Search Criteria: Research Area is "Neurobiology Research"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 002052 | B6.129P2-Apoetm1Unc/J | Level 1 |
| 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. | ||
| 001026 | BALB/cByJ | Level 1 |
| BALB/c mice are particularly well known for the production of plasmacytomas following injection with mineral oil, forming the basis for the production of monoclonal antibodies. Although not all BALB/c substrains have been examined for plasmacytoma induction, substrains derived from the Andervont (An) lineage (which includes BALB/cByJ) typically are susceptible, while those descended from BALB/cJ are resistant (see: Potter M ,1985). Mammary tumor incidence is normally low, but infection with mammary tumor virus by fostering to MMTV+ C3H mice dramatically increases tumor number and age of onset. BALB/c mice develop other cancers later in life including reticular neoplasms, primary lung tumors, and renal tumors. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in both BALB/cJ and BALB/cByJ substrains. BALB/cByJ has a deletion in the Qa2 subregion of the murine MHC. | ||
| 000651 | BALB/cJ | Level 1 |
| BALB/c mice are particularly well known for the production of plasmacytomas following injection with mineral oil forming the basis for the production of monoclonal antibodies. Although not all BALB/c substrains have been examined for plasmacytoma induction, substrains derived from the Andervont (An) lineage (which includes BALB/cByJ) typically are susceptible, while those descended from BALB/cJ are resistant (see: Potter M ,1985). Mammary tumor incidence is normally low but infection with mammary tumor virus by fostering to MMTV+ C3H mice dramatically increases tumor number and age of onset. BALB/c mice develop other cancers later in life including reticular neoplasms, primary lung tumors, and renal tumors. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in both BALB/cJ and BALB/cByJ substrains.
White et al. reported a variation in thioglycolate medium-induced peritoneal leukocyte recruitment in 4 analyzed s
..... | ||
| 000659 | C3H/HeJ | Level 1 |
| C3H/HeJ mice are used as a general purpose strain in a wide variety of research areas including cancer, immunology and inflammation, sensorineural, and cardiovascular biology. C3H/HeJ mice and all other Jackson substrains are homozygous for the retinal degeneration 1 mutation (Pde6brd1), which causes blindness by weaning age. There is also a high incidence of hepatomas in C3H mice (reportedly 72-91% in males at 14 months, 59% in virgin females, 30-38% in breeding females). Despite the lack of exogenous mouse mammary tumor virus (MMTV), virgin and breeding females may still develop some mammary tumors later in life. C3H/HeJ mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 00066
..... For more information please see the full phenotype on the strain data sheet | ||
| 000664 | C57BL/6J | Level 1 |
| C57BL/6 is the most widely used inbred strain. It is commonly used as a general purpose strain and background strain for the generation of congenics carrying both spontaneous and induced mutations. Although this strain is refractory to many tumors, it is a permissive background for maximal expression of most mutations. C57BL/6J mice are used in a wide variety of research areas including cardiovascular biology, developmental biology, diabetes and obesity, genetics, immunology, neurobiology, and sensorineural research. C57BL/6J mice are also commonly used in the production of transgenic mice. Overall, C57BL/6 mice breed well, are long-lived, and have a low susceptibility to tumors. Primitive hematopoietic stem cells from C57BL/6J mice show greatly delayed senescence relative to BALB/c and DBA/2J. This is a dominant trait. Other characteristics include: 1) a high susceptibility to diet-induced obesity, type 2 diabetes, and atherosclerosis; 2) a high incidence of microphthalmia and other a
..... For more information please see the full phenotype on the strain data sheet | ||
| 000671 | DBA/2J | Level 1 |
| DBA/2J is a widely used inbred strain that is valuable in a large number of research areas, including cardiovascular biology, neurobiology, and sensorineural research. Its characteristics are often contrasted with those of the C57BL/6J inbred strain (Stock No. 000664). DBA/2J mice show a low susceptibility to developing atherosclerotic aortic lesions (20 to 350 um2 atherosclerotic aortic lesions /aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). They also exhibit high-frequency hearing loss beginning roughly at the time of weaning/adolescence (between 3-4 weeks of age) and becoming severe by 2-3 months of age. This strain possesses three recessive alleles that cause progressive cochlear pathology initially affecting the organ of Corti. Decreasing anteroventral cochlear nucleus volume decreases and neuron loss parallel the progression of peripheral hearing loss. Young
..... For more information please see the full phenotype on the strain data sheet | ||
| 001976 | NOD/ShiLtJ | Level 1 |
| Diabetes in NOD/ShiLtJ mice is characterized by insulitis, a leukocytic infiltrate of the pancreatic islets. Marked decreases in pancreatic insulin content occur in females at about 12 weeks of age and several weeks later in males. Onset of diabetes is marked by moderate glycosuria and by a non-fasting plasma glucose higher than 250 mg/dl. Diabetic mice are hypoinsulinemic and hyperglucagonemic, indicating a selective destruction of pancreatic islet beta cells. Susceptibility to IDDM in NOD/ShiLtJ mice is polygenic, and environment, including housing conditions, health status, and diet, exerts a strong effect on penetrance. NOD/ShiLtJ females are more widely used than males because the onset of IDDM symptoms occurs earlier and with a higher incidence (90-100% by 30 weeks of age). NOD/ShiLtJ males develop IDDM at a frequency of between 40-60% by 30-40 weeks of age. Male mice are useful for certain applications, including pharmaceutical studies, "accelerated transfer" of IDDM, and some <
>
..... For more information please see the full phenotype on the strain data sheet | ||
| 000691 | 129X1/SvJ | Level 2 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson, et al., 1997.
In response to challenge, 129S1/SvImJ mice develop immune-mediated nephritis characterized by proteinuria, glome
..... | ||
| 000646 | A/J | Level 2 |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A inbred strain is used widely used in cancer and immunology research. It is highly susceptible to cortisone-induced congenital cleft palate. It has a high incidence of spontaneous lung adenomas, and lung tumors readily develop in response to carcinogens. A high percentage of mammary adenocarcinomas (a large proportion of acinar-type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. A/J mice fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid, and 15% fat) fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/cdJ, Sto
..... | ||
| 000648 | AKR/J | Level 2 |
| Originally inbred at the Rockefeller Institute, AKR mice are widely used in cancer research for their high leukemia incidence (60-90%) and in immunology as a source of the Thy1.1 (theta AKR) antigen. AKR/J mice are viremic from birth, and express the ecotropic retrovirus AKV in all tissues. The hair interior defect (hid) mutation, a strain characteristic of AKR mice, causes alterations in hair development that is only evident microscopically. Adrenocortical lipid depletion (ald) in AKR mice is caused by a mutation in sterol O-acyltransferase 1 (Soat1), and leads to a truncated SOAT1 protein. AKR/J mice are relatively resistant to aortic lesion formation on a semi-synthetic high fat diet and are hyporesponsive to diets containing high levels of fat and cholesterol. | ||
| 001801 | C57BL/10ScSn-Dmdmdx/J | Level 2 |
| The X-linked dystrophin gene (Dmd) is highly expressed in muscle cells and encodes a cytoskeletal protein which localizes to the inner face of the sarcolemma. Dystrophin molecules bind to cytoskeletal F-actin and transmembrane beta-dystroglycan as part of a complex, multimolecular unit that mediates signaling between the intracellular cytoskeleton and the extracellular matrix. The structure and localization also suggest that dystrophin is important for stabilizing the plasma membrane, particularly during contraction. The mdx mutation of Dmd is recessive and heterozygous females are visually indistinguishable from wild-type mice. Females homozygous and males hemizygous for the Dmdmdx allele retain a normal lifespan and can survive up to two years. Like human patients who suffer from one of the most common neuromuscular diseases, Duchenne muscular dystrophy (DMD), the Dmdmdx mutants do not express dystrophin and therefore have been
..... For more information please see the full phenotype on the strain data sheet | ||
| 000670 | DBA/1J | Level 2 |
| DBA/1J mice are widely used as a model for rheumatoid arthritis: immunization with type II collagen leads to the development of severe polyarthritis mediated by an autoimmune response. The incidence of collagen induced arthritis varies by experimental protocol, but is less than 100%. Similar to the human condition, mice with collagen-induced arthritis display synovitis and erosions of cartilage and bone. In addition, susceptibility in both humans and mice is linked to the expression of specific MHC class II molecules. DBA/1J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions on an atherogenic diet. In response to challenge, DBA/1J mice develop immune-mediated nephritis characterized by proteinuria, glomerulonephritis and tubulointerstitial disease (Xie et al., 2004). | ||
| 001140 | DBA/1LacJ | Level 2 |
| Historical reports indicate DBA/1J and DBA/1LacJ mice immunized with type II collagen develop a severe polyarthritis mediated by an autoimmune response. Recent in-house studies suggest that the response to collagen induction in the DBA/1LacJ strain is not as robust as indicated by earlier studies. Arthritis models such as B10.RIII-H2r H2-T18b/(71NS)SnJ (Stock No. 000457) and BUB/BnJ (Stock No. 000653) can be used as alternatives to DBA/1LacJ. Similar to the human condition, mice with collagen-induced arthritis display synovitis and erosions of cartilage and bone. In addition, susceptibility in both humans and mice is linked to the expression of specific MHC class II molecules. DBA/1 mice show a low susceptibility to developing atherosclerotic aortic lesions (20 to 350 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on a
..... For more information please see the full phenotype on the strain data sheet | ||
| 000486 | MRL/MpJ | Level 2 |
| The MRL/MpJ mice are large but docile to the point that males rarely fight. They are the parent and control strain for for MRL/MpJ-Faslpr (Stock Nos. 000485, 006825). Despite carrying the normal Fas gene, MRL/MpJ mice also exhibit autoimmune disorders, but symptoms are manifested much later in life compared to those the MRL/MpJ-Faslpr mice. Starting at about three months of age, levels of circulating immune complexes rise greatly in the MRL-Faslpr mouse but not in the wildtype control, MRL/MpJ. Also beginning at 3 months Faslpr mice exhibit very severe poliferative glomerulonephritis, whereas in the MRL/MpJ controls usually only mild glomerular lesions are detected. MRL/MpJ inbred female typically die at 73 weeks of age and males die at 93 weeks. This compares to a lifespan of 17 weeks in the female and 22 weeks for males in the mouse homozygous for Faslpr. See MRL/MpJ-Faslpr<
>
..... For more information please see the full phenotype on the strain data sheet | ||
| 000686 | SJL/J | Level 2 |
| SJL mice display a very high incidence of reticulum cell sarcomas resembling Hodgkin's disease by approximately one year of age. Sarcomas first appear in the Peyer's patches and mesenteric lymph nodes and later in the spleen, liver, thymus and other lymph nodes. Most of the tumors are mixed-cell types classified as type B reticulum cell neoplasms, but a few are type A histiocytomas. This strain is also characterized by extreme aggression in males and its susceptibility to experimental autoimmune encephalomyelitis (EAE) for multiple sclerosis research. SJL/J mice develop a spontaneous myopathy resulting from a splice-site mutation in the Dysferlin gene. This Dysfim allele has been shown to result in decreased levels of dysferlin protein in SJL/J mice and makes this strain a good model for limb girdle muscular dystrophy 2B. This spontaneous myopathy is characterized by a progressive loss of muscle mass and strength corresponding with an increase in muscle pathology incl
..... For more information please see the full phenotype on the strain data sheet | ||
| 100410 | WBB6F1/J-KitW/KitW-v/J | Level 2 |
| Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. KitW/KitW-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. KitW/KitW-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment. | ||
| 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 | ||
| 002810 | B6CBA-Tg(HDexon1)62Gpb/1J | Level 3 |
| This line is transgenic for the 5' end of the human HD gene carrying (CAG)115-(CAG)150 repeat expansions. The transgene is ubiquitously expressed. Transgenic mice exhibit a progressive neurological phenotype that mimics many of the features of HD, including choreiform-like movements, involuntary stereotypic movements, tremor, and epileptic seizures, as well as nonmovement disorder components, including unusual vocalization. They urinate frequently and exhibit loss of body weight and muscle bulk through the course of the disease. Neurologically they develop Neuronal Intranuclear Inclusions (NII) which contain both the huntingtin and ubiquitin proteins. Previously unknown, these NII have subsequently been identified in human HD patients. The age of onset of HD symptoms is reported to occur between 9 and 11 weeks. Commonly known as the "R6/2" strain. Transgenic mice develop hyperglycemia by 12 weeks of age with a corresponding decrease in insulin levels. Pancreatic beta cells develop
..... | ||
| 006494 | B6CBA-Tg(HDexon1)62Gpb/3J | Level 3 |
| This line is transgenic for the 5' end of the human HD gene carrying less than (CAG)150 repeat expansions. The transgene is ubiquitously expressed. Transgenic mice exhibit a progressive neurological phenotype that mimics many of the features of HD, including choreiform-like movements, involuntary stereotypic movements, tremor, and epileptic seizures, as well as nonmovement disorder components, including unusual vocalization. They urinate frequently and exhibit loss of body weight and muscle bulk through the course of the disease. Neurologically they develop Neuronal Intranuclear Inclusions (NII) which contain both the huntingtin and ubiquitin proteins. Previously unknown, these NII have subsequently been identified in human HD patients. The age of onset of HD symptoms is reported to occur between 9 and 11 weeks. Commonly known as the "R6/2" strain. Transgenic mice develop hyperglycemia by 12 weeks of age with a corresponding decrease in insulin levels. Pancreatic beta cells develop
..... | ||
| 002726 | B6SJL-Tg(SOD1*G93A)1Gur/J | Level 3 |
| Mice hemizygous for this SOD1-G93A (also called G93A-SOD1) transgene are viable and fertile, with transgenic expression of a G93A mutant form of human SOD1. This founder line (often referred to as G1H) is reported to have high transgene copy number. Hemizygotes exhibit a phenotype similar to amyotrophic lateral sclerosis (ALS) in humans; becoming paralyzed in one or more limbs with paralysis due to loss of motor neurons from the spinal cord. Transgenic mice have a life span of approximately 19-23 weeks. These SOD1-G93A (also called G93A-SOD1) transgenic mice may be useful in studying neuromuscular disorders, including Amyotrophic Lateral Sclerosis (ALS or Lou Gehrig's Disease). | ||
| 000662 | C57BLKS/J | Level 3 |
| Although C57BLKS/J is estimated to have more than 70% of its genome derived from C57BL/6J, these strains are phenotypically distinct. Diet-induced atherosclerotic lesions are much more severe in C57BLKS/J than in C57BL/6J or many other inbred strains. Compared with a panel of inbred strains, C57BLKS/J was found to have low total cholesterol and low HDL cholesterol when fed a normal diet and high total cholesterol and HDL cholesterol in an atherogenic diet. Paigen et al. found high levels of plasma bile salts in C57BLKS/J females after 8 weeks on an atherogenic diet. The mutations diabetes (Leprdb) and obese (Lepob) each express a much more severe phenotype on the C57BLKS/J background than on the C57BL/6J background. The Cpefat mutation causes severe obesity, hyperinsulinemia, and hyperglycemia on the C57BLKS/J background rather than the hyperinsulinemia, and mild obesity without hyperglycemia found on the HRS/J background. In
..... For more information please see the full phenotype on the strain data sheet | ||
| 000676 | LP/J | Level 3 |
| LP/J mice display a high susceptibility to audiogenic seizures. This strain is also reported to have a fairly high incidence of tumors that develop later in life, including mammary tumors, lymphoma, lung and soft-tissue sarcomas. LP/J mice are also homozygous for the spontaneous mutation piebald in the endothelin receptor type B gene (Ednrbs). The piebald spontaneous mutation is the result of a mutation in the endothelin receptor type B gene, Ednrb. Mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. They also have dark eyes. The white areas of the coat are completely lacking in neural crest-derived melanocytes, and there is a reduction in the number of melanocytes in the choroid layer of the eye is reduced. | ||
| 000680 | PL/J | Level 3 |
| PL/J mice show a moderate susceptibility to experimental allergic encephalitis (EAE) with late onset and high mortality. Reports of leukemia incidence vary from 50% in females and 19% in males to 80-90%. In addition to a low threshold to electroconvulsive seizures, PL/J mice are susceptible to handling and rhythmic tossing-induced seizures (Kitami T, et al, 2004). | ||
| 000690 | 129P3/J | Level 4 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently, 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson, et al., 1997. | ||
| 002065 | 129T2/SvEmsJ | Level 4 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson, et al., 1997. | ||
| 002213 | B6.129S4-Ngfrtm1Jae/J | Level 4 |
| 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 4 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 2- to 3-fold decreased sensitivity to NGF at embryonic day 15 and postnatal day 3, respectively. These ages coincide with the peak of naturally occurring cell death. p75-deficient embryonic hip
..... For more information please see the full phenotype on the strain data sheet | ||
| 003770 | B6.129X1-Trpv1tm1Jul/J | Level 4 |
| Mice that are homozygous 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 in dorsal root ganglia. Cultured dorsal root ganglia neurons and skin preparations display no, or markedly attenuated, response to vanilloid compounds, acidified environments or heat (43 degrees C). In intact wild type mice, a subcutaneous injection of vanilloid compounds into the hind paw elicits a pain response with subsequent swelling. No pain response is observed in homozygotes and swelling is noticeably reduced. Also absent is the profound reduction in body temperature following a subcutaneous injection of capsaicin. Homozygotes appear to display robust deficits in thermally evoked pain-related behavior and do not display an aversion to ingesting capsaicin-supplemented drinking water. | ||
| 003008 | B6;129S-Tnftm1Gkl/J | Level 4 |
| Mice homozygous for the Tnftm1Gkl targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does
..... For more information please see the full phenotype on the strain data sheet | ||
| 003243 | B6;129S-Tnfrsf1atm1Imx Tnfrsf1btm1Imx/J | Level 4 |
| Mice homozygous for both the Tnfrsf1atm1Imx and Tnfrsf1btm1Imx targeted mutations (p55 and p75 deficient) are viable and fertile. Double homozygous mutant mice fail to bind TNF. Thymus, spleen, and other lymphoid tissue are normal, indicating that TNF is not required for normal development of these organs. | ||
| 002633 | B6;129S4-Nos1tm1Plh/J | Level 4 |
| Mice homozygous for the Nos1tm1Plh targeted mutation are viable and fertile; however, they have enlarged stomachs and reduced stroke size. Hyperglycemic-euglycemic clamp studies demonstrate that homozygotes exhibit insulin resistance at the level of peripheral tissues. Homozygous males are reported to be more aggressive than normal wildtype siblings although this has not been confirmed in The Jackson Laboratory colony. These mice may be useful model for stroke research. | ||
| 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 tha
..... For more information please see the full phenotype on the strain data sheet | ||
| 000661 | C3H/HeSnJ | Level 4 |
| 000049 | C57BL/6J-KitW-v/J | Level 4 |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. | ||
| 002050 | NOR/LtJ | Level 4 |
| NOR/LtJ mice are insulitis resistant and diabetes free. NOR/LtJ mice still exhibit peripheral T-lymphocyte accumulation and defective peritoneal macrophage responses characteristic of NOD/LtJ mice. NOR/LtJ mice are matched at the diabetogenic H2g7 complex to NOD/LtJ. | ||
| 000726 | RBF/DnJ | Level 4 |
| The RBF inbred strain arose from crosses with wild mice, originally known as "tobacco mouse", captured in Valle di Poschiavo in S.E. Switzerland. The wild mice originally known as 'tobacco mouse' because of the coat colour. The strain was transferred to Dr. M. Davisson (Dn) in 1981 and subsequently to the production colony of The Jackson Laborotory (J). Mice are homozygous for Robertsonian translocation Rb(1.3)1Bnr, Rb(8.12)5Bnr and Rb(9.14)6Bnr. This strain is useful for production of antibody producing hybridomas. | ||
| 000692 | WB/ReJ KitW/J | Level 4 |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. The lack of germ cells in homozygous mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. | ||
| 004337 | 129(Cg)-Foxg1tm1(cre)Skm/J | Repository- Live |
| This strain expresses Cre recombinase from the endogenous Foxg1 locus. Forkhead box G1 is required for telencephalon development and is expressed specifically in the telencephalon and discrete head structures. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs in the telencephalon, anterior optic vesicle (developing lens and retina), otic vesicle, facial and head ectoderm, olfactory epithelium, mid-hindbrain junction and pharyngeal pouches. Mice that are homozygous for the targeted mutation die perinatally. Heterozygous mutant mice are viable, fertile, 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 of telencephalic development. | ||
| 006373 | 129-Braftm1Sva/J | Repository- Live |
| Homozygous "floxed B-raf" (B-raff/f) mice are viable and fertile with normal B-raf protein expression. When bred to mice expressing Cre recombinase under the control of a promoter of interest, exon 12 of the targeted gene is deleted in the tissue of interest. These mutant mice may be useful in neurological studies such as Ras/Raf and MEK/ERK signaling, synaptic (neural) plasticity, learning and memory. For example, when crossed to a strain expressing Cre recombinase in nervous tissue (see Stock No. 003771), this mutant mouse strain may be useful in studies of neuron development. For example, when crossed to a strain expressing interferon inducible Cre recombinase (see Stock No. 003755), this mutant mouse strain may be useful in studies of extraembryonic mammmalian development. | ||
| 006830 | 129-Dysftm1Kcam/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable, fertile and show a normal growth rate. Mice develop a slowly progressive muscular dystrophy. By the age of 2 months, a few individual necrotic and centrally nucleated fibers can be detected throughout the muscle; the number increases with age. By 8 months, the muscle develops all of the pathological characteristics of muscular dystrophy (e.g. regenerating fibers, split fibers, muscle necrosis with macrophage infiltration and fat replacement). The severity of the pathology varies in different muscles. Muscle fibers are defective in Ca2+-dependent sarcolemma resealing/repair. No protein product from the targeted gene is detected in skeletal muscle microsomes. This mutant mouse strain represents a model that may be useful in studies of muscle disease and repair. | ||
| 004293 | 129-Shhtm2Amc/J | Repository- Live |
| Mice that are homozygous for the Shhtm2Amc targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This conditional mutant contains two loxP sites flanking exon 2 of the targeted allele. Cre-mediated recombination excises exon 2 and some surrounding intronic sequence, generating a null allele. When the conditional mutant is crossed with a ubiquitously-expressing Cre recombinase carrier to remove Shh activity in the early embryo, the resulting phenotype resembles the Shh null mutation. These conditional mutant mice may be mated to strains expressing Cre recombinase to study the effects of temporal and tissue-specific ablation of the targeted allele. This mutant mouse strain represents a model that may be useful in studies of developmental defects resulting from disruption of Shh-dependent pathways.
When bred to a strain expressing Cre recombinase under the control of a tet
..... | ||
| 001137 | 129P1/ReJ | Repository- Live |
| For a complete history of the numerous 129 substrains please refer to Simpson, et al., 1997. Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. Most recently 129 mice are widely used strain in the production of targeted mutations due to the availability of several lines of embryonic stem cells. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of substrains into three major groups: parental substrains, steel substrains and "ter" substrains. Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. | ||
| 000641 | 129P1/ReJ-Lama2dy/J | Repository- Live |
| Mice homozygous for the dystrophia-muscularis spontaneous mutations (Lama2dy and Lama2dy-2J) are characterized by progressive weakness and paralysis beginning at about 3 1/2 weeks of age. The hindlimbs are affected first, later the axial and forelimb musculature. Death usually occurs before 6 months of age, and mutant mice are usually sterile. Skeletal muscle shows degenerative changes with proliferation of sarcolemmal nuclei, increase in amount of interstitial tissue, and size variation among individual muscle fibers. In the dorsal and ventral roots of the peripheral nerves, both spinal and cranial, Schwann cells fail to separate and ensheathe axons so that groups of closely apposed naked axons, normally seen only in early stages, persist into adulthood. In the rest of the PNS, the basement membrane of Schwann cells is interrupted by gaps, the internodal gap in the nodes of Ranvier is lengthened, and there is delayed onset of myelination with fewer
..... For more information please see the full phenotype on the strain data sheet | ||
| 007965 | 129S-Dvl1tm1Awb/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 MEF (mouse embryonic fibroblasts) derived from homozygotes. Homozygotes exhibit diminished social interaction behavior, do not barber or trim whiskers of cagemates, show subordinance in social dominance tests, do not sleep huddled together and do not build nests. Although mutants have an attenuated prepulse inhibition of acoustic and tactile startle (sensorimotor gating of the startle reflex), they do not exhibit any deficits in locomotor or cognitive function. This mutant mouse strain may be useful in studies of social behavior, sensorimotor gating, and possibly psychiatric disorders. | ||
| 004545 | 129S-Npytm1Rpa/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 Northern or Western blot analysis of brain or adrenal gland tissue. Beta-galactosidase activity assays and in situ hybridization demonstrate similar expression patterns for the lacZ gene and the endogenous wildtype gene. Spontaneous seizures are exhibited by some mice at age 6 to 8 weeks. Homozygous mice are susceptible to seizures induced by GABA antagonist treatment. Mutant mice have an increased sensitivity to leptin treatment which results in a greater initial reduction of food intake and weight loss when compared to wildtype mice. This mutant mouse strain may be useful in studies related to the role of neuropeptide Y in obesity. | ||
| 008002 | 129S-Pafah1b1tm2Awb/J | Repository- Live |
| These mice possess loxP sites flanking exons 3 through 6 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. Histological analysis of brains from homozygotes reveals slightly wider CA1 and CA3 regions and a split in CA2 region in the hippocampus. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 3 through 6 deleted in the cre-expressing tissue(s). | ||
| 007587 | 129S-Park2tm1Rpa/J | Repository- Live |
| Mice carrying this mutation are viable, fertile, and display no apparent defects or abnormalities. Mutations in the human homolog of this gene are associated with autosomal juvenile parkinsonism, a heritable form of Parkinson's disease. | ||
| 002779 | 129S-Parp1tm1Zqw/J | Repository- Live |
| Mice that are homozygous null for the targeted gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Although a shortened transcript is generated, no enzymatic activity is detected in tissues. Proliferation of homozygous-null fibroblasts and thymocytes is impaired following gamma-radiation in comparison to cells derived from wild-type mice. Older mice are susceptible to spontaneous development of skin disease. A significant portion of older mice ( ~30%) can be expected to exhibit epidermal hyperplasia. Null mice are also less susceptible to damage induced by the neurotoxin MPTP. | ||
| 006409 | 129S1.Cg-Tg(APPSw)40Btla/J | Repository- Live |
| These 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. This mutant mouse strain represents a model that may be useful in studies of 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 vary from that originally described. A publication (Lehman et al. 2003 Hum Mol Genet 12:2949) compar
..... | ||
| 002753 | 129S6/SvEvTac-Atmtm1Awb/J | Repository- Live |
| Mice homozygous for the Atmtm1Awb targeted mutation display many of the characteristics of ataxia telangiectasia, including growth retardation, neurologic dysfunction, infertility, defects in T lymphocyte maturation, and extreme sensitivity to gamma-irradiation. Most homozygotes develop thymic lymphoma between 2 and 4 months of age. Heterozygous mice display no abnormalities through eight months of age. | ||
| 006555 | A.129(B6)-Tg(APPSw)40Btla/J | Repository- Live |
| These 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). This mutant mouse strain represents a model that may be useful in studies of 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 p
..... | ||
| 000647 | A/WySnJ | Repository- Live |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A inbred strain is used widely used in cancer and immunology research. It is highly susceptible to induction of congenital cleft palate by cortisone. It has a high incidence of spontaneous lung adenomas and lung tumors readily develop in response to carcinogens. High percentage of mammary adenocarcinomas (a large proportion acinar type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. Unlike A/J mice, A/WySnJ mice carry a spontaneous mutation in Tnfrsf13c and exhibit a significant loss of mature B cells (Miller, et al., 1991, Lentz et al., 1996, Shulga-Morskaya et al., 2004). | ||
| 005136 | A/WySnJ-ctl/J | Repository- Live |
| Mice homozygous for the ctl mutation are easily recognizable at birth by their curly or bent tails. | ||
| 003070 | ALR/LtJ | Repository- Live |
| ALS/LtJ (Stock No. 003072) and ALR/LtJ inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. ALR/LtJ mice are of particular interest to investigators studying the immunogenetics of NOD/LtJ mice in that the ALR/LtJ MHC haplotype (H2gx) is a variant of the diabetogenic NOD H2g7 haplotype. The (H2gx) haplotype is identical to the H2g7 haplotype from the H2-K end of the complex through the class II and class III region distal to Hsp70. However, at the distal H2-D end of the complex, ALR/LtJ mice have a rare H2-Dgx allele. Despite the similarities to the NOD/ShiLtJ mice, ALR/LtJ mice do not develop
..... For more information please see the full phenotype on the strain data sheet | ||
| 003072 | ALS/LtJ | Repository- Live |
| ALS/LtJ and ALR/LtJ (Stock No. 003070) inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. By 34 wk of age, both untreated ALS/Lt and ALR/Lt males fed a 6% fat-containing chow diet attain a mean body weight of around 50 grams. Genome wide scan comparison shows that ALS/LtJ mice are more closely related to NON/ShiLtJ mice (they share the H2nb1 haplotype) than to NOD/ShiLtJ. Like two other ICR-derived inbred strains selected in Japan (NON and NSY), alloxan-untreated ALS/Lt males exhibit impaired glucose tolerance when tested by intraperitoneal administration of glucose. However, unlike NON/ShiLt males, which exhibit impaired glucose tolerance in the presence
..... For more information please see the full phenotype on the strain data sheet | ||
| 001673 | AXB1/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001681 | AXB10/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001683 | AXB12/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001826 | AXB13/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB13/PgnJ and AXB14/PgnJ are considered ?sister strains? being identical throughout much of the genome but differing in large regions of Chromosomes 11, 12, 13, and in small regions of a few other Chromosomes. Because these two strains are "near congenics" a nomenclature change has been made to update AXB14/PgnJ to AXB13a/PgnJ. In general, 'sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a ?near congenic? for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their suscepti
..... | ||
| 001685 | AXB15/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001687 | AXB19/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB18/Pgn, AXB19/Pgn, and AXB20/Pgn were found to be highly similar in their overall genomes, but with particular Chromosomes differing between them. Two of these "sister" strains were renamed. AXB19/Pgn was designated the primary strain since it has the best traceable history, and therefore its name remained unchanged. AXB18/Pgn was renamed AXB19a/Pgn and AXB20/Pgn was renamed AXB19b/Pgn. In general, the "sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a "near congenic" for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalu ..... For more information please see the full phenotype on the strain data sheet | ||
| 001686 | AXB19a/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB18/Pgn, AXB19/Pgn, and AXB20/Pgn were found to be highly similar in their overall genomes, but with particular Chromosomes differing between them. Two of these "sister" strains were renamed. AXB19/Pgn was designated the primary strain since it has the best traceable history, and therefore its name remained unchanged. AXB18/Pgn was renamed AXB19a/Pgn and AXB20/Pgn was renamed AXB19b/Pgn. In general, the "sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a "near congenic" for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalu ..... For more information please see the full phenotype on the strain data sheet | ||
| 001688 | AXB19b/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB18/Pgn, AXB19/Pgn, and AXB20/Pgn were found to be highly similar in their overall genomes, but with particular Chromosomes differing between them. Two of these "sister" strains were renamed. AXB19/Pgn was designated the primary strain since it has the best traceable history, and therefore its name remained unchanged. AXB18/Pgn was renamed AXB19a/Pgn and AXB20/Pgn was renamed AXB19b/Pgn. In general, the "sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a "near congenic" for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalu ..... For more information please see the full phenotype on the strain data sheet | ||
| 001674 | AXB2/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001690 | AXB23/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001691 | AXB24/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001676 | AXB4/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001677 | AXB5/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001678 | AXB6/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001679 | AXB8/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 000578 | B6 x STOCK Tyrc-ch Bmp5se +/+ Myo6sv/J | Repository- Live |
| Mice homozygous for the Snell's waltzer spontaneous mutation (Myo6sv) show to a marked degree the typical circling, head-tossing, deafness, and hyperactivity of other mutant mice of this type. Homozygous mutant mice are recognizable by the age of 1 week. The abnormalities of the inner ear consist of degeneration of the entire neuroepithelium comprising the organ of Corti, the saccular and utricular maculae, and the cristae of all three semicircular canals. Although viability of homozygotes is nearly normal, breeding ability is reduced and males are more reliable breeders than females.
Specific cytoskeletal components are critical for specific cellular structures. The microvilli of intestinal brush border cells in Myo6sv homozygotes are shorter than normal. While myosin 6 is not critical for the development of hair cell stereocilia, it is essential for their maintenance. At birth the stereocilia appear nearly normal with only occasional stereocil
..... | ||
| 006963 | B6(101)-Mdh1am1H/LvtJ | Repository- Live |
| Homozygotes die at approximately embryonic day 17.5 (E17.5), but heterozygotes are viable and fertile. Homozygous embryos are nearly colorless, are approximately half the size of heterozygous and wildtype littermates, and show altered or delayed brain/body development. There may be a vascular defect. Decreased expression of this gene has previously been implicated with cases of schizophrenia. | ||
| 004684 | B6(129P2) Nos2tm1Lau-chtl/J | 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. | ||
| 004608 | B6(Cg)-Htra2mnd2/J | Repository- Live |
| Mice homozygous for the recessive Htra2mnd2 mutation have a basal ganglia disorder initially described as an early onset motor neuron disease. This is first outwardly evident by 21 to 24 days of age as an unsteady gait with extended hind limbs, repetitive movements and episodes of sudden arrests. This progresses to include severe muscle atrophy, hunched posture, increased imbalance, chorea, dystonia, and progressive akinesis. A failure to gain weight becomes evident shortly after the onset of the other symptoms and by 35 days of age wildtype littermates are twice as heavy as the mutants. Body fat is not detectable at necropsy. Both the spleen and the thymus drop from normal weights at 23 days of age to 10% of normal at 30 days of age and the thymic corticomedullary junction is lost. Death usually occurs within two weeks of disease onset, by 40 days of age. The growth retardation is not the primary cause since disease is not delayed by intragastric feeding.
..... | ||
| 008149 | B6(Cg)-Snord116tm1.1Uta/J | Repository- Live |
| Mice homozygous for this Snord116del (1-loxP or knockout) allele are viable and fertile. As the Snord116 gene cluster is imprinted and expressed only from the paternal allele, mice with paternal inheritance of the deletion lack expression of the targeted Snord116 small nucleolar RNAs (snoRNAs) gene cluster in brain tissues. Similarly, paternal transmission of the mutant allele is required to obtain the mutant phenotype in offspring. Affected heterozygotes (paternal deleted/maternal wildtype) recapitulate a subset of Prader-Willi syndrome (PWS) characteristics, including early-onset postnatal growth retardation, delayed sexual maturation, increased anxiety, motor learning deficit and hyperphagia (but not obesity). Other reported abnormalities include altered metabolic fuel usage, prolonged meal time, and increased levels of circulating ghrelin. These Snord116del mice may be useful in studying growth and feeding regulation, mechanisms of obesity, and pa
..... For more information please see the full phenotype on the strain data sheet | ||
| 008118 | B6(Cg)-Snord116tm1Uta/J | Repository- Live |
| Mice homozygous for this 2-loxP (floxed) allele are viable and fertile, with loxP sites flanking the Snord116 small nucleolar RNAs (snoRNAs) gene cluster. When bred to mice that express Cre recombinase, the resulting offspring will have this gene cluster deleted in the cre-expressing tissue(s). Because the Snord116 gene cluster is imprinted and only expressed from the paternal allele, breeding 2-loxP males with cre-expressing females may be required to generate deleted offspring with the knockout phenotype. The donating investigator reports that the distance between the two loxP sites (~140 kb) may reduce the recombination efficiency in somatic cells. As deletions of the Snord116 cluster are associated with Prader-Willi syndrome (PWS), mice carrying the 2-loxP (floxed) allele may be useful in generating conditional mutations for studying the role of Snord116 in growth and feeding regulation, mechanisms of obesity, and patho
..... For more information please see the full phenotype on the strain data sheet | ||
| 004640 | B6(MOR)-Tmhshscy/J | Repository- Live |
| Mice homozygous for the Tmhshscy mutation circle rapidly, shake their heads from side to side, fail to swim, and are congenitally deaf. Although hair cells appear normal at birth, they degenerate. At 4 months of age, degeneration of the organ of Corti is also found, more pronounced in the basal region of the cochlea than the apex, with loss of inner and outer hair cells and decreased spiral ganglia (Longo-Guess et al., 2005). | ||
| 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 | ||
| 006257 | B6.129-Aldh5a1tm1Kmg/J | Repository- Live |
| Homozygous mutation of this gene results in reduced body weight, ataxia, seizures, gliosis of the hippocampus, and eventual status epilepticus. From 19-26 days of age, repetitive tonic-clonic seizures results in more than 95% mortality. Biochemical assays shows complete ablation of the endogenous enzymatic activity in the brains, livers, hearts, and kidneys of homozygous mutant mice. Homozygotes have increased levels of GHB and GABA in liver and brain tissues, as well as in urine. Phenotype can be rescued to varying degrees utilizing a number of both pharmacotherapeutic and gene therapeutic approaches. Although heterozygous mice have approximately 50% of the endogenous enzyme activity compared to wildtype mice, they are viable and fertile. Mice with this targeted mutation may be useful in studying succinate semialdehyde dehydrogenase (SSADH) deficiency and to explore the effect of GABA and GHB accumulation on central nervous system development and function. | ||
| 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. | ||
| 006836 | B6.129-Dag1tm1Kcam/J | Repository- Live |
| Heterozygotes are viable and fertile, but homozygous embryos exhibit gross developmental abnormalities beginning around 6.5 days of gestation. This lethality is attributed to a disruption of Reichert’s membrane, an extra-embryonic basement membrane. Laminin and collagen IV are specifically disrupted. No detectable transcript or protein is produced from this allele in homozygous embryos. Northern blot analysis of skeletal muscle RNA shows that transcript levels in heterozygotes are only 10-20% lower than those in wild-type mice. This mutant mouse strain represents a model that may be useful in studies of muscular dystrophies linked to dystrophin-glycoprotein complexes, and developmental processes. | ||
| 006874 | B6.129-Gabra4tm1.2Geh/J | Repository- Live |
| Mice homozygous for this GABAA-R alpha4F allele are viable and fertile. These mutant mice have loxP sites flanking exon 3 of the targeted gene. When bred to Cre-recombinase expressing mice, offspring will have a deletion of exon 3 in the cre expressing tissue(s). These "floxed" mice may be useful in neurological studies including behavior and neurotransmitter function. Of note, several strains bearing gamma-aminobutyric acid (GABA-A) receptor mutations are available from this donating investigator (Dr. Gregg Homanics, University of Pittsburgh), including Gabra1 (Stock No. 004318), Gabra4 (Stock No. 006874), Gabra6 (Stock No. 002710), Gabrb3 (Stock No. 002711), Gabrd (Stock No.
..... | ||
| 007708 | B6.129-Gt(ROSA)26Sortm1(HD*103Q)Xwy/J | Repository- Live |
| Mice heterozygous for the RosaHD mutant allele are viable and fertile. These mice have the neuropathogenic polyQ-mutant variant of the human Huntingtin protein (mhtt-exon1; 103Q) inserted into the Gt(ROSA)26Sor locus. Expression of mhtt-exon1 is blocked by an upstream loxP-flanked transcriptional STOP sequence. When bred to mice with a Cre recombinase gene under the control of a promoter of interest, the STOP sequence is deleted in the tissue of interest, and mhtt-exon1 expression is observed. As these RosaHD mutant mice allow cre-conditional expression of the neuropathogenic mhtt-exon1 protein, they may be useful in studying Huntington's disease (HD) or other polyQ disorders. Of note, sequencing of the polyQ region (using mice from the 11th backcross) indicate the actual number of repeats to be 98. For example, when bred to strains expressing cre in brain tissues (such as Nestin-Cre (see Stock No. 003771
..... | ||
| 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. | ||
| 006146 | B6.129-Smn1tm1Jme/J | Repository- Live |
| Mice homozygous for this SMNF7 floxed allele are viable and fertile and do not display any gross physical or behavioral abnormalities. Mutant mice exhibit no transcript splicing defects. Cre-mediated recombination of the loxP-flanked sequences results in deletion of exon 7 of the targeted gene. As mutations of this exon are implicated in 95% of all human spinal muscular atrophy (SMA), these mice may be useful in studying SMA or other neuromuscular degenerative diseases.
When crossed to a strain expressing Cre recombinase in neurons (see Stock No. 005938, Stock No. 006297, and Stock No. 006663), this mutant mouse strain may be useful as a model of SMA. When crossed to a strain expressing Cre recombinase in striated muscle fibers (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 005300 | B6.129-Tg(APPSw)40Btla/J | Repository- Live |
| These 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 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. 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 investigator reports i
..... For more information please see the full phenotype on the strain data sheet | ||
| 004146 | B6.129-Tg(Pcp2-cre)2Mpin/J | Repository- Live |
| These transgenic mice express a cre gene inserted into exon 4 of a Pcp2 gene. Mice homozygous for the insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Recombinase activity is observed in most Purkinje cells and some retinal bipolar neurons. Small amounts of activity are observed in an unidentified population of cells of the central nervous system tissue. Recombination is first observed around postnatal day 6 and is fully established 2 to 3 weeks after birth. | ||
| 003890 | B6.129P2(C)-Mecp2tm1.1Bird/J | Repository- Live |
| Homozygous null mice are viable and appear normal at birth. No Mecp2 gene product (mRNA or protein) is detected in tissues. Mobility problems are apparent at 3-8 weeks of age. Mice exhibit hindlimb clasping and uneven breathing. An uneven wearing of teeth associated with misalignment of the jaws is observed in 50% of the animals. Adult males do not mate and their testes remain internal although sperm are present in the cauda epididymis. Symptom progression is variable, but mice can be expected to undergo weight loss, shivering, continued mobility problems before succumbing. Expected lifespan is about 50-60 days. Heterozygous female mice display mobility problems and hindlimb clasping starting at about 6 months, but the symptoms appear not to be progressive. This mutant mouse strain represents a model that may be useful in studies related to Rett Syndrome. Importation of this model was supported in part by the Rett Syndrome Research Foundation. | ||
| 006084 | B6.129P2(Cg)-Foxg1tm1(cre)Skm/J | Repository- Live |
| This strain expresses Cre recombinase from the endogenous Foxg1 locus. Forkhead box G1 is required for telencephalon development and is expressed specifically in the telencephalon and discrete head structures. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs in the telencephalon, anterior optic vesicle (developing lens and retina), otic vesicle, facial and head ectoderm, olfactory epithelium, mid-hindbrain junction and pharyngeal pouches. Mice that are homozygous for the targeted mutation die perinatally. Heterozygous mutant mice are viable, fertile, normal in size. On the C57BL/6 background, forebrain volume in heterozygotes is substantially reduced especially in the cerebral cortex (40.7%), striatum (29.7%), and hippocampus (18.6%). In the adult, the thalamus is reduced in volume by 21.6%. This mutant mouse strain represents a model that ma
..... For more information please see the full phenotype on the strain data sheet | ||
| 002053 | B6.129P2-Apobtm1Unc/J | Repository- Live |
| The Apobtm1Unc targeted mutation produces a truncated form of the apolipoprotein B protein (APOB70)and no apoB100 that is similar to human familial hypobetalipoproteinemia condition. Expression of apoB48 is not altered. Homozygous mice show greatly reduced levels of plasma APOB, beta-lipoproteins, and total cholesterol. They also have reduced plasma triglyceride concentrations, fasting chylomicronemia, and reduced high density lipoprotein (HDL) cholesterol. Homozygotes also have a high incidence of exencephaly and hydrocephaly. Heterozygous mice show a slight increase over wildtype in the incidence of hydrocephaly. | ||
| 007566 | B6.129P2-Clip2tm1.1Gal/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable and fertile. Female homozygotes adults have lower body weights and smaller body length when compared to wildtype. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of brain tissue. A splice acceptor site introduced into the lacZ reporter cassette results in a hybrid Clip2-lacZ transcript. Beta galactosidase staining is observed primarily in the hippocampus and in other areas of the brain. Homozygotes exhibit a mild growth retardation. The average copus callosum volume is significantly smaller than wildtype. Homozygotes and heterozygotes exhibit abnormal behavior indicative of hippocampal defects. In contextual fear-conditioning tests, mutant mice have a diminished response, although in cued fear-conditioning tests mutant mice exhibit normal behavior. Synaptic plasticity in the CA1 area of the hippocampus is decreased in mutant mice. Both heterozygotes and homozygotes e
..... For more information please see the full phenotype on the strain data sheet | ||
| 005786 | B6.129P2-Cnr2tm1Dgen/J | Repository- Live |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 004744 | B6.129P2-Esr1tm1Ksk/J | Repository- Live |
| At birth, mice homozygous for the targeted allele are viable and normal in size and appearence. Female mice exhibit ovaries that lack corpora lutea and hypoplastic uteri that are unresponsive to estrogen. In males, below normal testis weight is associated with a diminished sperm count (10% of normal). Homozygous females are infertile. The fertility of homozygous males is greatly reduced, but not abolished. | ||
| 007808 | B6.129P2-Grin3btm1Yaha/J | Repository- Live |
| Mice homozygous for this NR3B (Grin3b) mutant allele are viable and fertile, with no RNA from the targeted allele expressed in adult spinal cord. Homozygotes show a moderate but significant impairment in motor learning or coordination, decreased body weight with age, and decreased activity in their home cages. In addition, homozygous mice exhibit highly increased social interactions with their familiar cage mates in their home cage, with moderately increased anxiety-like behavior and decreased social interaction in novel environments. These NR3B (Grin3b) mutant mice may be useful in neurobiological studies; specifically studies involving NMDA receptor and NR3B function in cranial and spinal somatic motor neurons. | ||
| 004595 | B6.129P2-Htttm2Detl/J | Repository- Live |
| Mice homozygous for the targeted allele are viable and fertile. At 15-40 weeks of age mice carrying this allele on a segregating C57BL/6 and 129P2 background exhibit an abnormal gait, clasping behavior and diminished exploratory activity. Infrequent tonic-clonic like seizures may also be observed. Mice with a higher percentage of C57BL/6 in their genetic background develop behavioral and neurological phenotypes at a much later age (70-100 weeks). (Heng MY et al. 2007) Mutant mice may be noticeably smaller than wild-type littermates. Increased glial fibrillary acidic protein immunoreactivity is present in the striatum and ubiquititin- and huntingtin-positive neuronal intranuclear inclusions (NIIs) are detected throughout the dorsal striatum, nucleus accumbens and to a lesser extent other regions of the brain. Onset of symptoms occurs earlier for homozygotes than for heterozygotes.This mutant mouse strain represents a model that may be useful in studies related to Huntington's di
..... For more information please see the full phenotype on the strain data sheet | ||
| 007999 | B6.129P2-Sorl1Gt(Ex255)Byg/J | Repository- Live |
| 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. | ||
| 005439 | B6.129S-Mecp2tm1Hzo/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable and fertile. A truncated gene product (protein) is detected by immunohistochemical analysis of brain tissue. By 6 weeks of age, male mutant mice begin to exhibit tremors, progressive motor dysfunction, oily disheveled fur, hypoactivity, myoclonic seizures, and kyphosis. Approximately 10% of male mutants die between 10 and 12 months of age. Heterozygous female mice exhibit a milder phenotype. All mutant male mice and 62% of female heterozygotes exhibit a repetitive clasping movement of their forelimbs and exhibit tremors. The Donating Investigator reports that the myoclonic seizures, kyphosis and reduced survival were observed in aged male mutants on a 129/SvEv genetic background. This mutant mouse strain may be useful in studies of Rett Syndrome. The Howard Hughes Medical Institute and the National Institutes of Health supported the creation of this model. Importation of this model was supported by the Rett Syndrome Rese
..... | ||
| 005540 | B6.129S-Tnftm1Gkl/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does not affect the degree of obe
..... For more information please see the full phenotype on the strain data sheet | ||
| 008087 | B6.129S1-Bchetm1Loc/J | Repository- Live |
| 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
..... | ||
| 006600 | B6.129S1-Mnx1tm4(cre)Tmj/J | Repository- Live |
| Mice heterozygous for this HB9cre targeted mutation are viable and fertile, with cre expression replacing HB9 (Hlxb9 or Mnx1) expression. Under control of the endogenous upstream elements, cre expression is directed to motor neurons. In heterozygotes, cre expression coincides with HB9 expression. Homozygous HB9cre mice die at or soon after birth, with expression of Cre recombinase likewise directed to motor neurons but no expression of endogenous HB9. When these HB9cre mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination in the resulting offspring leads to deletion of the flanked sequences in Mnx1/HB9 expressing cells; making them useful in neurodevelopmental studies of homeobox genes, motor neuron function and differentiation, and the central nervous system. | ||
| 005628 | B6.129S2-Emx1tm1(cre)Krj/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This strain expresses Cre recombinase from the endogenous Emx1 locus. Western blot analysis of cortical brain tissue does not detect reduced endogenous gene product (protein). When crossed with a strain containing a loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs in approximately 88% of the neurons of the neocortex and hippocampus, and in the glial cells of the pallium, mimicking the pattern of expression of the endogenous gene. This mutant mouse strain represents a model that may be useful in studies of forebrain development and function. | ||
| 007557 | B6.129S2-Oprd1tm1Kff/J | Repository- Live |
| Mice homozygous for this delta-opioid receptor mutant allele (DOR-) are viable and fertile. DOR-selective ligand binding is absent in vitro on brain membranes from homozygous mice. Unlike mutant mice deficient in kappa- or mu-opioid receptors (Stock No. 007558 or 007559, respectively), homozygous DOR- mutants exhibit increased anxiety and depressive-like behavior but no alteration of spontaneous pain perception. Homozygous DOR- mice also have increased ethanol self-administration and increased inflammatory pain. These DOR mutant mice may be useful in studying the biological activity of opioids andanalgesics, mechanical nociception, inflammatory pain, and emotional disorders.
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 ch
..... | ||
| 007558 | B6.129S2-Oprk1tm1Kff/J | Repository- Live |
| Mice homozygous for this kappa-opioid receptor mutant allele (KOR-) are viable and fertile. KOR-selective ligand binding is absent on brain membranes from homozygous mice. In contrast to mutant mice deficient of delta- or mu-opioid receptors (Stock No. 007557 or 007559), KOR- homozygotes have normal mechanical pain thresholds, but greatly increased sensitivity to chemical visceral pain. KOR- homozygotes also exhibit normal spontaneous stress responses (unlike delta-opioid receptor null mice). Homozygous KOR- mice also show decreased ethanol self-administration and decreased THC-conditioned place aversion. These KOR mutant mice may be useful in studying biological activity of opioids, analgesics, spinally mediated thermal nociception and chemical visceral pain thresholds. 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. These mut
..... | ||
| 007559 | B6.129S2-Oprm1tm1Kff/J | Repository- Live |
| Mice homozygous for this mu-opioid receptor mutant allele (MOR-) are viable and fertile. MOR-selective ligand binding is absent on brain membranes from homozygous mice. Homozygous MOR- mice exhibit a lack of morphine analgesia, reward, and withdrawal. This is accompanied by decreased mechanical, thermal, and chemical pain thresholds. Homozygous MOR- mice also show decreased ethanol self-administration and decreased THC-conditioned place aversion. In contrast to mutant mice deficient of delta- or kappa-opioid receptors (Stock No. 007557 or 007558, respectively), MOR- homozygotes exhibit hypolocomotive spontaneous stress responses. Indeed, the reduced anxiety and depressive-like behavior observed in MOR- mutants is in stark contrast to kappa-opioid receptor deficient mice. These MOR mutant mice may be useful in studying the biological activity of opioids, analgesics, and responses to mechanical, chemical and thermal nociception at a supraspinal level. In an attempt to offer alleles
..... | ||
| 005301 | B6.129S2-Tg(APP)8.9Btla/J | Repository- Live |
| 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. | ||
| 007668 | B6.129S4(Cg)-Arntltm1Weit/J | Repository- Live |
| Mice homozygous for this conditional (floxed) allele possess loxP sites flanking exon 8 of the targeted gene and are viable and fertile, with circadian behavioral rhythms indistinguishable from wildtype littermates. When bred to mice that express Cre recombinase, the resulting offspring will have the exon encoding the ARNTL (BMAL1) basic helix-loop-helix (bHLH) domain deleted in the cre-expressing tissue(s). These Bmal1-floxed mutant mice may be useful in generating conditional mutations (whole-mouse or tissue-specific) to study the role of circadian clock/circadian rhythm in physiological and behavioral regulation.
For example, when crossed to a strain expressing Cre recombinase in the retina (see Stock No. 005105), this mutant mouse strain may be useful in studies of the circadian clock of the retina. | ||
| 006490 | B6.129S4-Abcb7tm1Mdf/J | Repository- Live |
| Homozygous mice are viable and fertile with no reported neurological or hematological abnormalities. These mutant mice have loxP sites flanking exons 9 and 10 of the endogenous gene. When bred to Cre recombinase expressing mice, exons 9 and 10 are deleted in the offspring dependent on the tissue specificity of the Cre recombinase expressing parent. The donating investigator reports that the null allele is not transmissible due to an effect on the extraembryonic tissues. This mutant may be useful in studying cytosolic Fe-S cluster assembly and metabolism, Friedreich ataxia, anemia, and hematopoiesis.
When bred to a strain expressing Cre recombinase in liver (see Stock No. 003574 for example), this mutant mouse strain may be useful in studies of hepatocyte iron metabolism.
When bred to a strain expressing Cre recombinase in epiblast derived cells (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 002266 | B6.129S4-Bdnftm1Jae/J | Repository- Live |
| Mice heterozygous for the Bdnftm1Jae mutation show about half normal levels of Bdnf mRNA, but appear normal. Mice homozygous for the Bdnftm1Jae mutation are smaller than normal siblings and most die within the second postnatal week. They have defective coordination of movements and balance. They also exhibit head bobbing and spinning during periods of hyperactivity. There are rare survivors to adulthood. There is excessive degeneration in all sensory ganglia examined, including the vestibular ganglion. Motor neurons are not affected. BDNF can prevent death of central motor neurons and other neurons in vitro, but does not affect these in vivo. | ||
| 005246 | B6.129S4-Grin1tm2Stl/J | Repository- Live |
| These mice possess loxP sites flanking approximately 12kb of sequence of the targeted gene that encodes the entire transmembrane domain and C-terminal region. 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 a strain expressing Cre recombinase in the CA3 region of the hippocampus (see Stock No. 006474 for example), this mutant mouse strain may be useful in studies of associative memory recall. When bred to a strain expressing Cre recombinase in the CA1 region of the hippocampus (see Stock No. 005359 for example), this mutant mouse strain may be useful in studies of nonspacial memory. | ||
| 002986 | B6.129S4-Nos1tm1Plh/J | Repository- Live |
| Mice homozygous for the Nos1tm1Plh targeted mutation are viable and fertile; however, they have enlarged stomachs and reduced stroke size. Hyperglycemic-euglycemic clamp studies demonstrate that homozygotes exhibit insulin resistance at the level of peripheral tissues. Homozygous males are reported to be more aggressive than normal wildtype siblings although this has not been confirmed in The Jackson Laboratory colony. These mice may be useful model for stroke research. | ||
| 006582 | B6.129S4-Park2tm1Shn/J | Repository- Live |
| Homozygous mice are viable and fertile, and exhibit grossly normal brain morphology. Western blot analysis using antibody specific to C-terminal sequences indicates the absence of full length gene product. RT-PCR shows that exon 2 splices to exon 4, skipping exon 3 entirely, resulting in a frame shift and a premature stop codon in exon 5. While EGFP transcripts are present, little parkin-EGFP fusion protein is detectable by Western analysis. Homozygous mice have increased extracellular dopamine concentration in the striatum. Further, medium-sized striatal spiny neurons require greater currents to induce synaptic responses, suggesting a reduction in synaptic excitability in the absence of the endogenous gene. Homozygotes also exhibit deficits in behavioral paradigms sensitive to dysfunction of the nigrostriatal pathway. The numbers of dopaminergic neurons in the substantia nigra, however, are normal up to the age of 24 months, in contrast to the substantial loss of nigral neurons charac
..... For more information please see the full phenotype on the strain data sheet | ||
| 006406 | B6.129S4-Tg(APPSwLon)96Btla/J | Repository- Live |
| 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 wildtype 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 | Repository- Live |
| 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. | ||
| 004936 | B6.129S6(Cg)-Spp1tm1Blh/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) is detected by RT-PCR analysis of embryonic fibroblasts and kidney. Immunohistochemical analysis of kidney and bone tissue also fails to detect gene product (protein). Homozygotes exhibit disorganized ultrastructural wound matrix remodeling and defective macrophage infiltration and accumulation at sites of injury and infection. Experimentally induced hyperoxaluria results in renal tubule deposition of calcium oxalate crystals. Accelerated ectopic calcification mineralization in soft tissues occurs after subcutaneous implantation of glutaraldehyde-fixed aortic valve tissue. Mutant macrophage response to mycobacteria infection and pulmonary granulomatous response and inflammation are impaired. According to a recent publication (Hsieh et al 2006 Cancer Res 2006 66:7119-27), mutant mice treated with a skin chemical
..... For more information please see the full phenotype on the strain data sheet | ||
| 007969 | B6.129S6-Dvl1tm1Awb/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 MEF (mouse embryonic fibroblasts) derived from homozygotes. Homozygotes exhibit diminished social interaction behavior, do not barber or trim whiskers of cagemates, show subordinance in social dominance tests, do not sleep huddled together and do not build nests. Although mutants have an attenuated prepulse inhibition of acoustic and tactile startle (sensorimotor gating of the startle reflex), they do not exhibit any deficits in locomotor or cognitive function. This mutant mouse strain may be useful in studies of social behavior, sensorimotor gating, and possibly psychiatric disorders.
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 wa
..... | ||
| 006852 | B6.129S6-Per2tm1Jt/J | Repository- Live |
| Mice homozygous for this "mPer2Luc" mutation are viable and fertile with no developmental or morphological differences compared to wildtype littermates. Expression of PERIOD2::LUCIFERASE (or mPER2::LUC) fusion protein during peak periods is similar to endogenous pPER2 patterns. Homozygous mice have normal entrainment and circadian behaviors. These mPer2Luc knock-in mice may be useful as a real-time reporter of circadian dynamics in different tissues. | ||
| 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. | ||
| 003232 | B6.129S7-Chrna7tm1Bay/J | Repository- Live |
| Mice homozygous for the Chrna7tm1Bay mutation are viable and fertile. Neuropathological and histochemical assessment of the brain reveals no abnormalities. High-affinity nicotine binding sites are present but there is an absence of high-affinity 125alpha-BGT sites. Homozygotes lack rapidly desensitizing, methyllycaconitine-sensitive, nicotinic currents that are present in hippocampal neurons. | ||
| 003819 | B6.129S7-Per2tm1Brd/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display gross physical or behavioral abnormalities. A mutant transcript, if translated, would generate a protein with an 87 amino acid deletion. When maintained in constant darkness, two phenotypic components are exhibited: a shortened circadian period and a loss of persistent circadian rhythmicity. When housed under constant light, homozygotes exhibit normal activity rhythm but a period length of less than 24 hours. Female homozygotes, 9-12 months of age, exhibit low reproductive success and produce small litters when compared to wildtype. This mutant mouse strain may be useful in studies related to the regulation of the sleep-wake cycle. | ||
| 002973 | B6.129S7-Sod2tm1Leb/J | Repository- Live |
| Mice homozygous for the Sod2tm1Leb targeted mutation die within 21 days after birth. They exhibit severe wasting and are clearly much smaller, weaker,and less coordinated than their wildtype and heterozygous littermates. Homoyzotes exhibit several novel pathogenic phenotypes including severe anemia, degeneration of neurons in the basal ganglia and brainstem, progressive motor disturbances, and myocardial injury. | ||
| 002222 | B6.129S7-Twist1tm1Bhr/J | Repository- Live |
| Homozygotic embryos for the Twist1tm1Bhr targeted mutation die | ||