Search Criteria: Strain Type is "Chemically Induced Mutation"

Strains from the Research Colonies of Jackson Laboratory Scientists

JAX® Mice Strains

Stock
Number
Strain Name
 
Strain Description
Standard Supply
002020 C57BL/6J-ApcMin/J
Level 3
The C57BL/6J-ApcMin/J strain is highly susceptible to spontaneous intestinal adenoma formation. Homozygous mice are not viable. It was initially reported that one hundred percent of the C57BL/6J-ApcMin heterozygous mice raised on a high fat diet develop in excess of 30 adenomas throughout the intestinal tract and most die by 120 days of age. Heterozygotes also develop anemia. (Moser et al., 1990, Su et al., 1992). A small number of C57BL/6J-ApcMin heterozygous female mice develop mammary tumors. A subsequent publication indicates that this strain may carry a dominant modifier (Mom2) gene that reduces the number and incidence of polyp formation in C57BL/6J-ApcMin heterozygous mice (Silverman et al., 2002).
006963 B6(101)-Mdh1am1H/LvtJ
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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.
006863 C3Fe.B6-Mcm4chaos3/J
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Mice homozygous for this ENU-induced F345I hypomorphic allele (Chaos3) are viable, fertile, and overtly indistinguishable from normal littermates. Homozygous, but not heterozygous, mice have slightly reduced wildtype protein levels in mouse embryonic fibroblasts (MEFs). Whereas Chaos3 heterozygotes show mildly elevated (2- to 5-fold) micronucleus frequencies compared with wildtype, homozygotes have an approximate 20-fold increase with over 7% of erythrocytes containing micronuclei. MEFs from homozygous mice exhibit mild defects (cell proliferation, S phase and G2/M populations), and are highly susceptible to chromosome breakage following treatment with the DNA replication inhibitor aphidicolin. On a congenic C3HeB/FeJ background, greater than 80% of homozygous females exhibit mammary adenocarcinomas with a mean latency of 12 months, while males have no tumor incidence. These Chaos3 mice provide a novel, non-transgenic model of breast cancer, and may be useful for s .....
For more information please see the full phenotype on the strain data sheet
008253 C57BL/6J-Clcn1adr-mto9J/J
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This allele of myotonia is slightly milder in severity than the original adr-mto mutation.
006926 C57BL/6J-EgfrVel/J
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Mice homozygous for this mutation have an embryonic lethal phenotype, failing to develop past embryonic days 13.5. Heterozygous mice are viable, fertile, do not display any behavioral abnormalities and are born with open eyelids and curly vibrissae. Adult heterozygotes often have small eyes and corneal opacity with excessive secretions at the eyelid edges. MEFs (mouse embryonic fibroblasts) exhibit reduced migratory ability, approximately 53% of wildtype controls. Histological analysis of homozygous E12.5 embryos reveals placental defects. This mutant mouse strain may be useful in studies of development and as a visible dominant marker for the Egfr allelic series.
006699 C57BL/6J-Pcsk1N222D/J
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Mice homozygous for this ENU-induced "Pc1N222D" mutation are viable and fertile, although the donating investigator reports that homozygous breeders have diminished reproductive performance. Unlike mice homozygous for the traditional knockout allele, Pc1N222D homozygotes are not runted. Homozygous mice exhibit obesity, abnormal proinsulin processing and multiple endocrinological defects. Increased energy intake and a more efficient metabolism contribute to the obesity. Defective proinsulin processing leads to glucose intolerance, but neither insulin resistance nor diabetes develop despite obesity. Obesity is associated with impaired autocatalytic and neuropeptide processing. These mutant mice are a model of human PC1 deficiency, and may be useful in studying obesity, fat metabolism, propeptide processing, and neuroendocrinology.
004766 C57BL/6J-Pde6brd1-2J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Pde6b2J entry.
005037 C57BL/6J-Ticam1Lps2/J
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Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This single base pair deletion mutation was induced by ENU mutagenesis. Unlike wildtype macrophages, macrophages derived from these animals fail to respond to synthetic lipid A, endotoxin lipopolysaccharide (LPS), and dsRNA with production of tumor necrosis factor (TNF). Macrophages are less susceptible to LPS-induced cytotoxicity. Nitrous oxide and type I interferon production in activated macrophages is impaired. Homozygotes exhibit increased susceptibility to mouse cytomegalovirus. Although homozygotes are resistant to challenges with LPS, the mice will become ill and some may die. This mutant mouse strain may be useful in studies of immunodeficiency and host response to bacterial endotoxins and viruses.
006128 STOCK Otofdeaf5Jcs/Kjn
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005445 A.B6 Tyr+-Cybanmf333/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf333 entry.
005098 A.B6 Tyr+-Spnb4qv-7J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Spnb4qv-7J entry.
006026 A.B6 Tyr+-nmf282/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf282 entry.
005012 A.B6 Tyr+-Myo5ad-l31J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page.
002171 B6.129P2-Hprt1b-m3/J
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HPRT-embryonic stem cells were obtained by selecting for spontaneous mutation by incubation in medium containing 6-thioguanine. HPRT-males have no overt phenotype of abnormal behavior. The mutation is due to a large deletion in the Hprt gene. Mutant mice have no HPRT detectable by Western blot analysis and no detectable HPRT enzyme activity in brain homogenates. They appear to have normal brain purine content, but de novo purine synthesis is accelerated four- to fivefold. The Hprtb-m3 mutation has been used in preimplantation studies to determine when the maternal and paternal alleles of Hprt are activated during early embryonic development. Either administration of amphetamine or inhibition of adenine phosphoribosyltransferase (APRT) activity stimulates locomotor and stereotypic behaviors in HPRT-deficient mice. However, the null mutant for both Hprt and Aprt does not show the characteristics of Lesch-Nyhan disease.
006558 B6.Cg-H2bm1 Tg(GUSB)4Sly/SndsJ
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Mice that are homozygous for this transgene and the Gusbmps allele have approximately 20-fold higher beta-glucuronidase enzyme activity than wildtype controls. Distribution of human enzyme activity throughout various tissues mimics the endogenous mouse enzyme activity pattern. Of note, mice homozygous for both the transgene and the Gusbmps allele do not exhibit an accumulation of undegraded glycosaminoglycans. These transgenic mice do not carry the Gusbmps allele. Mice that are hemizygous for this transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of lysomal storage diseases and mucopolysaccharidosis VII (Sly syndrome).
004852 B6;129-Crb1rd8/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Crb1rd8 (Crb1nmf144) entry.
005043 B6;129-nmf166/J
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Mice homozygous for the nmf166 mutation have lens extrusion cataracts and deep anterior chambers at 12 weeks of age. View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf166 entry.
005048 B6;129-nmf291/J
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By approximately 11 weeks of age mice homozygous for this ENU-induced mutation develop splayed hind feet, a lumbering gait, and jump into the air intermittently. The phenotype progresses to include spasms of the hind and front limbs that can result in falling over. Both female and male homozygotes breed, but the reproductive window is shortened by the progressive physical impairments.

For additional information on nmf291 view the web page on the Neuroscience Mutagenesis Facility web site.

005689 B6;129S1-hlb349A/J
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For information on Hlb349A view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
006810 B6;129S4-hlb258/J
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For information on hlb258 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
005520 B6;CByJ-Cacna1atg-6J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Cacna1atg-6J entry.
005050 B6;CByJ-Cacna2d2du-3J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf299 entry.
005633 B6;CByJ-Dstdt-38J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Dstdt-38J entry.
005463 B6;CByJ-Scn8a7J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Scn8a7J entry.
005753 B6;CByJ-Spnb4qv-9J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf470 entry.
005750 B6;CByJ-nmf375/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf375 entry.
005636 B6;CByJ-nmf418/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf418 entry.
005751 B6;CByJ-nmf419/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf419 entry.
006033 B6;CByJ-nmf445/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf445 entry.
000125 B6By.Cg-Sox18Ra Pt Os/J
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The Sox18Ra and Sox18Ra-J alleles cause a less severe phenotype than the Sox18Ra-Op allele. The Sox18Ra and Sox18Ra-J alleles are similar mutations and give a very similar phenotype. The Sox18Ra allele has been more broadly described in the literature and will be covered here. Heterozygotes are viable and fertile. Heterozygotes have developmentally retarded sinus hair growth apparent at embryonic day 16.5 and retarded development of pelage follicles apparent by embryonic day 17.5. Thus, heterozygotes have slightly shorter vibrissae evident at birth, and can be distinguished at three days of age by their pink skin which, due to the abnormally sparse development of the coat, fails to darken like that of wildtype siblings. A paucity of fur is apparent by nine days of age and persists throughout life. Compared with the wild type pelage, Sox18Ra/+ coats have longer g .....
For more information please see the full phenotype on the strain data sheet
002388 B6Ros.Cg-Dmdmdx-2Cv/J
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Mice carrying the Dmdmdx-2Cv mutation display a phenotype similar to the original Dmdmdx mutation. Dmdmdx-3Cv mutant mice display a faint dystrophin immunofluorescence in skeletal sarcolemma and skeletal muscle in contrast to the other mutants which show no dystrophin reactivity. This is similar to a group of human DMD patients. This mutant has a low frequency of revertants. The Dmdmdx-4Cv and Dmdmdx-5Cv strains have 10 times fewer revertants than the Dmdmdx and Dmdmdx-2Cv strains as viewed in quadricep cross-sections. This is not attributable to genetic background or viral infections. These reversion rate differences may be attributable to differences in the location of the point mutation. The large number of revertants in Dmdmdx mutants has complicated the analysis of gene or cell therapies. These mutants are more useful for this purpose. All .....
For more information please see the full phenotype on the strain data sheet
002377 B6Ros.Cg-Dmdmdx-3Cv/J
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Dmdmdx-3Cv mutant mice display a faint dystrophin immunofluorescence in skeletal sarcolemma and skeletal muscle in contrast to the other mutants which show no dystrophin reactivity. This is similar to a group of human DMD patients. This mutant has a low frequency of revertants. The Dmdmdx-4Cv and Dmdmdx-5Cv strains have 10 times fewer revertants than the Dmdmdx and Dmdmdx-2Cv strains as viewed in quadricep cross-sections. This is not attributable to genetic background or viral infections. These reversion rate differences may be attributable to differences in the location of the point mutation. The large number of revertants in Dmdmdx mutants has complicated the analysis of gene or cell therapies. These mutants are more useful for this purpose. All these strains are also hemizygous for Hprta and Pgk1a (both are on the X chromosome).
002378 B6Ros.Cg-Dmdmdx-4Cv/J
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The Dmdmdx-4Cv and Dmdmdx-5Cv strains have 10 times fewer revertants than the Dmdmdx and Dmdmdx-2Cv strains as viewed in quadricep cross-sections. This is not attributable to genetic background or viral infections. These reversion rate differences may be attributable to differences in the location of the point mutation. The large number of revertants in Dmdmdx mutants has complicated the analysis of gene or cell therapies. These mutants are more useful for this purpose. All these strains are also hemizygous for Hprta and Pgk1a (both are on the X chromosome).
002379 B6Ros.Cg-Dmdmdx-5Cv/J
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Mice carrying the Dmdmdx-5Cv mutation have 10 times fewer revertants than the Dmdmdx and Dmdmdx-2Cv strains as viewed in quadricep cross-sections. This is not attributable to genetic background or viral infections. These reversion rate differences may be attributable to differences in the location of the point mutation. The large number of revertants in Dmdmdx mutants has complicated the analysis of gene or cell therapies. These mutants are more useful for this purpose. This strain is also hemizygous for Hprta and Pgk1a (both are on the X chromosome).
004122 BALB/cByJ-Nmf31/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Nmf31 entry.
002232 BTBR-Pahenu2/J
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Homozygous mutant mice show severe hyperphenylalanemia. They are hypopigmented unless maintained on a low phenylalanine diet. Females are fertile but do not rear their young when maintained on a standard mouse diet. The coat color of the background strain, BTBR +T tf/tf, is black and tan (at/at). This strain is also homozygous for the gene tufted (tf/tf) resulting in various molting patterns in the mouse coat. These effects, limited to the mouse coat, may make the mice appear malformed.
002231 BTBR.Cg-Pahenu1/J
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Homozygous mutant mice show a delay in the clearing of a load of phenylalanine.
002662 C.Cg-Fechm1Pas/J
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Homozygous mutants are recognizable by the intense yellow color of their sera, gross bilirubinemia, and, especially in albino mice, jaundice. Photosensitivity is evidenced by the appearance of inflammatory skin lesions, often becoming ulcerous, under standard mouseroom conditions (fluorescent light). Mutants do not differ from their normal littermates in body size or weight, nor are they retarded in growth. They exhibit hepatomegaly and splenomegaly, leading to enlarged abdomens after several months of age. Although mutants are not anemic at one month old, normocytic anemia develops with age.
005011 C57BL/6J-Agtpbp1pcd-6J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Agtpbp1pcd-6J entry.
005921 C57BL/6J-Aqp2F204V/J
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Mice homozygous for this mutation are viable with normal body size and lifespan. Homozygotes are fertile, but females usually die during labor. The predicted valine for phenylalanine substitution at amino acid 204 of the mutant protein (F204V) leads to an enrichment in kidney cells of a normally short-lived, intermediately glycosylated 31 kDa isoform and to a reduction in the mature, glycosylated protein level. The mutant AQP2F204V protein is mis-localized in kidney collecting duct cells, and fails to translocate to the apical cell surface in response to desmopressin. Homozygous mice exhibit excessive water consumption and urination, normal plasma glucose levels, and no glucose in the urine. Mutant mice are unable to concentrate urine and exhibit severe hydronephrosis. The presence of some mature, glycosylated protein and a defective, but not completely absent, desmopressin response in homozygous mutant mice likely permits their survival. Heterozygous mice are viable and fer .....
For more information please see the full phenotype on the strain data sheet
004764 C57BL/6J-Cdh23v-8J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Cdh23v-8J entry.
004819 C57BL/6J-Cdh23v-9J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Cdh23v-9J entry.
005253 C57BL/6J-Clcn1adr-mto6J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Clcn1adr-mto6J entry.
005465 C57BL/6J-Clcn1adr-mto7J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Clcn1adr-mto7J entry.
002923 C57BL/6J-Clockm1Jt/J
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Heterozygous mice show a lengthening of their circadian period by about 1 hour. Homozygous mice show a lengthening of 4 hours followed by a loss of circadian rhythm. Mice homozygous for this mutation are viable. Male homozygotes are fertile while female homozygotes appear to have reduced fertility.
004829 C57BL/6J-Dstdt-36J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Dstdt-3J entry.
005560 C57BL/6J-Dstdt-37J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Dstdt-37J entry.
004109 C57BL/6J-Glra1nmf11/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Glra1nmf11 entry.
005447 C57BL/6J-Grid2ho-16J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf62 entry.
005561 C57BL/6J-Grm1nmf373/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Grm1nmf373 entry.
005322 C57BL/6J-Gusbmps-3J/J
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000996 C57BL/6J-Hbbd3th/J
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005691 C57BL/6J-Hlb280/J
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For information on Hlb280 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
005060 C57BL/6J-Hlb290/J
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For information on Hlb290 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
008507 C57BL/6J-Hlb320/J
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For information on Hlb320 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
005495 C57BL/6J-Hlb398/J
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For information on Hlb398 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
008411 C57BL/6J-Hlb426/J
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For information on Hlb426 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
008509 C57BL/6J-Hlb446/J
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For information on Hlb446 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
006423 C57BL/6J-Hlb468/J
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For information on Hlb468 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
008263 C57BL/6J-Hlb476/J
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008504 C57BL/6J-Hlb477/J
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For information on Hlb477 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
008506 C57BL/6J-Hlb529/J
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Mice homozygous for this ENU induced mutation exhibit elevated HDL cholesterol.
008505 C57BL/6J-Hlb561/J
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Mice homozygous for this ENU induced mutation exhibit elevated HDL cholesterol.
008499 C57BL/6J-Hlb589/J
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Mice homozygous for this ENU induced mutation exhibit elevated HDL cholesterol.
008262 C57BL/6J-Hlb594/J
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005342 C57BL/6J-Il7hlb368/J
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For information on hlb368 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
004820 C57BL/6J-Kcne12J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Kcne12J entry.
005748 C57BL/6J-Kcnq1vtg-3J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Kcnq1vtg-3J entry.
004703 C57BL/6J-Kcnq2Nmf134/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Kcnq2Nmf134 entry.
005635 C57BL/6J-Lama2dy-7J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Lama2dy-7J entry.
005061 C57BL/6J-LdlrHlb301/J
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For information on Ldlrhlb301 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
005579 C57BL/6J-Ltahlb382/J
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For information on hlb382 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
005749 C57BL/6J-Myo6sv-3J/J
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005468 C57BL/6J-Myo7ash1-11J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Myo7ash1-11J entry.
004851 C57BL/6J-Nmf128/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Nmf128 entry.
005007 C57BL/6J-Nmf191/J
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At 12 weeks of age, the retinas of Nmf191 carriers were found to be grainy, although electroretinographic recordings were normal. View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Nmf191 entry.
004821 C57BL/6J-Nmf193/J
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Carriers of Nmf193 have been found to have pan retinal photoreceptor degeneration of the outer nuclear layer. View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Nmf193 entry.
004832 C57BL/6J-Nmf220/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Nmf220 entry.
005014 C57BL/6J-Nox3het-4J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf250 entry.
004817 C57BL/6J-Npc1nmf164/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Npc1nmf164 entry.
004156 C57BL/6J-Pcdh15av-5J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Pcdh15av-5J entry.
005744 C57BL/6J-Relnrl-6J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Relnrl-6J entry.
008412 C57BL/6J-Rnl27/J
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For information on Rnl27 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
005047 C57BL/6J-Rorasg-3J/J
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Mice homozygous for this ENU-induced mutation are smaller than normal and, by 3.5 weeks of age on average, display splayed hind limbs and a leaning gait. They fall over on their sides and have difficulty regaining a walking position. A disorganized Purkinje cell layer and loss of granule cells has been found.

For additional information on Rorasg-3J view the web page on the Neuroscience Mutagenesis Facility web site.

004102 C57BL/6J-Scn8a4J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Scn8a4J entry.
004105 C57BL/6J-Scn8a5J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Scn8a5J entry.
005449 C57BL/6J-Spnb4qv-8J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf379 entry.
005638 C57BL/6J-Tmhshscy-2J/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Tmhshscy-2J entry.
008264 C57BL/6J-hlb145/J
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For information on hlb145 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
004517 C57BL/6J-hlb156/J
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For information on hlb156 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
004530 C57BL/6J-hlb15/J
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For information on hlb15 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
008508 C57BL/6J-hlb218/J
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For information on hlb218 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
005124 C57BL/6J-hlb219/J
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For information on hlb219 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
008265 C57BL/6J-hlb233/J
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007231 C57BL/6J-hlb243/J
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For information on hlb243 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
006422 C57BL/6J-hlb324B/J
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For information on hlb324B view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
005343 C57BL/6J-hlb381/J
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For information on hlb381 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
005496 C57BL/6J-hlb385/J
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For information on hlb395 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
005580 C57BL/6J-hlb388/J
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For information on hlb388 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
008269 C57BL/6J-hlb414/J
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For information on hlb414 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
008280 C57BL/6J-hlb454/J
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For information on hlb454 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
008497 C57BL/6J-hlb459/J
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For information on hlb459 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
008266 C57BL/6J-hlb495/J
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008261 C57BL/6J-hlb497/J
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008267 C57BL/6J-hlb520/J
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008268 C57BL/6J-hlb521/J
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008270 C57BL/6J-hlb52/J
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008498 C57BL/6J-hlb575/J
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Mice with this mutation exhibit an increased percentage of body fat on a standard laboratory chow diet.
004811 C57BL/6J-nmf110/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf110 entry.
004812 C57BL/6J-nmf111/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf111 entry.
004747 C57BL/6J-nmf118/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf118 entry.
004814 C57BL/6J-nmf127/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf127 entry.
004110 C57BL/6J-nmf12/J
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View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf12 entry.
005006 C57BL/6J-nmf131/J
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Homozygosity for the nm131 mutation can cause retinal dysplasia, retinal degeneration, vitreal fibroplasia, and, less commonly, cataracts or microphthalmia. This mutation has low penetrance.

View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf131 entry.

004765 C57BL/6J-nmf148/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf148 entry.
004816 C57BL/6J-nmf161/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf161 entry.
004818 C57BL/6J-nmf172/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf172 entry.
005008 C57BL/6J-nmf192/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf192 entry.
005009 C57BL/6J-nmf195/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf195 entry.
004823 C57BL/6J-nmf205/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf205 entry.
004830 C57BL/6J-nmf206/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf206 entry.
004831 C57BL/6J-nmf219/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf219 entry.
005095 C57BL/6J-nmf240/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf240 entry.
005010 C57BL/6J-nmf242/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf242 entry.
005096 C57BL/6J-nmf247/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf247 entry.
005101 C57BL/6J-nmf268/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf268 entry.
005298 C57BL/6J-nmf313/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf313 entry.
005329 C57BL/6J-nmf318/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf318 entry.
005255 C57BL/6J-nmf329/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf329 entry.
005448 C57BL/6J-nmf347/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf347 entry.
005741 C57BL/6J-nmf356/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf62 entry.
005467 C57BL/6J-nmf370/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf370 entry.
005469 C57BL/6J-nmf380/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf380 entry.
005451 C57BL/6J-nmf391/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf391 entry.
004085 C57BL/6J-nmf4/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf4 entry.
004442 C57BL/6J-nmf62/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf62 entry.
004468 C57BL/6J-nmf63/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf63 entry.
004470 C57BL/6J-nmf65/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf65 entry.
004472 C57BL/6J-nmf67/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf67 entry.
004656 C57BL/6J-nmf88/J
Repository-Cryopreserved
nmf88 mutants have an increased propensity for seizure triggered by PTZ or transcorneal stimulation. For further details see the Neuroscience Mutagenesis Facility web page for the nmf88 entry.
004107 C57BL/6J-nmf9/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf9 entry.
005421 CBy;B6-Bmp5cfe-se8J/J
Repository-Cryopreserved
005016 CByJ;B6-Cdh23v-10J/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Cdh23v-10J entry.
002919 STOCK Myo7ash1-7J/J
Repository-Cryopreserved
Myo7ash1-7J homozygotes exhibit circling behavior, a slight head tilt and side-to-side head bob. They develop progressive hearing loss, becoming totally deaf by 60 days of age. Heterozygotes are normal. (Samples et al., 2000). Mutations of the human ortholog of Myo7a, MYO7A, have been characterized in pedigrees of patients having Usher syndrome type 1 (USH1), an autosomal recessive disorder characterized by profound deafness, vestibular dysfunction and progressive retinitis pigmentosa (Weil et al., 1995; Weston et al., 1996; Adato et al., 1997; Levy et al., 1997; Liu et al., 1998; Espinos et al., 1998; Cuevas et al., 1998, 1999; Janecke et al., 1999). MYO7A mutations have also been identified in patients with autosomal dominant non-syndromic deafness (Liu et al., 1997) and autosomal recessive isolated deafness (Liu et al., 1997; Weil et al., 1997).
002812 STOCK Npr3stri/PasEiJ
Repository-Cryopreserved
Mice homozygous for the strigosus mutation are identifiable as early as six days of age by their elongated bodies and digits and a conical extension of the body at the base of the tail. Older mice are extremely thin and exhibit arachnodactyly, thoracic kyphosis, and, often, kinks in the tail. The strigosus mutation is milder than the longjohn alleles, which become humbacked at a younger age and have sacral kinks. Upon necropsy, homozygotes are found to lack normal body fat deposits. Skeletal analysis demonstrated delayed endochondral ossification, most obvious in the hind- and forepaws but affecting the entire skeleton. At embryonic day 10.5 all truncal vertebrae are present but enlarged.
005375 STOCK Trp53bp1hlb543/CloJ
Repository-Cryopreserved
000802 WB.Cg-Hbath-J/J
Repository-Cryopreserved

(147 stocks)         Back to Top

Strains from the Research Colonies of Jackson Laboratory Scientists

IMPORTANT NOTE: Price information is on the strain data sheet which can be viewed by clicking on the strain name.

Stock
Number
Strain Name
 
Strain Description
Standard Supply
005013C57BL/6J-GarsNmf249/J
Research Strain
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for GarsNmf249 entry.
005296C57BL/6J-nmf246/J
Research Strain
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf246 entry.

(2 stocks)         Back to Top


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