Search Criteria: Strain Type is "Chemically Induced Mutation"

New Strains Awaiting Transfer

JAX® Mice Strains

Stock
Number		 Strain Name
 
Strain Description		 Standard Supply
001060 B6.C-H2-Kbm1/ByJ
Level 4
002020 C57BL/6J-ApcMin/J
Level 4
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).
016158 129S1.B6-Zic2m1Nisw/J
Repository- Live
006228 B6.129S1-Nox3het-3J/GrsrJ
Repository- Live
Homozygotes completely lack otoconia, both in the utricle and the saccule, as early as embryonic day 14 and this persists in the adult. However, the rest of the inner ear appears morphologically normal and hearing is normal. Otoconia appear to be normal in heterozygotes. Homozygotes can be identified by a significant sideways tilting of the head. When dropped 30cm to a soft surface homozygotes fail to land on their feet. They also fail to orient and swim in water, but instead rotate underwater and require rescue.
002378 B6Ros.Cg-Dmdmdx-4Cv/J
Repository- Live
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).
006926 C57BL/6J-EgfrVel/J
Repository- Live
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.
012810 C57BL/6J-Enpp1asj/GrsrJ
Repository- Live
Homozygotes initially appear normal but by 2 months of age they hold their forepaws closer to the body and develop a slow hobbling gait due to joint calcification. Moderate to severe hearing loss is found by 3 months of age. Homozygotes may breed, but the ability to breed and maintain a litter is curtailed by progressive physical disability.
017307 C57BL/6J-Krt71Ca-17J/GrsrJ
Repository- Live
As with other caracul mutants, heterozygotes have a very wavy coat and curved vibrissae. The mutation can be detected when the coat first comes in at about 7 to 8 days of age, is easily recognized at 3 weeks of age, and remains ruffled throughout life but is less wavy with age.
005061 C57BL/6J-LdlrHlb301/J
Repository- Live
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 G to A transition mutation in exon 14, nucleotide 2096 was induced by ENU mutagenesis. The "Wicked High Cholesterol" (WHC) phenotype was mapped to the Ldlr, low density lipoprotein receptor, gene. Although total plasma cholesterol levels do not differ between sexes, when fed a standard chow diet for 5 weeks, homozygous WHC males exhibit higher triglyceride and HDL levels than homozygous WHC females. When fed Western diet for 5 weeks, mutant WHC males exhibit higher HDL levels than female WHC mutants. When fed an atherogenic diet for 5 weeks, WHC homozygotes of both sexes develop elevated total cholesterol levels of more than a 4 fold increase when compared to WHC homozygotes on standard chow diet. Cholesterol and HDL levels of WHC homozygotes fed atherogenic diet for 5 weeks remain elevated 1 month after resum .....
For more information please see the full phenotype on the strain data sheet
009345 C57BL/6J-Mstnlean/J
Repository- Live
Mice homozygous for this ENU-induced mutation, called the lean (Ln) allele of myostatin (MstnLn), are viable and fertile. The MstnLn allele alters mRNA splicing and results in an additional larger transcript containing a 128 basepair insert at the junction between exons 2 and 3. This insertion encodes an additional 4 amino acids before a premature stop codon (ASDNX), and is predicted to generate a truncated protein containing the Mstn signal sequence and propeptide, but lacking the ligand portion of the molecule. In addition to this abnormal splicing product, the mRNA from mutant males is also reduced in abundance by approximately 60% compared to wildtype males. When maintained on normal diet, homozygous (MstnLn/Ln) mice exhibit increased muscularity. When maintained on a high fat diet, homozygotes exhibit glucose tolerance, protection against overall insulin resistance, improved muscle and liver insulin sensitivity (with decreased .....
For more information please see the full phenotype on the strain data sheet
005037 C57BL/6J-Ticam1Lps2/J
Repository- Live
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.
010814 D2.B6-LdlrHlb301/J
Repository- Live
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 G to A transition mutation in exon 14, nucleotide 2096 was induced by ENU mutagenesis. The "Wicked High Cholesterol" (WHC) phenotype was mapped to the Ldlr, low density lipoprotein receptor, gene. Although total plasma cholesterol levels do not differ between sexes, when fed a standard chow diet for 5 weeks, homozygous WHC males exhibit higher triglyceride and HDL levels than homozygous WHC females. When fed Western diet for 5 weeks, mutant WHC males exhibit higher HDL levels than female WHC mutants. When fed an atherogenic diet for 5 weeks, WHC homozygotes of both sexes develop elevated total cholesterol levels of more than a 4 fold increase when compared to WHC homozygotes on standard chow diet. Cholesterol and HDL levels of WHC homozygotes fed atherogenic diet for 5 weeks remain elevated 1 month after resum .....
For more information please see the full phenotype on the strain data sheet
012655 FVB.A-Irf6clft1/BeiJ
Repository- Live
Mice that are homozygous for this hypomorphic allele are characterized by an abnormal adhesion between the tongue and palate. Approximately 63% of E18.5 mutants exhibit a partial fusion of the anterior palate, the remaining mutants exhibit a complete cleft of the secondary palate. Oral adhesions between the palate and tongue are first observed by E12.5. In addition, a small number of mutants exhibit syndactyly, short forelimbs, curly tail, and hind limbs that appear fused to the body. This mutant mouse strain may be useful in studies of cleft palate and Van der Woude Syndrome.

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

013100 FVB.C-Prdm16csp1/J
Repository- Live
Mice heterozygous for the csp1 ENU-induced mutation, are viable, fertile, and normal in size. Homozygous mutants exhibit the cleft palate (CP) phenotype and perinatal lethality with respiratory failure. The occurrence of the CP phenotype in homozygous csp1 mice drops to 9% after backcrossing onto the C57BL/6J background for four generations, although 93% of these mice still die shortly after birth and still exhibit respiratory failure. Approximately 6% of heterozygous mutant mice exhibit the (CP) phenotype. These csp1 mice possess a C to A mutation within intron 6 of the PR domain containing 16 (Prdm16) gene, resulting in vairable absence of exon 7 and early termination within exon 8. It is unclear if this truncated PRDM16 protein is stable in csp1. The CP phenotype of these csp1 mice is exhibited by micrognathia and failed palate shelf elevation due to physical obstruction by the tongue, resembling human Pierre Robin sequence (PRS)-like .....
For more information please see the full phenotype on the strain data sheet
014645 STOCK Sec24bY613X/J
Repository- Live
Mice heterozygous for this ENU-induced mutation (Sec24bY613X), are viable and fertile, although the donating investigator reports that 33% of homozygous mice are dead or dying by E18.5. Sec24b is a cargo-sorting member of the core complex of the COPII endoplasmic reticulum (ER)-Golgi transport vesicle, and is critical for neural tube closure. These mice contain a premature stop codon in exon 9 of the Sec24 related gene family, member B (Sec24b) gene. Sec24bY613X homozygotes develop craniorachischisis, a fully open neural tube from the midbrain-hindbrain boundary to the most caudal end of the neural tube. These mice exhibit deficits in convergent extension and other planar cell polarity phenotypes. At E18.5, 45% of embryos exhibit omphalocele and 99% exhibit eyelid fusion failure. Also, outer and inner cochlear hair cells periodically fall out of phase and are abnormally aligned. These mutant mice may be useful in studying planar cel .....
For more information please see the full phenotype on the strain data sheet
004766 C57BL/6J-Pde6brd1-2J/J
Research Strain
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Pde6b2J entry.
005296 C57BL/6J-nmf246/J
Research Strain
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf246 entry.
010918 129S1.B6-Szt2m1Frk/Frk
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any electroencephalograhic, neurosensory or motor abnormalities. Although mice do not exhibit spontaneous seizures, non-invasive kindling produces an earlier latency to first minimal clonic seizure than C57BL/6J controls (4 tests vs. 7-8 tests). This mutant mouse strain may be useful in studies of epilepsy susceptibility.

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

005445 A.B6 Tyr+-Cybanmf333/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf333 entry.
005098 A.B6 Tyr+-Spnb4qv-7J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Spnb4qv-7J entry.
006026 A.B6 Tyr+-Pde6anmf282/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf282 entry.
005012 A.B6 Tyr+-Myo5ad-l31J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page.
006963 B6(101)-Mdh1am1H/LvtJ
Cryopreserved - Ready for recovery
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.
006559 B6.C-H2-Kbm1/ByBir-Gusbmps/BrkJ
Cryopreserved - Ready for recovery
Mice homozygous for the Gusbmps allele exhibit skeletal dysplasia as well as cognitive, hearing and visual deficits. Lifespan of the homozygotes is approximately six months. Homozygotes lack the lysomal enzyme, beta-glucoronidase, and, as a result, glycosaminoglycans accumulate in tissues throughout the body. Female homozygotes rarely conceive and do not lactate. This strain is a model for the human lysomal storage disease, mucopolysaccharidosis type VII.
000256 B6.C-H2-Kbm1/ByBir-Gusbmps/J
Cryopreserved - Ready for recovery
Mice homozygous for the Gusbmps allele exhibit skeletal dysplasia as well as cognitive, hearing and visual deficits. Lifespan of the homozygotes is approximately six months. Homozygotes lack the lysomal enzyme, beta-glucoronidase, and, as a result, glycosaminoglycans accumulate in tissues throughout the body. Female homozygotes rarely conceive and do not lactate. This strain is a model for the human lysomal storage disease, mucopolysaccharidosis type VII.
006558 B6.Cg-H2-Kbm1 Tg(GUSB)4Sly/SndsJ
Cryopreserved - Ready for recovery
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).
001373 B6.Cg-Ldhab/J
Cryopreserved - Ready for recovery
004852 B6;129-Crb1rd8/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Crb1rd8 (Crb1nmf144) entry.
005048 B6;129-Rnu2nmf291
Cryopreserved - Ready for recovery
U2 small nuclear RNA (Rnu2-8) is one of five small nuclear RNAs, which comprise the spliceosome machinery and are responsible for the splicing of pre-mRNAs. The ethylmethanesulfonate (EMS)-induced nmf291 allele is a 5 base pair deletion, which results in alternative splicing defects, including the retention of small introns. Mice homozygous for the mutation exhibit mild tremors beginning at 4 weeks of age and progress to truncal ataxia by 12 weeks of age. The ataxia is characterized by splayed hind feet, a lumbering gait and a tendency to intermittently jump into the air. Granule cell degeneration begins at 4 weeks of age and occurs mainly in the cerebellum, but later progresses to the dentate gyrus region of the hippocampus. Mice heterozygous for the mutation develop late onset (2 years) tremors and some granule cell degeneration. Both female and male homozygotes breed, but the reproductive window is shortened by the progressive physical impairments. This .....
For more information please see the full phenotype on the strain data sheet
005043 B6;129-nmf166/J
Cryopreserved - Ready for recovery
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.
005689 B6;129S1-hlb349A/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable and fertile. Screening of third generation mice (G3) on atherogeneic diet identified a 12 week old male (born 12/28/2002) with a weight of 30.71 grams and body fat of 22.38%. Females appear to be more severely affected than males. This mutant mouse strain may be useful in studies of obesity.
006810 B6;129S4-hlb258/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 6 week old female (born 12/04/2002) with a plasma fibrinogen level of 67.4 mg/dl, which is approximately 61% lower than controls. This mutant mouse strain may be useful in studies of blood coagulation and hemophilia.
005520 B6;CByJ-Cacna1atg-6J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Cacna1atg-6J entry.
005050 B6;CByJ-Cacna2d2du-3J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf299 entry.
005633 B6;CByJ-Dstdt-38J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Dstdt-38J entry.
005463 B6;CByJ-Scn8a7J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Scn8a7J entry.
005753 B6;CByJ-Spnb4qv-9J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf470 entry.
005750 B6;CByJ-nmf375/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf375 entry.
005636 B6;CByJ-nmf418/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf418 entry.
005751 B6;CByJ-nmf419/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf419 entry.
006033 B6;CByJ-nmf445/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf445 entry.
000125 B6By.Cg-Sox18Ra Pt Os/J
Cryopreserved - Ready for recovery
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
Cryopreserved - Ready for recovery
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
Cryopreserved - Ready for recovery
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).
002379 B6Ros.Cg-Dmdmdx-5Cv/J
Cryopreserved - Ready for recovery
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
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Nmf31 entry.
002232 BTBR-Pahenu2/J
Cryopreserved - Ready for recovery
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
Cryopreserved - Ready for recovery
Homozygous mutant mice show a delay in the clearing of a load of phenylalanine.
002662 C.Cg-Fechm1Pas/J
Cryopreserved - Ready for recovery
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.
013059 C3.B6-Erbb3m3329Ddg/J
Cryopreserved - Ready for recovery
Mice homozygous for the Erbb3 (v-erb-b2 erythroblastic leukemia viral oncogene homolog 3 (avian)) I449S loss-of-function mutation are embryonic lethal at day 14.5 (E14.5). Mutant embryos exhibit extreme defasciculation of all major peripheral branches of the dorsal root ganglia (DRG). While the major dorsal and lateral projections form and are dissociated, all of the secondary and tertiary branches are absent. Upon reaching their superficial target, the axonal projections are splayed out almost randomly within the dermatome. Additionally, mutant embryos have complete loss of the mandibular branch of the trigeminal ganglia with defasciculation of the ophthalmic branch. This strain may be useful in studies of nerve development.
006863 C3Fe.B6-Mcm4chaos3/J
Cryopreserved - Ready for recovery
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
012946 C3Fe.B6-Scn8a8J/Frk
Cryopreserved - Ready for recovery
Mice that are homozygous for this chemically-induced allele exhibit small size, a weak and unsteady gait and a high incidence of spike wave discharges (SWD). On a mixed C57BL/6J and C3HeB/FeJ background, SWD burst frequency is recorded at 4-5 Hz. Homozygous mice die by 21 days, however, with additional care (see husbandry), mice can survive to 7 weeks. In mixed background heterozygotes, the SWD burst frequency is 7-9 Hz; SWD are characterized by high amplitude, significant duration and high frequency and occur between periods of locomotor activity. This mutant mouse strain may be useful in studies of human absence epilepsy.

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

005469 C57BL/6J-Agrnnmf380/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf380 entry.
005011 C57BL/6J-Agtpbp1pcd-6J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Agtpbp1pcd-6J entry.
006153 C57BL/6J-Akt3Nmf350/JFrk
Cryopreserved - Ready for recovery
Mice carrying this dominant missense point mutation in the thymoma viral proto-oncogene 3 (Akt) gene exhibit a low seizure threshold in response to electroconvulsive threshold testing or pentylenetetrazol (PTZ) administration, sporadic tonic-clonic seizures, brain enlargement and ecotopic neurons in the dentate hilus and molecular layer of the hippocampus. This mutant mouse strain may be useful in studies of AKT signalling and epilepsy.
005921 C57BL/6J-Aqp2F204V/J
Cryopreserved - Ready for recovery
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
005598 C57BL/6J-Arsbm1J/GrsrJ
Cryopreserved - Ready for recovery
Mice homozygous for the Arsbm1J mutation have a combination of delayed muscle and nerve degeneration along with a skeletal phenotype consisting of a shortened snout, wide-set eyes and shortened limbs that becomes more noticeable with age. Mutants can be poor breeders yielding small litters. Of 10 litters the average number of pups was 3.9.
004764 C57BL/6J-Cdh23v-8J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Cdh23v-8J entry.
004819 C57BL/6J-Cdh23v-9J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Cdh23v-9J entry.
005253 C57BL/6J-Clcn1adr-mto6J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Clcn1adr-mto6J entry.
005465 C57BL/6J-Clcn1adr-mto7J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Clcn1adr-mto7J entry.
005095 C57BL/6J-Clcn2nmf240/J
Cryopreserved - Ready for recovery
Homozygotes exhibit grainy retinas by 3 weeks of age which progresses into large white patches distributed across the entire retina by 12 weeks of age. At 10 days of age the apical processes of the retinal pigment epithelium are abnormally elongated, by 14 days of age the retinal outer nuclear layer is reduced in thickness and contains pyknotic nuclei and the photoreceptor outer segments are disorganized and shortened. By 3 weeks of age the photoreceptor layer is reduced to one to two layers of cells and the outer segments are not visible. Both dark and light adapted flash electroretinograms show reduced amplitude responses as early as 14 days of age and this worsens progressively to near zero by 26 days of age. Male infertility is associated with decreased weight of the testes and epididymides and azoospermia as early as 6 weeks of age with severe degradation of spermatogenesis. Progressive leukoencephalopathy is also found, with vacuoles in the white matter tracts and cerebellum .....
For more information please see the full phenotype on the strain data sheet
005255 C57BL/6J-Cldn9nmf329/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf329 entry.
002923 C57BL/6J-Clockm1Jt/J
Cryopreserved - Ready for recovery
Mice heterozygous for this Clockdelta19 mutation (also called Clockmut or Clockm1Jt) 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. Homozygous mice are viable. Male homozygotes are fertile, but female homozygotes appear to have reduced fertility.
013612 C57BL/6J-Dnahc5b2b002Clo/J
Cryopreserved - Ready for recovery
This c.13169T>C Dnahc5 (dynein, axonemal, heavy chain 5) point mutation was identified in an ENU screen for recessive cardiovascular development phenotypes in Dr. Cecilia Lo's laboratory, NHLBI Cardiovascular Development Consortium (CvDC). It was recovered from G1 sperm and associated with the phenotype described described here. Because G1 sperm were cryopreserved, additional incidental mutations are also segregating in this strain.

Homozygotes demonstrate laterality defects, including situs inversus totalis, and heterotaxy. Congenital heart disease (CHD) is marked by double outlet right ventricle (DORV), atrioventricular septal defects (AVSD), superior-inferior ventricles, and likely other structural heart defects.

004829 C57BL/6J-Dstdt-36J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Dstdt-3J entry.
005560 C57BL/6J-Dstdt-37J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Dstdt-37J entry.
004109 C57BL/6J-Glra1nmf11/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Glra1nmf11 entry.
005447 C57BL/6J-Grid2ho-16J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf334 entry.
005561 C57BL/6J-Grm1nmf373/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Grm1nmf373 entry.
005322 C57BL/6J-Gusbmps-3J/J
Cryopreserved - Ready for recovery
005691 C57BL/6J-Hlb280/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) after 5 weeks on atherogenic high fat diet identified a 13 week old female (born 9/9/2002) with a 4 hour fasted plasma HDL of 136 mg/dl and total cholesterol of 486 mg/dl, which is approximately 174% and 485% (respectively) higher than controls. This mutant mouse strain may be useful in studies of hypercholesterolemia.
005060 C57BL/6J-Hlb290/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified an 8 week old male (born 11/25/2002) with a 4 hour fasted plasma glucose of 516 mg/dl, which is approximately 137% higher than controls. Two siblings were similarly affected. This mutant mouse strain may be useful in studies of diabetes and hyperglycemia.
008507 C57BL/6J-Hlb320/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified an 8 week old female (born 1/5/2003) with a 4 hour fasted plasma total cholesterol of 35 mg/dl and an HDL of 26 mg/dl, which is approximately 58% and 48% lower than controls, respectively. One female sibling was similarly affected. This mutant mouse strain may be useful in studies of hypercholesterolemia.
008411 C57BL/6J-Hlb426/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on atherogenic diet for 1 week identified a female (born 3/31/2004) with a a systolic blood pressure of 142 +/- 12 mmHg, which is approximately 30% higher than controls. Retest 6 weeks later confirmed the phenotype. This mutant mouse strain may be useful in studies of hypertension.
008509 C57BL/6J-Hlb446/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 6 week old male (born 5/27/2002) with a 4 hour fasted plasma high density lipoprotein (HDL) of 112.2 mg/dl. Retesting one week later confirmed this observation with a reading of 120.6 mg/dl. This mutant mouse strain may be useful in lipoprotein studies.
006423 C57BL/6J-Hlb468/J
Cryopreserved - Ready for recovery
Mice carrying the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 11 week old male (born 1/19/2005) with a heart rate of 854 bpm. Repeat testing on week later measured a heart rate of 870 bpm confirming the phenotype. This mutant mouse strain may be useful in studies of tachycardia.
008263 C57BL/6J-Hlb476/J
Cryopreserved - Ready for recovery
008504 C57BL/6J-Hlb477/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 8 week old male (born 3/18/2005) with a 4 hour fasted plasma high density lipoprotein (HDL) of 106 mg/dl. Retesting one week later confirmed this observation with a reading of 107 mg/dl. This mutant mouse strain may be useful in lipoprotein studies.
008506 C57BL/6J-Hlb529/J
Cryopreserved - Ready for recovery
Mice homozygous for this ENU induced mutation exhibit elevated HDL cholesterol.
008505 C57BL/6J-Hlb561/J
Cryopreserved - Ready for recovery
Mice homozygous for this ENU induced mutation exhibit elevated HDL cholesterol.
008503 C57BL/6J-Hlb586/J
Cryopreserved - Ready for recovery
Mice homozygous for this ENU induced mutation exhibit elevated plasma HDL cholesterol.
008499 C57BL/6J-Hlb589/J
Cryopreserved - Ready for recovery
Mice homozygous for this ENU induced mutation exhibit elevated HDL cholesterol.
008500 C57BL/6J-Hlb592/J
Cryopreserved - Ready for recovery
Mice homozygous for this ENU induced mutation exhibit elevated plasma HDL cholesterol.
008262 C57BL/6J-Hlb594/J
Cryopreserved - Ready for recovery
005342 C57BL/6J-Il7hlb368/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified an 8 week old male (born 4/7/2003) with a CBC of 1.50 x 103 WBC/ul (84% lower than controls); testing two weeks later produced a result of 2.51 WBC/ul (74% lower than controls). This mutant mouse strain may be useful in studies of leukopenia.
004820 C57BL/6J-Kcne12J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Kcne12J entry.
005748 C57BL/6J-Kcnq1vtg-3J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Kcnq1vtg-3J entry.
004703 C57BL/6J-Kcnq2Nmf134/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Kcnq2Nmf134 entry.
005094 C57BL/6J-Lama1nmf223/J
Cryopreserved - Ready for recovery
Homozygotes have retinal vasculopathy, characterized by vitreal fibroplasias and vessel tortuosity. There is thinning of the peripheral inner nuclear layer and variable cell loss in the retinal ganglion cell layer, along with reduced dark and light adapted electroretinogram amplitudes. There is abnormal migration of retinal astrocytes into the vitreous and the persistence of hyaloid vaculature. While targeted disruption of the alpha 1 laminin gene causes a more severe phenotype, including the absence of the inner limiting membrane, this hypomorph nevertheless displays ectopic cells and blood vessels within the vitreous indicative of reduced integrity of the inner limiting membrane.
005635 C57BL/6J-Lama2dy-7J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Lama2dy-7J entry.
005638 C57BL/6J-Lhfpl5hscy-2J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Lhfpl5hscy-2J entry.
005579 C57BL/6J-Ltahlb382/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3)identified a non-fasted female (born 10/9/2003) with an increased white blood cell count of 15.39 x 103 cells/ul, which is approximately 92% higher than controls. This mutant mouse strain may be useful in studies of leukocytosis.
004110 C57BL/6J-Mertknmf12/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf12 entry.
005124 C57BL/6J-Mplhlb219/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 6 week old female (born 8/14/2002) with a platelet count of 106 x 103 cells/ul, which is approximately 91% lower than controls. This mutant mouse strain may be useful in studies of thrombocytopenia.
005749 C57BL/6J-Myo6sv-3J/J
Cryopreserved - Ready for recovery
005468 C57BL/6J-Myo7ash1-11J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Myo7ash1-11J entry.
004851 C57BL/6J-Nmf128/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Nmf128 entry.
005007 C57BL/6J-Nmf191/J
Cryopreserved - Ready for recovery
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.
004832 C57BL/6J-Nmf220/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Nmf220 entry.
005014 C57BL/6J-Nox3het-4J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf250 entry.
004817 C57BL/6J-Npc1nmf164/J
Cryopreserved - Ready for recovery
Npc1 is a transmembrane protein involved in endosomal lipid sorting and trafficking. The nmf164 allele is a point mutation, which results in partial functional loss of the protein. In comparison to mice carrying Npc1spm (Stock #002760) and Npc1m1N (Stock #003092), the nmf164 phenotype has a delayed onset and models a more slowly progressing form of human Niemann-Pick C disease. Mice exhibit age-dependent ataxia, impaired motor and strength capabilities, shortened lifespan (112 +/- 4 days), weight loss, progressive accumulation of sphingomyelin and glycosphingolipids in the liver and spleen (sphingomyelinosis), and abnormal cholesterol levels in liver. In the brain, phenotypic characteristics include: loss of cerebellar Purkinje cells, an increase in the GM2 and GM3 gangliosides, abnormal astrocyte and microglial cell activation, abnormal cholesterol levels in neurons, and acoustic startle response abnormalities. This mutant mou .....
For more information please see the full phenotype on the strain data sheet
005008 C57BL/6J-Nphp4nmf192/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf192 entry.
004156 C57BL/6J-Pcdh15av-5J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Pcdh15av-5J entry.
006699 C57BL/6J-Pcsk1N222D/J
Cryopreserved - Ready for recovery
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.
006249 C57BL/6J-Plxna2nmf454/J
Cryopreserved - Ready for recovery
Due to aberrant migration of granule cells during development, mice homozygous for the nmf454 mutation have a hypercellular molecular layer of the cerebellum with many ectopic granule cells in the molecular layer.
004821 C57BL/6J-Prph2Nmf193/J
Cryopreserved - Ready for recovery
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.
005744 C57BL/6J-Relnrl-6J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Relnrl-6J entry.
008791 C57BL/6J-Rnl11/Pgn
Cryopreserved - Ready for recovery
Mice homozygous for this ENU induced mutation exhibit decreased kidney function as measured by an increased albumin/creatinine ratio (ACR).
016255 C57BL/6J-Rnl16/BPgn
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 20 week old male with an increased blood urea nitrogen (BUN) of 34 mg/dL. Testing one week later confirmed the increased BUN value (34 mg/dL). This mutant mouse strain may be useful in studies of kidney function.
008793 C57BL/6J-Rnl18/Pgn
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 20 week old male with an increased blood urea nitrogen (BUN) of 36 mg/dL. Testing one week later confirmed the increased BUN value (33 mg/dL). This mutant mouse strain may be useful in studies of kidney function.
008794 C57BL/6J-Rnl20/Pgn
Cryopreserved - Ready for recovery
Mice homozygous for this ENU induced mutation exhibit decreased kidney function as measured by an increased albumin/creatinine ratio (ACR).
008795 C57BL/6J-Rnl23/Pgn
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 20 week old male (born 3/28/2006) with an increased blood urea nitrogen (BUN) of 37 mg/dL. Testing one week later confirmed the phenotype (BUN=55 mg/dL). This mutant mouse strain may be useful in studies of kidney function and blood homeostasis.
008796 C57BL/6J-Rnl25/APgn
Cryopreserved - Ready for recovery
Mice homozygous for this ENU induced mutation exhibit decreased kidney function as measured by increased blood/urea/nitrogen levels (BUN). In the F2 and F3 generations, some animals exhibited increased albumin/creatinine ratios (ACR). In succeeding generations, mice with elevated ACR were bred to establish the "A" line. Mice with elevated BUN were bred to establish the "B" line (Stock No. 016256).
016256 C57BL/6J-Rnl25/BPgn
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 20 week old male with an increased blood urea nitrogen (BUN) of 34 mg/dL. Testing one week later confirmed the increased BUN value (35 mg/dL). This mutant mouse strain may be useful in studies of kidney function.
008412 C57BL/6J-Rnl27/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 20 week old male (born 5/17/2006) with an increased blood urea nitrogen (BUN) of 47 mg/dL. Testing one week later confirmed the increased BUN value (52 mg/dL). This mutant mouse strain may be useful in studies of kidney function.
016916 C57BL/6J-Rnl27/Pgn
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 20 week old male with an increased blood urea nitrogen (BUN). Testing one week later confirmed the increased BUN value. This mutant mouse strain may be useful in studies of kidney function.
008798 C57BL/6J-Rnl29/Pgn
Cryopreserved - Ready for recovery
Mice homozygous for this ENU induced mutation exhibit decreased kidney function as measured by increased blood/urea/nitrogen levels (BUN).
008801 C57BL/6J-Rnl32/Pgn
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 20 week old male (born 6/25/2006) with an increased blood urea nitrogen (BUN) of 37 mg/dL. Testing one week later confirmed the phenotype (BUN=35 mg/dL). This mutant mouse strain may be useful in studies of kidney function and blood homeostasis.
008803 C57BL/6J-Rnl43/Pgn
Cryopreserved - Ready for recovery
Mice homozygous for this ENU induced mutation exhibit decreased kidney function as measured by increased blood/urea/nitrogen levels (BUN).
005047 C57BL/6J-Rorasg-3J/J
Cryopreserved - Ready for recovery
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.

005096 C57BL/6J-Rpgrip1nmf247/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Rpgrip1nmf247 entry.
005495 C57BL/6J-Scarb1Hlb398/J
Cryopreserved - Ready for recovery
Mice carrying this mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified an 8 week old male (born 2/5/2004) with a 4 hour fasted total cholesterol of 190 mg/dl and a high density lipoprotein (HDL) of 146 mg/dl, which is approximately 62% and 102%, respectively, higher than controls. Retesting one week later confirmed these results. This is a dominant mutation affecting 5 out of 6 of the F1 progeny. This mutant mouse strain may be useful in studies of hypercholesterolemia.
004102 C57BL/6J-Scn8a4J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Scn8a4J entry.
004105 C57BL/6J-Scn8a5J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Scn8a5J entry.
005449 C57BL/6J-Spnb4qv-8J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf379 entry.
008785 C57BL/6J-Stk39Rnl5/Pgn
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 20 week old male (born 11/21/2002) with an increased albumin-creatinine ratio of 22 mg/g. Retesting one week later confirmed this observation with a reading of 91 mg/g. This mutant mouse strain may be useful in studies of albuminuria.
008264 C57BL/6J-hlb145/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 7 week old female (born 4/16/2002) with a white blood cell count of 2.7 x 103 cells/ul, which is approximately 66% lower than controls. Retesting 2 weeks later confirmed the phenotype. This mutant mouse strain may be useful in studies of leukopenia.
004517 C57BL/6J-hlb156/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 6 week old male (born 5/27/2002) with a neutrophil level of 27.4%, which is approximately 130% higher than controls. This mutant mouse strain may be useful in studies of neutrophilia.
004530 C57BL/6J-hlb15/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 9 week old female (born 4/15/2001) with a mean systolic blood pressure of 133 +/- 16 mmHg, which is approximately 22% higher than controls. This mutant mouse strain may be useful in studies of hypertension.
008508 C57BL/6J-hlb218/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 8 week old male (born 9/15/2002) with a n4 hour fasted plasma total cholesterol of 17 mg/dl and HDL cholesterol of 15 mg/dl, which is approximately 85% and 79% lower than controls, respectively. This mutant mouse strain may be useful in studies of cholesterol homeostasis.
008265 C57BL/6J-hlb233/J
Cryopreserved - Ready for recovery
007231 C57BL/6J-hlb243/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) after more than 5 weeks atherogenic diet identified a 13 week old female (born 9/04/2002) with a 4 hour fasted plasma total cholesterol of 517 mg/dl and HDL of 129 mg/dl, which is approximately 522% and 160% higher, respectively, than controls. One sibling was similarly affected. This mutant mouse strain may be useful in studies of diet-induced hypercholesterolemia.
006422 C57BL/6J-hlb324B/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 12 week old male (born 9/30/2002) with a low bone mineral content and density as determined by DEXA analysis. Retesting at 18 weeks of age, when bone development has stabilized, confirmed this phenotype. This mutant mouse strain may be useful in studies of bone mineralization.
005343 C57BL/6J-hlb381/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 6 week old male (born 1/7/2004) with a platelet count of 24 x 103 cells/ul,which is approximately 98% lower than controls. One sibling was similarly affected. This mutant mouse strain may be useful in studies of neutrophilia.
005496 C57BL/6J-hlb385/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 7 week old female (born 12/13/2003) with a complete blood count (CBC) of 3.2 x 103 white blood cells (WBC)/ul, approximately 60% lower than controls. Retesting 2 weeks later confirmed the phenotype. This mutant mouse strain may be useful in studies of leukopeniia.
005580 C57BL/6J-hlb388/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) identified a fasted 8 week old male (born 12/25/2003) with a plasma HDL level of 97.6 mg/dl, which is approximately 35% higher than controls. HDL levels were 106.9 mg/dl when the mouse was retested one week later. This mutant mouse strain may be useful in studies of hypercholesterolemia.
008269 C57BL/6J-hlb414/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 9 week old male (born 2/15/2004) exhibiting a hyper-response to methacholine (MCH). Absolute Penh values are as follows: saline control 0.46(0.66), 5mg/ml MCH 0.64(0.60), 10 mg/ml MCH 0.92(1.28), 20 mg/ml MCH 4.54(12.48). Second run values are in parenthesis. This mutant mouse strain may be useful in studies of asthma and airway hyper-responsiveness (AHR).
010952 C57BL/6J-hlb444/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified an 8 week old male (born 9/15/2004) with a 4 hour fasted plasma triglyceride level of 187 mg/dl, which is increased in comparison to controls. Retesting one week later confirmed this observation with a reading of 204 mg/dl. This mutant mouse strain may be useful in studies of triglyceride and lipid homeostasis.
008280 C57BL/6J-hlb454/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on atherogenic diet identified a 9 week old male (born 9/12/2004) exhibiting a hyper-response to methacholine (MCH). Absolute Penh values are as follows: 5mg/ml MCH 0.1.37(0.98), 10 mg/ml MCH 2.01(1.94), 20 mg/ml MCH 11.47(5.28). Second run values are in parenthesis. Two siblings were similarly affected. This phenotype has been validated by an invasive resistance evaluation using a flexivent protocol. This mutant mouse strain may be useful in studies of asthma and airway hyper-responsiveness (AHR).
008497 C57BL/6J-hlb459/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 11 week old male (born 11/8/2004) with a heart rate of 805 bpm. Repeat testing one week later confirmed the phenotype (822 bpm). This mutant mouse strain may be useful in studies of tachycardia.
008266 C57BL/6J-hlb495/J
Cryopreserved - Ready for recovery
008261 C57BL/6J-hlb497/J
Cryopreserved - Ready for recovery
008267 C57BL/6J-hlb520/J
Cryopreserved - Ready for recovery
008268 C57BL/6J-hlb521/J
Cryopreserved - Ready for recovery
008270 C57BL/6J-hlb52/J
Cryopreserved - Ready for recovery
010955 C57BL/6J-hlb541/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a male with an increased percentage of fat in comparison to controls. This mutant mouse strain may be useful in studies of obesity.
010956 C57BL/6J-hlb560/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) identified a mouse with elevated plasma triglycerides. This mutant mouse strain may be useful in studies of cardiovascular research and metabolism.
008498 C57BL/6J-hlb575/J
Cryopreserved - Ready for recovery
Mice with this mutation exhibit an increased percentage of body fat on a standard laboratory chow diet.
008640 C57BL/6J-hlb583/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the mutation are viable and fertile. Screening of third generation mice (G3) on standard chow identified a male with an increased percentage of fat. This mutant mouse strain may be useful in studies of obesity.
005330 C57BL/6J-hpbk/GrsrJ
Cryopreserved - Ready for recovery
Mice homozygous for the humpback mutation appear normal at wean age, but by 5 weeks of age can be distinguished by thoracic kyphosis and scrawniness. Both phenotypes progress with age, and sudden death is common in adults. Histology reveals myopathy. Homozygotes females are not able to deliver pups and homozygous males develop phimosis so do not breed.
004811 C57BL/6J-nmf110/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf110 entry.
004812 C57BL/6J-nmf111/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf111 entry.
004747 C57BL/6J-nmf118/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf118 entry.
004814 C57BL/6J-nmf127/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf127 entry.
005006 C57BL/6J-nmf131/J
Cryopreserved - Ready for recovery
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
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf148 entry.
004816 C57BL/6J-nmf161/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf161 entry.
004818 C57BL/6J-nmf172/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf172 entry.
005009 C57BL/6J-nmf195/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf195 entry.
004823 C57BL/6J-nmf205/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf205 entry.
004830 C57BL/6J-nmf206/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf206 entry.
004831 C57BL/6J-nmf219/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf219 entry.
005010 C57BL/6J-nmf242/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf242 entry.
005101 C57BL/6J-nmf268/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf268 entry.
005298 C57BL/6J-nmf313/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf313 entry.
005329 C57BL/6J-nmf318/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf318 entry.
005448 C57BL/6J-nmf347/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf347 entry.
005741 C57BL/6J-nmf356/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf356 entry.
005467 C57BL/6J-nmf370/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf370 entry.
005451 C57BL/6J-nmf391/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf391 entry.
004085 C57BL/6J-nmf4/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf4 entry.
004442 C57BL/6J-nmf62/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf62 entry.
004468 C57BL/6J-nmf63/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf63 entry.
004470 C57BL/6J-nmf65/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf65 entry.
004472 C57BL/6J-nmf67/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf67 entry.
004656 C57BL/6J-nmf88/J
Cryopreserved - Ready for recovery
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
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf9 entry.
005421 CBy;B6-Bmp5cfe-se8J/J
Cryopreserved - Ready for recovery
Homozygotes have small, round ear pinnae with ridges along the perimeter and both ears are affected. This mutation is 100% penetrant. Unlike short ear mutations of this gene, skeletal abnormalities were not detected by X-ray for this mutant. Both males and females are fertile.
005016 CByJ;B6-Cdh23v-10J/J
Cryopreserved - Ready for recovery
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Cdh23v-10J entry.
000806 LT.Cg-Ldhab/J
Cryopreserved - Ready for recovery
008607 STOCK Aspanur7/J
Cryopreserved - Ready for recovery
Mice homozygous for this ENU-induced mutation, the neurological 7 (nur7) allele of Aspa (Aspanur7), are viable and fertile, although the donating investigator reports homozygotes are poor breeders. The Aspanur7 mutation encodes a Q193X transition that generates a nonsense codon and results in a predicted 120 amino acid truncation of the protein. While mutant Aspa mRNA expression is reduced by 40% (compared to wildtype), no truncated Aspa protein expression is reported in homozygous oligodendrocytes or brain tissue. Homozygous mice display early-onset spongy degeneration of central nervous system myelin with increased NAA levels similar to that observed in Canavan disease; an Aspa-deficiency-induced fatal childhood autosomal recessive leukodystrophy. Homozygous mice are easily distinguished at 21 days of age by their small body size and a wide-based ataxic gait. Neurological disease progresses with age to tremors and seizures. These Aspa> .....
For more information please see the full phenotype on the strain data sheet
007863 STOCK Dnahc5hlb612/JClo
Cryopreserved - Ready for recovery
The ENU generated hlb612 allele contains an in-frame deletion in a dynein gene (Dnahc5) commonly associated with human primary ciliary dyskinesia (PCD). Thirty-six percent of homozygotes exhibit situs inversus totalis and hydrocephaly and die between 2-4 weeks of age. Forty percent of homozygotes die before or shortly after birth and exhibit heterotaxy with structural heart defects and cardiovascular anomalies including discordant atrioventricular and ventricular outflow situs, atrial/pulmonary isomerisms, artery alignment defects, interrupted inferior vena cava and dextrocardia. Electronmicroscopy reveals that the outer dynein arms of the respiratory cilia are greatly reduced in number. Respiratory cilia exhibit a wide variation in orientation. Cilia in the airway epithelia are immotile or slow and dsykinetic. Heterozygous mice do not have situs defects, however, respiratory cilia exhibit some reduction in the number of outer dynein arms. This strain may be use .....
For more information please see the full phenotype on the strain data sheet
015824 STOCK Hmx1dmbo/KjnJ
Cryopreserved - Ready for recovery
Mice homozygous for the dumbo mutation have low set, laterally protruding ears. They are smaller in overall body size than normal, with males weighing about half that of normal littermates at three days of age and lagging behind through nine days of age. Most have microphthalmia. This mutation causes perinatal lethality such that approximately 40% fewer homozygotes than predicted by standard Mendelian genetics are found at three weeks of age. Further assessment showed that most of the homozygous death occurs within the first three days of life and is strongly associated with exencephaly. This strain is a model for oculo-auricular syndrome.
008581 STOCK Largemyd-3J/GrsrJ
Cryopreserved - Ready for recovery
Mice homozygous for the myodystrophy 3 Jackson mutation generally begin to display evidence of muscle degeneration at two to three months of age, although some exhibit symptoms as early as wean age. Inability to splay the hind legs outward when held up by the tail is an initial phenotype and this progresses with age to include swaying gait then dragging of the hind legs. Homozyogtes also display retinoschisis and males are sterile.
002919 STOCK Myo7ash1-7J/J
Cryopreserved - Ready for recovery
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
Cryopreserved - Ready for recovery
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.
006128 STOCK Otofdeaf5Jcs/Kjn
Cryopreserved - Ready for recovery
005375 STOCK Trp53bp1hlb543/CloJ
Cryopreserved - Ready for recovery
000802 WB.Cg-Hbath-J/J
Cryopreserved - Ready for recovery
016157 129S1.B6-Shroom3m1Nisw/J
Under Development - Now Accepting Orders
Mice heterozygous for the ENU-induced mutation, Shroom3C5745T, are viable and fertile, although homozygotes die shortly before birth. These mice possess a C to T mutation in the codon for amino acid residue 1663 results in an arginine to cysteine change in the shroom family member 3 (Shroom3) gene. These mice exhibit complete exencephaly (hind-mid-forebrain), cleft face, and body wall defects. These mutant mice may be useful in studying embryonic development.
016926 BTBR T+ tf-Fbxl3Ovtm/J
Under Development - Now Accepting Orders
Ovtm ENU-induced mutants contain an A to G transition at nucleotide in exon 5 of the F-box and leucine-rich repeat protein 3 (Fbxl3) gene that defines an amino acid change from isoleucine to threonine at residue 364. While homozygous males are viable, fertile, and normal in size, homozygous females are viable and normal in size, but are often infertile. FBXL3 is part of the SKP1-CUL1-F-box-protein (SCF) ubiquitin protein ligase complex which mediates phosphorylation-dependent ubiquitination. Homozygotes have a long circadian period of ~26 hours. These mice may be useful for studying circadian rhythm modulation.
016131 C57BL/6J-Sec61a1m1Gek/J
Under Development - Now Accepting Orders
Mice homozygous for the ENU-induced missense mutation, called Sec61a1Y344H, are viable and fertile. By ~4 weeks of age, homozygous males and females maintained on a high-fat diet (~58% kcal from fat) become diabetic (hyperglycemic) with hypoinsulinemia; the result of endoplasmic reticulum (ER) stress-induced apoptosis of pancreatic β-cells. In addition to diabetes, these mice exhibit other metabolic, endocrinological, and growth abnormalities (including hyperlipidemia, hepatosteatosis, hypercholesterolemia, hypertriglyceridemia, and, in older mice, hepatic cirrhosis). Homozygous mice maintained on a chow diet (~5% kcal from fat) become diabetic by ~10 weeks of age; exhibiting hyperglycemia, hypoinsulinemia, glucose intolerance, and pancreatic β-cell loss. Heterozygous mice have an intermediate hypoinsulinemic phenotype on high-fat diet. These Sec61a1Y344H mutant mice may be useful in studying diabetes, ER protein trafficking/processing/sec .....
For more information please see the full phenotype on the strain data sheet
017537 C57BL/6J-Tmem173gt/J
Under Development - Now Accepting Orders
These Tmem173gt chemically-induced (ENU) mutant mice carry a missense mutation in exon 6 of the transmembrane protein 173 (Tmem173 or Sting) gene, which results in an isoleucine-to-asparagine change in amino acid 199, in the C-terminal of the protein. No gene product (protein) is detected by Western blot analysis of bone marrow-derived macrophages from homozygotes. Thioglycolate-elicited peritoneal macrophages isolated from homozygotes do not produce type I interferons (IFN-β) in response to cyclic dinucleotides (c-di-GMP) or Listeria monocytogenes infection. Mice homozygous for the mutation are viable and fertile.

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New Strains Awaiting Transfer

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

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

Stock
Number		Strain Name
 
Strain Description		Standard Supply
013561B6(129S1)-Pgap1m1Nisw/J
Awaiting Transfer from the Donor
Mice homozygous for this ENU-derived Pgap1 mutant display head truncations on the C57BL/6 genetic background. This strain may be useful in studies of development.
016175C.B6-Clockm1Jt/J
Awaiting Transfer from the Donor
This strain carries the Clock (circadian locomotor output cycles kaput) delta 19 ENU mutation on a BALB/cJ genetic background. This strain may be useful in studies of circadian rhythm.
017461C57BL/6-Mia2cpto/J
Awaiting Transfer from the Donor
These Mia2cpto ENU-induced mutant mice possess a missense mutation in exon 3 of the melanoma inhibitory activity 2 (Mia2) gene. These mutant mice may be useful in studying the regulation and secretion of circulating cholesterol and triglycerides.
016091C57BL/6-Ptprcltng/J
Awaiting Transfer from the Donor
These lightning mice possess an ENU-induced point mutation (F503S) in the Ptprc gene and may be useful in studying the differential regulation of TCR signaling by altered CD45 expression levels.

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New Strains Awaiting Transfer The Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion.

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

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