Search Criteria: Research Area is "Neurobiology Research: Alzheimer's Disease"
| 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. Recent 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 3 |
| 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 | ||
| 004462 | B6C3-Tg(APPswe,PSEN1dE9)85Dbo/J | Level 4 |
| 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 | ||
| 006409 | 129S1.129(Cg)-Tg(APPSw)40Btla/J | Repository- Live |
| 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. 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) segregating for transgene copy number; one with lower trangene copy number (Stock No. 006409) and one with higher transgene copy number (Stock No. 008609). At the ..... | ||
| 007069 | AKR.129P2(B6)-Apoetm1Unc/J | Repository- Live |
| 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-characterized> ..... | ||
| 004684 | B6(129P2) Nos2tm1Lau-chtl/GrsrJ | Repository- Live |
| 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. | ||
| 005999 | B6(SJL)-Tg(SBE/Tk-luc)7Twc/J | Repository- Live |
| 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 | ||
| 004714 | B6.129-Bace1tm1Pcw/J | Repository- Live |
| 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. | ||
| 007251 | B6.129-Mapttm1Hnd/J | Repository- Live |
| 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. | ||
| 005300 | B6.129-Tg(APPSw)40Btla/J | Repository- Live |
| 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 | ||
| 007685 | B6.129P2-Psen1tm1Vln/J | Repository- Live |
| 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 ..... | ||
| 002213 | B6.129S4-Ngfrtm1Jae/J | Repository- Live |
| 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 | Repository- Live |
| 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. | ||
| 005491 | B6.Cg-Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J | Repository- Live |
| 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/J | Repository- Live |
| 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. | ||
| 005864 | B6.Cg-Tg(APPswe,PSEN1dE9)85Dbo/J | Repository- Live |
| 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 | ||
| 007575 | B6.Cg-Tg(CAG-Ngb,-EGFP)1Dgrn/J | Repository- Live |
| 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 ..... | ||
| 007004 | B6.Cg-Tg(Camk2a-tTA)1Mmay/DboJ | 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 (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 | ||
| 004633 | B6.Cg-Tg(GFAP-APOE*3)37Hol Apoetm1Unc/J | Repository- Live |
| 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 | ||
| 004631 | B6.Cg-Tg(GFAP-APOE*4)1Hol Apoetm1Unc/J | Repository- Live |
| 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 | ||
| 007673 | B6.Cg-Tg(Gad1-EGFP)3Gfng/J | Repository- Live |
| 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 | ||
| 008321 | B6.Cg-Tg(Npy-MAPT/GFP*)1Rck/J | Repository- Live |
| 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 | Repository- Live |
| 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 | ||
| 006293 | B6.Cg-Tg(PDGFB-APPSwInd)20Lms/2J | Repository- Live |
| 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. This mutant mouse strain represents a model that may be useful in studies of the pathogenesis of Familial Alzheim ..... For more information please see the full phenotype on the strain data sheet | ||
| 008324 | B6.Cg-Tg(Pmch-MAPT/GFP*)1Rck/J | Repository- Live |
| These mice express a tau (MAPT)-cyan green fluorescent protein (GFP) 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/GFP*)1Rck/J | Repository- Live |
| 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. | ||
| 008596 | B6.Cg-Tg(Prnp-Abca1)EHol/J | Repository- Live |
| 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 ..... | ||
| 008364 | B6;129-Chattm1(cre/Esr1)Nat/J | Repository- Live |
| 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. | ||
| 007605 | B6;129P-Psen1tm1Vln/J | Repository- Live |
| 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. | ||
| 002596 | B6;129P2-Nos2tm1Lau/J | Repository- Live |
| 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-Chattm1(cre)Lowl/J | Repository- Live |
| Homozygous mice maintained at The Jackson Laboratory 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. | ||
| 008636 | B6;C-Tg(Prnp-APP695*/EYFP)49Gsn/J | Repository- Live |
| 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/J | Repository- Live |
| 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 (Stock No. 00 ..... For more information please see the full phenotype on the strain data sheet | ||
| 008169 | B6;C3-Tg(Prnp-MAPT*P301S)PS19Vle/J | Repository- Live |
| These transgenic mice express the P301S mutant 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 approximately nine months of a ..... For more information please see the full phenotype on the strain data sheet | ||
| 000231 | B6;C3Fe a/a-Csf1op/J | Repository- Live |
| 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. | ||
| 006554 | B6SJL-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/J | Repository- Live |
| 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 (Abeta-42). 5XFAD mice generate Abeta-42 almost exclusively and rapidly accumulate massive cerebral levels. 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. In addition, these mice have reduced synaptic marker protein levels, increased p25 levels, neuron loss, and memory impairment in the Y-maze test. 5XFA ..... For more information please see the full phenotype on the strain data sheet | ||
| 008833 | C57BL/6-Tg(Camk2a-UBB)3413-1Fwvl/J | Repository- Live |
| These transgenic mice express the mutant human ubiquitin B, UBB+1, under the direction of the mouse Camk2a, calcium/calmodulin-dependent protein kinase II alpha, promoter. In hemizygotes, mutant transcript is expressed at 49% of the endogenous levels. The transgene is expressed in neurons of the cortex, hippocampus, amygdala and striatum. Hemizygous transgenic mice exhibit diminished ubiquitin-proteasome system activity with a resulting increase in ubiquitinated proteins in the cortex. Transgenic mice display a reduced synaptic plasticity in the hippocampus and impaired spatial learning. Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical abnormalities. This mutant mouse strain may be useful in studies of neurodegenerative diseases such as Alzheimer's and Huntington disease. | ||
| 007027 | C57BL/6-Tg(Thy1-APPSwDutIowa)BWevn/J | Repository- Live |
| 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 | ||
| 006618 | C57BL/6-Tg(tetO-COX8A/EYFP)1Ksn/J | Repository- Live |
| 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. | ||
| 007677 | CB6-Tg(Gad1-EGFP)G42Zjh/J | Repository- Live |
| 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. While transgene expression (EGFP expression) is published as early as postnatal day 0 (P0) with high expression levels throughout postnatal development, 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 in vivo. Of note, this GAD67-GFP strain is one of many fluorescent GABAerg ..... | ||
| 007072 | CByJ.129P2(B6)-Nos2tm1Lau/J | Repository- Live |
| 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 | ||
| 007067 | D2.129P2(B6)-Apoetm1Unc/J | Repository- Live |
| 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 ..... | ||
| 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). | ||
| 006143 | FVB/N-Tg(Thy1-cre)1Vln/J | Repository- Live |
| 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. | ||
| 008051 | NOD.129P2(B6)-Ctsbtm1Jde/RclJ | Repository- Live |
| 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 ..... | ||
| 004779 | STOCK Mapttm1(EGFP)Klt/J | Repository- Live |
| 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. | ||
| 006340 | STOCK Tg(Gad1-EGFP)98Agmo/J | Repository- Live |
| 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 | ||
| 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 | ||
| 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 ..... | ||
| 006555 | A.129(B6)-Tg(APPSw)40Btla/J | 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). These R1.40 transgenic mice may be useful in studying the pathogenesis of Familial Alzheimer's Disease and possible therapeutic treatments.
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 va ..... | ||
| 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. | ||
| 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. | ||
| 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. | ||
| 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 ..... | ||
| 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. | ||
| 006406 | B6.129S4-Tg(APPSwLon)96Btla/J | 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 (see Stock No. 005300). 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. | ||
| 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 | ||
| 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*2)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 | ||
| 008323 | B6.Cg-Tg(Mc4r-MAPT/GFP*)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. | ||
| 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/J | 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 | ||
| 007051 | B6.Cg-Tg(tetO-APPSwInd)102Dbo/J | 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 tauopathies. For example, when bred to a strain expressing tTA in brain tissues (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 007052 | B6.Cg-Tg(tetO-APPSwInd)107Dbo/J | 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 tauopathies. For example, when bred to a strain expressing tTA in brain tissues (see Stock No. ..... | ||
| 007049 | B6.Cg-Tg(tetO-APPSwInd)885Dbo/J | 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 tauopathies. For example, when bred to a strain expressing tTA in brain tissues (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 008476 | B6;129-Ncstntm1Sud/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 005618 | B6;129P2-Bace2tm1Bdes/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. 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 | 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. | ||
| 003378 | B6C3-Tg(APP695)3Dbo Tg(PSEN1)5Dbo/J | Cryopreserved - Ready for recovery |
| 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/J | Cryopreserved - Ready for recovery |
| 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. When bred to a strain expressing rtTA or tTA in brain tissues (see Stock No. 003010, for example), this mutant mouse strain may be useful in studies of Alzheimer's Disease. | ||
| 003741 | B6D2-Tg(Prnp-MAPT)43Vle/J | Cryopreserved - Ready for recovery |
| 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 | ||
| 002328 | C.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 | ||
| 003375 | C3B6-Tg(APP695)3Dbo/J | Cryopreserved - Ready for recovery |
| 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 | Cryopreserved - Ready for recovery |
| 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 | ||
| 005706 | C57BL/6-Tg(tetO-CDK5R1/GFP)337Lht/J | Cryopreserved - Ready for recovery |
| 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; ..... | ||
| 006472 | D2.129(B6)-Tg(APPSw)40Btla/J | 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). These R1.40 transgenic mice may be useful in studying the pathogenesis of Familial Alzheimer's Disease and possible therapeutic treatments.
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 va ..... | ||
| 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 | Cryopreserved - Ready for recovery |
| 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 ..... 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. | ||
| 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. | ||
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