOH-terminus which releases a soluble 23 amino acid peptide. In the transgenic fusion protein, Abeta1-42 is fused to the C terminus of the BRI protein at the furin-like cleavage site such that cleavage results in efficient Abeta1-42 secretion into the lumen or extracellular space. Therefore, these mice specifically express the Abeta1-42 isoform in the absence of human amyloid beta protein precursor (APP) overexpression. In contrast to BRI-Abeta40 transgenic mice (Tg(Prnp-ITM2B/APP695*40)1Emcg), hemizygous BRI-Abeta42 mice accu .....
For more information please see the full phenotype on the strain data sheet
008850 B6;SJL-Tg(Mt1-LDLR)93-4Reh/AgnJ
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Mice hemizygous for this MMT-I-hLDLR transgene (hLDLRTg mice) are viable and fertile, with human low density lipoprotein receptor (hLDLR) expression controlled by the mouse metallothionein 1 gene (Mt1) promoter sequences. The donating investigator reports that homozygous mice are not viable. Expression of hLDLR mRNA is highest in liver, moderate in kidney, small intestine, and heart, and lowest in brain and pancreas. Treatment with cadmium sulfate (CdSO4) stimulates transcription from the metallothionein promoter and results in higher levels of hLDLR expression. This overexpression of functional LDLR in transgenic mice results in greatly increased clearance of LDLR ligands (LDL, apoprotein B-100 and apoprotein E) from plasma when compared to wild-type mice. These hLDLRTg mice may be useful for studying the role of apolipoproteins and their receptors, lipid transport and lipoprotein metabolism in a wide variety of disease (including atherosclerosis, Alzheimer's disease, and hepat .....
For more information please see the full phenotype on the strain data sheet
003378 B6C3-Tg(APP695)3Dbo Tg(PSEN1)5Dbo/J
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These transgenic mice express human presenilin 1 (A246E variant) and a chimeric amyloid precursor protein (APPSwe). The mouse prion protein promoter directs expression of both transgenes. Elevated levels of the AB1-42(43) peptide is detected in brain homogenates. By nine months of age, histological examination of brain tissue reveals numerous amyloid deposits resembling those observed in the brains of patients with Alzheimer's disease (AD). The number of amyloid deposits increases dramatically between the ages of 10 and 12 months. These mice provide a useful model for studying the underlying mechanism of amyloid deposition, a process implicated in AD.
006004 B6C3-Tg(tetO-APPSwInd)885Dbo/Mmjax
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Hemizygous mice are viable and fertile. These transgenic mice express a chimeric mouse/human amyloid precursor protein (APP) bearing the Swedish (KM570/571NL) and Indiana (V617F) mutations associated with Alzheimer's disease (APPswe/ind) under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of tissue-specific promoters , APPswe/ind transgene expression can be regulated in the appropriate tissue of the bitransgenic offspring with the tetracycline analog, doxycycline.

Note that tet alone may affect neuronal degeneration and behavioral phenotypes, depending on the genetic background used (see Han et al, J. Neurosci., 2012).

When bred to a strain expressing rtTA or tTA in brain tissues (B6;CBA-Tg(Camk2a-tTA)1Mmay/J), this mutant mouse strain may be useful i .....
For more information please see the full phenotype on the strain data sheet

003741 B6D2-Tg(Prnp-MAPT)43Vle/J
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These transgenic mice express the human fetal tau MAPT isoform under the direction of the mouse prion protein promoter. Hyperphosphorylated, insoluble MAPT protein is widely expressed in neurons of the CNS at levels approximately ten-fold higher than the endogenous mouse counterpart. Mice homozygous for the transgenic insert die at about three months of age. In the hemizygous mice intraneural inclusions that stain positive with T14, a monoclonal antibody specific for MAPT, are observed in brain and spinal cord tissue at 1 month of age. The number of inclusions increases until 6-9 months of age. Transmission electron microscopy studies of these inclusions reveals tightly packed aggregates of randomly arranged 10-20 nm straight filaments. Mice suffer progressive, age-dependant neuronal damage, motor weakness and gliosis. These mice recapitulate key features of tauopathies and provide a model for studying the underlying mechanism of related diseases such as FTDP-17, Alzheimer's and .....
For more information please see the full phenotype on the strain data sheet
016556 B6N.129-Ptpn5tm1Pjlo/J
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In this STEP KO strain, a neo cassette replaces the catalytic site of the protein tyrosine phosphatase, non-receptor type 5 (Ptpn5) gene, abolishing gene expression. Homozygotes are viable, fertile, and normal in size. Striatal enriched protein phosphatase (STEP) is a neuron-specific tyrosine phosphatase which regulates synaptic plasticity following glutamatergic and dopaminergic input. Expressed mainly in the striatum, hippocampus, amygdala, and cortex of the brain, glutamate-activated STEP controls synaptic plasticity through limiting the duration of ERK 1/2 MAP kinase activity and by endocytosis of glutamate receptors. Activation of ERK1/2 in STEP-expressing regions of the brain is required for memory formation and learning. STEP levels are also shown to be increased in prefrontal cortex of Alzheimer's Disease (AD) models. Homozygous STEP KO mice lack expression of all STEP isoforms, and exhibit enhanced phosphorylation of ERK1/2 in the striatum, hippocampus .....
For more information please see the full phenotype on the strain data sheet
024841 B6N.Cg-Tg(Prnp-MAPT*P301S)PS19Vle/J
Cryopreserved - Ready for recovery
012621 C.129S(B6)-Chrna3tm1.1Hwrt/J
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These α3[5] nAChR mice contain a mutation designed to introduce 5 nucleotide mutations to exon 5 of mouse nicotinic acetylcholine receptor (nAChR) neuronal α3 subunit and a loxP-flanked neomycin (neo) resistance cassette upstream of exon 5. Mice that are heterozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The α3[5] allele contains mutations in the loop C region corresponding to residues from the α1 subunit of nAchR from Torpedo californica, the Pacific electric ray, conveying α-bungarotoxin (αBTX) sensitivity. This mutation allows for direct visualization, by staining with rhodamine-conjugated αBTX, of α3[5] nAChR-containing superior cervical ganglia (SCG) neurons. Less than 2% of homozygous mice on a C57BL/6 or 129S background survived beyond 70 days and all pups are runted, whereas 60% of homozygotes survi .....
For more information please see the full phenotype on the strain data sheet
002328 C.129S2-Plautm1Mlg/J
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Homozygotes develop normally, are fertile and have a normal life span. Rectal prolapse of a non-infectious origin develops in 9% of homozygotes and/or extensive non-healing ulcerations occur at the eyelids and around the face. Small, focal fibrin deposits are occasionally seen in the intestines and in the sinusoids of the liver, and excessive fibrin deposits are seen in ulcerated skin or prolapsed rectum. Pulmonary clot lysis is comparable to that seen in normal wildtype siblings. Endotoxin induced venous thrombosis is increased over normal wildtype siblings. Fibrin dissolution by PLAU-deficient macrophages is greatly reduced but macrophage invasion into the peritoneal cavity after thioglycollate injection is unaffected. Homozygous knockout mice have increased levels of Abeta42 and Abeta40 in plasma. Brain Abeta levels are not significantly different than controls. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a .....
For more information please see the full phenotype on the strain data sheet
003375 C3B6-Tg(APP695)3Dbo/Mmjax
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These transgenic mice express the human amyloid precursor protein bearing the Swedish (K670N/M671L) mutation and develop amyloid deposits in brain tissue by 18-20 months of age. These mice provide a useful model for studying the underlying mechanism of amyloid deposition, a process implicated in Alzheimer's disease (AD).
005087 C57BL/6-Tg(Camk2a-IDE)1Selk/J
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These transgenic mice express human insulin-degrading enzyme (IDE) under the direction of the mouse calcium/calmodulin-dependent protein kinase II alpha (Camk2a) promoter. Transgene expression is approximately 2 fold relative to wildtype controls, as detected by quantitative Western blot analysis and protease activity assay. The levels of soluble alpha beta-amyloid X-40 and soluble alpha beta-amyloid X-42 are reduced in 2 to 3 month old transgenic mice. Mice that are hemizygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed to B6.Cg-Tg(PDGFB-APPSwInd)20Lms/2J (Stock No. 006293) mice, amyloid beta plaque burden in the resulting double transgenic mice is reduced by half. This mutant mouse strain may be useful in studies of Alzheimer's Disease, specifically the enhancement of amyloid beta-protein degradation.
005086 C57BL/6-Tg(Camk2a-MME)3Selk/J
Cryopreserved - Ready for recovery
These transgenic mice express human membrane metallo-endopeptidase (MME) under the direction of the mouse calcium/calmodulin-dependent protein kinase II alpha (Camk2a) promoter. Transgene expression is approximately 8 fold relative to wildtype controls, as detected by quantitative Western blot analysis and protease activity assay. The levels of soluble alpha beta-amyloid X-40 and soluble alpha beta-amyloid X-42 are reduced in 2 to 3 month old transgenic mice. Mice that are hemizygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Transgenic mice have poor reproductive performance. When crossed to B6.Cg-Tg(PDGFB-APPSwInd)20Lms/2J (Stock No. 006293) mice, amyloid beta plaques do not develop in the resulting double transgenic mice. This mutant mouse strain may be useful in studies of Alzheimer's Disease, specifically the enhancement of amyloid beta .....
For more information please see the full phenotype on the strain data sheet
008833 C57BL/6-Tg(Camk2a-UBB)3413-1Fwvl/J
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Homozygous UBB+1 tg line 3413 mice are viable and fertile, with the mouse CamkIIα promoter directing expression of a mutant human ubiquitin B (UBB+1) protein associated with disease-specific aggregates in tauopathies and polyglutamine diseases. In hemizygous mice, UBB+1 transcripts are expressed at ~49% of the endogenous levels. UBB+1 tg line 3413 mice overexpress human UBB+1 specifically in neurons throughout the postnatal brain (cortex, hippocampus, amygdala, striatum and brain stem), with strongest neuronal expression in the forebrain. Hemizygous mice exhibit diminished ubiquitin-proteasome system activity with a resulting increase in ubiquitinated proteins in the cortex. UBB+1 tg line 3413 mice have deficits in spatial memory, contextual memory and hippocampal synaptic plasticity, as well as altered expression of cerebral cortical proteins involved in energy metabolism. Concordant with high expre .....
For more information please see the full phenotype on the strain data sheet
010800 C57BL/6-Tg(Thy1-PTGS2)300Kand/J
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Mice hemizygous for the human Thy-1-COX-2 transgene (hCOX-2 transgene) are viable and fertile, with expression of human COX-2 (PTGS2 or PGE2) directed primarily to neurons of the amygdala, striatum, cerebral cortex, and hippocampus by the murine Thy1.2 expression cassette. These moderate overexpressing C57BL/6J COX-2 transgenic line 300 mice have PGE2 levels that are ~10-12-fold greater than non-transgenic controls (compared to ~25-40-fold overexpression in line 303; see Stock No. 010703). At approximately 12 months of age, COX-2 transgenic mice develop an age-dependent deficit in spatial memory. Around 20 months of age, a less pronounced, but significant deterioration in performance of non-spatial memory tasks develops. Further progressive memory impairments are observed over time. These cognitive deficits are associated with parallel age-dependent increases in cortical neuronal apoptosis and glial activation. Transgenic m .....
For more information please see the full phenotype on the strain data sheet
010703 C57BL/6-Tg(Thy1-PTGS2)303Kand/J
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Mice hemizygous for the human Thy-1-COX-2 transgene (hCOX-2 transgene) are viable and fertile, with expression of human COX-2 (PTGS2 or PGE2) directed primarily to neurons of the amygdala, striatum, cerebral cortex, and hippocampus by the murine Thy1.2 expression cassette. These overexpressing C57BL/6J COX-2 transgenic line 303 mice have PGE2 levels that are ~25-40-fold greater than non-transgenic controls (compared to ~10-12-fold overexpression in line 300; see Stock No. 010800). At approximately 12 months of age, COX-2 transgenic mice develop an age-dependent deficit in spatial memory. Around 20 months of age, a less pronounced, but significant deterioration in performance of non-spatial memory tasks develops. Further progressive memory impairments are observed over time. These cognitive deficits are associated with parallel age-dependent increases in cortical neuronal apoptosis and glial activation. Transgenic mice exhib .....
For more information please see the full phenotype on the strain data sheet
005706 C57BL/6-Tg(tetO-CDK5R1/GFP)337Lht/J
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Hemizygous transgenic mice are viable, fertile, normal in size and do not display any behavioral abnormalities. Mice homozygous for this transgene may not be viable. When these transgenic mice are bred with mice expressing the tetracycline-controlled transactivator protein (tTA) under the regulation of a tissue-specific promoter, expression of the CDK5R1/GFP fusion protein in the appropriate tissue of the bitransgenic offspring can be regulated by doxycycline administration. These mice may be useful in studies of Alzheimer's disease and other neurodegenerative tauopathies, amyotrophic lateral sclerosis (ALS), Niemann Pick Type C (NPC) disease, and Parkinson's disease.

Note: this transgenic strain was designed to breed with Tg(Camk2a-tTA) transgenic mice, (Stock No. 003010), a transgenic strain that expresses tTA in forebrain neurons. The resulting bitransgenic offspring exhibit the hallmark phenotype of Alzheimer's disease; .....
For more information please see the full phenotype on the strain data sheet

006618 C57BL/6-Tg(tetO-COX8A/EYFP)1Ksn/J
Cryopreserved - Ready for recovery
Hemizygotes are viable and fertile. These transgenic mice express a mitochondrial-specific EYFP fusion protein under the control of a tetracycline-responsive promoter element (TRE;tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of tissue-specific promoter, tissue-specific expression of EYFP in mitochondria of the bitransgenic offspring can be regulated with the tetracycline analog, doxycycline.

When bred to a strain expressing rtTA or tTA in forebrain neurons (see Stock No. 003010 for example), this mutant mouse strain may be useful in studies of neuronal mitochondrial dysfunction.

006472 D2.129(B6)-Tg(APPSw)40Btla/Mmjax
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These R1.40 transgenic mice express all mRNA and protein isoforms of the human amyloid beta (A4) precursor protein APP containing the Familial Alzheimer's Disease (FAD) Swedish mutation K670N/M671L. Transgene expression (mRNA and full-length protein) is 2 to 3 fold the endogenous mouse App expression level in the hemizygous state in brain tissue as revealed by RT-PCR and Western Blot analysis. Transgene expression pattern mimics endogenous mouse gene expression patterns. The donating investigator reports increased mortality in young homozygous animals (higher incidence in females). 3 to 4 month old transgenic mice, maintained on a C57BL/6J background, exhibit spontaneous seizure-like events (abnormal spiking) in EEG readings, without abnormal behavior and are more susceptible to kainic acid induced seizures (Vogt et al. Neurobiol Aging 2009). These R1.40 transgenic mice may be useful in studying the pathogenesis of Familial Alzheimer's Disease and possible therapeu .....
For more information please see the full phenotype on the strain data sheet
007067 D2.129P2(B6)-Apoetm1Unc/J
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Mice homozygous for the Apoetm1Unc mutation show a marked increase in total plasma cholesterol levels that are unaffected by age or sex. Fatty streaks in the proximal aorta are found at 3 months of age. The lesions increase with age and progress to lesions with less lipid but more elongated cells, typical of a more advanced stage of pre-atherosclerotic lesion. Moderately increased triglyceride levels have been reported in mice with this mutation on a mixed C57BL/6 x 129 genetic background. Aged APOE deficient mice (>17 months) have been shown to develop xanthomatous lesions in the brain consisting mostly of crystalline cholesterol clefts, lipid globules, and foam cells. Smaller xanthomas were seen in the choroid plexus and ventral fornix. Recent studies indicate that APOE deficient mice have altered responses to stress, impaired spatial learning and memory, altered long term potentiation, and synaptic damage.

In an attempt to offer alleles on well-charac .....
For more information please see the full phenotype on the strain data sheet

013732 FVB-Tg(NPEPPS)1Skar/J
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These mice express a human aminopeptidase puromycin sensitive (hPSA or NPEPPS) gene directed by its endogenous promoter/enhancer regions on a BAC transgene. Mice hemizygous for the transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. PSA is a cytosolic aminopeptidase that hydrolyzes N-terminal amino acids. PSA is considered to have neuroprotective qualities due to its ability to degrade certain proteins associated with neurodegenerative diseases (TAU and polyglutamine expansion repeat-containing proteins). hPSA overexpression is seen in the cerebral cortex, spinal cord, cerebellum, hippocampus, and brain stem at a 2-3 fold greater level than endogenous PSA. hPSA activity is also increased in muscle, kidney, and liver. These mice may be useful for studying PSA protection in neurodegenerative disorders.
013156 FVB-Tg(tetO-CDK5R1*)1Vln/J
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These tetO-CDK5R1* mice express a truncated human cyclin-dependent kinase 5, regulatory subunit 1 (CDKR1 or p35) cDNA sequence, also referred to as p25, under the control of a tetracycline operator (tetO; also called tetracycline-responsive element (TRE, TetRE) or tet-operator). The N-terminal truncated isoform of p35 is p25. Unlike p35, which is membrane bound in postmitotic neurons in the brain, p25 is non-tethered and expression is seen in all cellular compartments of neuronal somata and dendrites. Mice that are hemizygous for this transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred with another mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), CDK5R1 expression can be regulated with the tetracycline analog doxycycline (dox) in the resulting double mutant offspring. For example, when bred to a strain expressing .....
For more information please see the full phenotype on the strain data sheet
002329 FVB.129S2-Plautm1Mlg/J
Cryopreserved - Ready for recovery
Homozygotes develop normally, are fertile and have a normal life span. Rectal prolapse of a non-infectious origin develops in 9% of homozygotes and/or extensive non-healing ulcerations occur at the eyelids and around the face. Small, focal fibrin deposits are occasionally seen in the intestines and in the sinusoids of the liver, and excessive fibrin deposits are seen in ulcerated skin or prolapsed rectum. Pulmonary clot lysis is comparable to that seen in normal wildtype siblings. Endotoxin induced venous thrombosis is increased over normal wildtype siblings. Fibrin dissolution by PLAU-deficient macrophages is greatly reduced but macrophage invasion into the peritoneal cavity after thioglycollate injection is unaffected. Homozygous knockout mice have increased levels of Abeta42 and Abeta40 in plasma. Brain Abeta levels are not significantly different than controls. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a .....
For more information please see the full phenotype on the strain data sheet
003753 FVB/N-Tg(Eno2CDK5R1)1Jdm/J
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These transgenic animals display a robust expression of the amino terminal proteolytic fragment p25 of human CDK5R1. Expression is detected in the amygdala, thalamus/hypothalamus, cerebral cortex, and cerebellum. The p25 fragment acts as a positive allosteric regulator of cyclin-dependent kinase 5 (Cdk5), a kinase known to phosphorylate the microtubule-binding protein tau. A two-fold increase in the catalytic activity of Cdk5 is observed in these mice. In contrast to wildtype control mice, brains from 4-month-old exhibit the presence of tau and neurofilament phosphoepitopes. Utlrastructurally, axonal swelling in neurons from the amygdala and spinal cord is observed. Affected neurons possess numerous, abnormally clustered mitochondria and lysosomes, with some evidence of cytoskeletal disorganization. Mice exhibit whole-body tremors at 4-9 weeks of age and enhanced open-field locomotor activity. Aspects of this phenotype are similar to Alzheimer's, Pick's and other n .....
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022350 MRL.Cg-Nos2tm1Lau Faslpr/J
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Mice that are homozygous for these targeted mutation and spontaneous mutant alleles are viable, fertile, and develop immune complex proliferative glomerulonephritis similar to that observed in MRL/MpJ-Faslpr/J (JAX Stock No. 000485) mice. Double mutant mice exhibit more superoxide production in the renal cortex and increased anti-dsDNA antibody production when compared to MRL/MpJ-Faslpr/J wildtype controls.
008051 NOD.129P2(B6)-Ctsbtm1Jde/RclJ
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Mice homozygous for the Ctsb targeted mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Northern blot analysis of kidney total RNA indicates a lack of transcript in homozygous mutant mice. An absence of Ctsb protein in homozygous mutant mice was determined by Western blot analysis of kidney lysosomal protein extracts. The proteolytic activity of the endogenous protein was found to be absent using an assay involving liver lysosomal extracts, obtained from homozygous mutant mice, and a fluorogenic substrate (Halangk et al. 2000).

The donating investigator indicates that the diabetes incidence in homozygous mutant NOD mice is significantly reduced (28%) compared to wildtype NOD (69%), while heterozygous mice are modestly protected from diabetes (50%) at six months of age. Histological analysis of the pancreas from non-diabetic homozygous mice indicate that insulitis is present but at much lower levels .....
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007069 STOCK Apoetm1Unc/J
Cryopreserved - Ready for recovery
Mice homozygous for the Apoetm1Unc mutation show a marked increase in total plasma cholesterol levels that are unaffected by age or sex. Fatty streaks in the proximal aorta are found at 3 months of age. The lesions increase with age and progress to lesions with less lipid but more elongated cells, typical of a more advanced stage of pre-atherosclerotic lesion. Moderately increased triglyceride levels have been reported in mice with this mutation on a mixed C57BL/6 x 129 genetic background. Aged APOE deficient mice (>17 months) have been shown to develop xanthomatous lesions in the brain consisting mostly of crystalline cholesterol clefts, lipid globules, and foam cells. Smaller xanthomas were seen in the choroid plexus and ventral fornix. Recent studies indicate that APOE deficient mice have altered responses to stress, impaired spatial learning and memory, altered long term potentiation, and synaptic damage.

In an attempt to offer alleles on well-characteri .....
For more information please see the full phenotype on the strain data sheet

008390 STOCK Apptm1Sud/J
Cryopreserved - Ready for recovery
These targeted mutant (knock-in line ADF) mice carry an insertion incorporating a truncated exon 16 of the mouse amyloid beta (A4) precursor protein (App) gene as well as the Swedish mutant exon 16 and London/Dutch mutations of exon 17. Truncated exon 16 is incorporated into the sAPPbeta-FLAG transcript, but exon 17 is not expressed. No overt phenotype has been observed. Homozygotes are viable and fertile. This strain may be useful in studies of Alzheimer's disease.
012640 STOCK Hdac2tm1.2Rdp/J
Cryopreserved - Ready for recovery
These HDAC2KO mutant mice lack exons 5-6 of the mouse histone deacetylase 2 (Hdac2) gene. Mice that are homozygous for this allele are viable, with reduced fertility, and are born at a twofold lower frequency than expected from a normal Mendelian ratio. Homozygous mutants are about 25% smaller than wild-type and heterozygote littermates. These mice have an increased synapse number and enhanced memory formation. This strain may be useful for studying the functional and structural synaptic changes and neuronal adaptive responses implicated in memory formation and storage.
004808 STOCK Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the targeted allele and hemizygous for the transgene are viable and fertile. Although no endogenous mouse MAPT is detected, all six isoforms (including both 3R and 4R forms) of human MAPT are expressed. Hyperphosphorylated MAPT is detected in cell bodies and dendrites by three months of age. Paired helical filaments of aggregated insoluble MAPT can be isolated from brain tissue as early as two months of age. These mutant mice may be useful in studies examining the relationship between human MAPT and Alzheimer's disease pathogenesis.
014092 STOCK Tg(ACTB-tTA2,-MAPT/lacZ)1Luo/J
Cryopreserved - Ready for recovery
Homozygous CAG-stop-tTA2 transgenic mice are viable and fertile. CAG-stop-tTA2 transgenic mice harbor the ii-CAG-stop-tTA2-IRES-tau-lacZ-ii transgene; designed with a loxP-flanked transcriptional STOP cassette preventing transcription of the downstream modified tetracycline-regulated transactivator (tTA2). The ii-CAG-stop-tTA2-IRES-tau-lacZ-ii transgene is flanked by two copies of the chicken β-globin HS4 insulator on each side to preserve expression fidelity (see additional information below). When bred to mice that express a tamoxifen-inducible Cre recombinase (CreERT2), administration of tamoxifen to the double mutant offspring allows the CreERT2 fusion protein to enter the nucleus of the cre-expressing cells; this deletes the STOP cassette and results in expression of tTA2. The donating investigator reports that tau-lacZ fusion protein expression in the tamoxifen-treated double mutant offspring is faint. Of note, the donating investigator h .....
For more information please see the full phenotype on the strain data sheet
006340 STOCK Tg(Gad1-EGFP)98Agmo/J
Cryopreserved - Ready for recovery
Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Enhanced Green Fluorescent Protein (EGFP) under the direction of the mouse Gad1 (glutamic acid decarboxylase 1 or GAD67) promoter. In the neocortex, EGFP expression is detected predominantly in layers 5B and 6, and to a lesser extent in layers 2/3. Low levels of fluorescence are detected in small cells with glial morphology. EGFP expression is also observed in area CA1 of the hippocampus, mainly in large interneurons in the oriens-alveus layers. In the neocortex of founder line 98 transgenic mice, fluorescence is observed in infragranular, calbindin immunoreactive interneurons with axonal arborizations in layer 1. In animals younger than two weeks of age, an increased number of EGFP labeled neurons is observed in the supragranular layers, and EGFP expression is also observed in some cells with pyramidal m .....
For more information please see the full phenotype on the strain data sheet
007577 STOCK Tg(Gt(ROSA)26Sor-BCHE*G117H)837Loc/J
Cryopreserved - Ready for recovery
Transgenic "G117H BChE" mice are viable and fertile. These mice express a mutant form of human butyrylcholinesterase (BCHE or BChE), harboring a single amino acid change at codon 117 (His for Gly), under the control of the ROSA26 promoter. This mutation has the unusual ability to hydrolyze organophosphorus toxicants (OP), as well as acetylcholine and is resistant to inhibition by OP. All tested tissues show G117H BChE enzymatic activity. In the founder mice and immediate offspring, plasma concentrations of the mutant protein are approximately 25% of endogenous wildtype mouse BChe. No reported abnormalities result from BChE overexpression in homozygous mutant mice. Transgenic mice injected with the OP echothiophate are protected from the severe toxicity and lethality observed in wildtype controls. This is the first transgenic mouse strain that expresses human BChE as well as the first mammal with hereditary OP resistance. These G117H BChE transgenic mice may be useful for biodefe .....
For more information please see the full phenotype on the strain data sheet
014544 STOCK Tg(tetO-ABL1*P242E*P249E)CPdav/J
Cryopreserved - Ready for recovery
Hemizygous AblPP transgenic mice are viable and fertile with no reported phenotypic abnormalities. The TRE-AblPP transgene has the Tet response element (TRE or tetO) upstream of a human c-Abl 1b isoform modified to harbor two amino acid substitutions (P242E/P249E) in the conserved proline residues of the SH2-SH3 linker region that render the protein constitutively active (AblPP). When bred with other mice expressing tetracycline-controlled transactivator protein (tTA) or reverse tetracycline-controlled transactivator protein (rtTA), AblPP expression in the resulting double mutant offspring can be regulated with tetracycline or its analog doxycycline (dox). As designed, AblPP transgenic mice have no reported levels of AblPP expression in the absence of tTA.

These AblPP transgenic mice allow Tet-Off/Tet-On expression of a constitutively active form of c-Abl, and may be may be useful for studying tau phosphorylation and the pathogenesis of neurodegeneration/neuroinflammatio .....
For more information please see the full phenotype on the strain data sheet

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New Strains Awaiting Transfer from the Donor

(See informational text following listing of strains)
How to Register Interest
Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.

View a Data sheet for New Strains Awaiting Transfer
Select the strain name to link to the strain data sheet.

Stock
Number
Strain Name
 
Strain Description
Standard Supply
024415B6.129S6(Cg)-Wwc1tm1.1Rlh/J
Awaiting Transfer from the Donor
This strain carries a targeted knockout of the mouse Wwc1 (KIBRA) gene and is useful in studies of synaptic plasticity, learning, and memory.
025820B6;CBA-Tg(CRH-MAPT/Topaz)1Rck/J
Awaiting Transfer from the Donor
These transgenic mice express Tau(MAPT)-Topaz GFP under the control of the mouse Crh promoter. Fluorescent expression in the brain is faithful to that of the Crh gene and the functional integrity of labeled cells is intact.

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New Strains Awaiting Transfer from the Donor
  • Receive periodic updates on the status of the colony AWAITING TRANSFER
  • Obtain advance notification of strain availability and opportunity to order prior to the strain being published as available
  • Provide input affecting speed and quantity of availability
The Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion.

It is VERY IMPORTANT that you register interest in strains Awaiting Transfer. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.

Additional Register Interest Strains

Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.

View a Data sheet for a Strain
Select the strain name to link to the strain data sheet.

Stock
Number
Strain Name
 
Strain Description
Standard Supply
012628B6.Cg-Apoetm3(APOE*4)Mae Ins2Akita Ldlrtm1(LDLR)Mae/J
In Progress
In "E4hAkita" mice, the mouse apolipoprotein E is replaced with a human apoE4 isoform and the mouse low density lipoprotein receptor is replaced with a transcript-stabilized human LDLR that expresses at three times that of wildtype endogenous levels. Also present is the Ins2Akita allele which causes insulin dependent diabetes. E4hAkita mice are diabetic with atherosclerosis and may be useful in applications related to the study of lipoprotein metabolism-related genes in diabetes, atherosclerosis, dyslipidemia, and vascular complications.
025119B6N(Cg)-Elk1tm1.1(KOMP)Vlcg/J
In Progress
This knockout/reporter mutant of the Elk1 (ELK1, member of ETS oncogene family) gene has been generated by the Knockout Mouse Phenotyping Program (KOMP2) at The Jackson Laboratory. The Elk1 gene encodes a transcription activator that plays a role in long term memory, addiction, and the onset of Alzheimer’s disease.

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It is VERY IMPORTANT that you Register Interest. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain.

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