JAX Mice Database - Major Histocompatibility Congenic

Search Criteria: Strain Type is "Major Histocompatibility Congenic"

Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development

JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
000465	B10.BR-H2^k H2-T18^a/SgSnJ	Level 2
	Some phenotypic parameters of the B10.BR-H2^k H2-T18^a/SgSnJ mice may have changed recently relative to the strain's previous performance. In order to confirm that a change had occurred and in order to better characterize any differences that may have arisen, animals were recovered from cryo-preserved embryos of the strain (Stock No. 004804) that had been frozen in 1991, and the two lines of B10.BR-H2^k H2-T18^a/SgSnJ were compared. Differences between the two strains have been identified in the CD4/CD8 ratios among several cell populations, and in some dendritic cell populations. As more information is gathered, this website will be updated. Both colonies of B10.BR-H2^k H2-T18^a/SgSnJ (Stock No's. 000465 and 004804) may exhibit white belly ..... For more information please see the full phenotype on the strain data sheet
000457	B10.RIII-H2^r H2-T18^b/(71NS)SnJ	Level 2
	This congenic strain develops chronic and relapsing experimental autoimmune encephalomyelitis (EAE) after immunization with myelin basic protein (MBP). Susceptibility is associated with the major histocompatibility complex (MHC) allele, H2^r, the T cell receptor V β8 chain, and other non MHC loci. This strain also is susceptible to induction of collagen-induced arthritis.
000469	B10.A-H2^a H2-T18^a/SgSnJ	Level 3

004804	B10.BR-H2^k H2-T18^a/SgSnJJrep	Level 3
	Some phenotypic parameters of the B10.BR-H2^k H2-T18^a/SgSnJ (Stock No. 000465) mice may have changed recently relative to the strain's previous performance. In order to confirm that a change has occurred and in order to better characterize any differences that may have arisen, animals were recovered from cryopreserved embryos of the strain (B10.BR-H2^k H2-T18^a/SgSnJJrep Stock No. 004804) that had been frozen in 1991, and the two lines of B10.BR-H2^k H2-T18^a/SgSnJ were compared. Differences between the two strains have been identified in the CD4/CD8 ratios among several cell populations, and in some dendritic cell populations. As more information is gathered, this website will be updated. Both colonies of B10.BR-H2^k H2-T18^a/SgSnJ (000465 and 004804) may exhibit whit ..... For more information please see the full phenotype on the strain data sheet
002024	B10.D1-H2^q/SgJ	Level 3

000461	B10.D2-Hc⁰ H2^d H2-T18^c/oSnJ	Level 3
	This congenic strain carries the H2^d haplotype from DBA/2J following six generations of backcrossing to C57BL/10Sn. This strain still carries the Hc⁰ allele from DBA/2J, making them serum C5 deficient. Mice have increased susceptibility to certain pathogens and impaired chemotactic responses of neutrophils. Allograft rejection is prolonged. The following inbred strains are also homozygous for the Hc⁰ allele: A/HeJ (Stock No. 000645), AKR/J (Stock No. 000648), DBA/2J (Stock No. 000671), NOD/LtJ (Stock No. 001976), NZB/BlNJ (Stock No. 000684), and SWR/J (Stock No. 000689).
000463	B10.D2-Hc¹ H2^d H2-T18^c/nSnJ	Level 3

000458	B10.PL-H2^u H2-T18^a/(73NS)SnJ	Level 3

000438	C3.SW-H2^b/SnJ	Level 3
	Male mice from the C3.SW-H2^b/SnJ congenic strain are predisposed to maturity-onset impairment of glucose tolerance and hyperinsulinemia with some mice exhibiting hyperglycemia. Symptoms occur much later, between 5 and 8 months of age, than most of the single gene obese and diabetic strains. In addition, male mice are susceptible to the diabetogenic effects of multiple low doses of streptozotocin (40 mg/kg BW.day X 5).
000471	A.SW-H2^s H2-T18^b/SnJ	Level 4

001060	B6.C-H2^bm1/ByJ	Level 4

006500	129.NOD-(D17Mit175-H2)/J	Repository- Live
	129S1.NOD-H2^g7 congenic mice are viable, fertile, normal in size, do not display any gross physical or behavioral abnormalities and are diabetes free. Because targeted mutations frequently are made using 129 ES cells, this strain may be useful for identifying Idds in 129 strains.
001649	A.BY H2^bc H2-T18^f/SnJ-Dstn^corn1/J	Repository- Live
	Mice homozygous for the recessive Dstn^corn1 mutation have abnormally proliferative basal corneal epithelial cells. Focal areas of corneal epithelial hyperplasia are found by one week of age, and neovascularization is found by 14 days of age when the eyes open. This neovascularization, which progresses during the first two months of age, is not found in mice homozygous for the Dstn^corn-2J allele (which is a point mutation leading to a change in a single amino acid residue). In both mutants the corneal epithelial cells show increased levels and altered organizational pattern of filamentous actin. The areas of thickened cortical epithelia yield a roughened, opaque corneal surface. At 4 weeks of age in Dstn^corn1 homozygotes, expression of keratin 14 and involucrin extend into the suprabasal layer in the areas of hyperplastic corneal epithelia. There is also an increase in the levels of expression of cofilin 1, lumican and kerat ..... For more information please see the full phenotype on the strain data sheet
000140	A.BY-H2^bc H2-T18^f/SnJ	Repository- Live
	Dr. George Snell, of The Jackson Laboratory, created this H2-congenic strain by crossing of mice of a non-inbred stock carrying the brachyury mutation (and therefore called BY) to mice of the A/Lilly inbred strain, then repeatedly backcrossing to the latter strain mice that proved resistant to A-derived tumors. A/Lilly was a subline of strain A that Snell obtained from the Lilly Company after the 1947 fire at The Jackson Laboratory; when it was learned that this strain was contaminated, Snell performed a single additional backcross to the A/WySn subline, taking it to generation N11 (Rodgers 2004; Klein 1989). The BY stock apparently was obtained from Dr. Dobrovolskaia-Zavadskaia, who described a short-tailed mouse sired by a gonadally-irradiated male; she believed the brachyury mutation not to have been caused by the radiation, but to have been a pre-existing spontaneous mutation (Dobrovoskaya-Zajadkaya 1927; Rodgers 2004). In a subsequent article, she described short tailed (b ..... For more information please see the full phenotype on the strain data sheet
000468	B10.A-H2^h2/(2R)SgSnJ	Repository- Live

006102	B10.Cg-H2^k Tg(Il2/NFAT-luc)83Rinc/J	Repository- Live
	Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The donating investigator reports that homozygous females in their colony are subfertile. These transgenic mice express luciferase under the regulation of the Il2 minimal promoter and 3 binding sites for the NFAT inducible nuclear factor involved in the regulation of interleukin-2 and other cytokine expression. Luciferase activity in these transgenic mice identifies NFAT-mediated transcription. These NFAT-luc transgenic mice may be useful be useful as reporters for NFAT-mediated expression during thymocyte development and selection and in studies related to signal transduction, apoptosis, and transcriptional regulation.
006100	B10.Cg-H2^k Tg(NFkB/Fos-luc)26Rinc/J	Repository- Live
	Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Mutant mice have the luciferase gene driven by two copies of the NF-kappaB (NF-kB or NFkB) regulatory element. The presence of nuclear NF-kB DNA binding activity (as detected by electrophoretic mobility shift assay [EMSA]) is consistent with luciferase reporter activity; these reporter mice identify NF-kB transcriptional activity in any tissue. These transgenic mice may be useful in studies of immunology, cellular signaling, signal transduction, apoptosis, and transcription factor function.
001953	B10.S-H2^s/SgMcdJ	Repository- Live

005717	B6(NOD) H2^g7-Sostdc1^shk/J	Repository- Live

001148	B6.AK-H2^k/FlaEgJ	Repository- Live

003625	B6.C-H2-Ab1^bm12/KhEg-Mc1r^e-J/J	Repository- Live

000359	B6.C-H2^d/bByJ	Repository- Live

007958	B6.Cg-H2^b3/FlaCmwJ	Repository- Live
	The Qa2, or Ped, complex includes four similar genes and is correlated with the rate of preimplantation embryo development. Qa2^positive mice are characterized by the fast Ped phenotype; Qa2^negative mice, which do not express the QA2 antigen, are characterized by the slow Ped phenotype. This strain, commonly known as B6.K1, is slow Ped or Qa2^negative. B6.K1 females have longer gestation times and smaller litter sizes than the control B6.K2 (Stock No. 007959) females. (Warner CM, 1993) At birth, B6.K1 pups are slighter lighter than B6.K2 pups, but they exhibit an accelerated growth, and by week 6 both male and female B6.K1 mice are significantly heavier than B6.K2 mice. (Watkins A, 2006) At 21 weeks of age, B6.K1 females exhibit elevated systolic blood pressure, and both sexes exhibit elevated serum angiotensin-converting enzyme (ACE) activity. (Watkin ..... For more information please see the full phenotype on the strain data sheet
007959	B6.Cg-H2^b4/FlaCmwJ	Repository- Live
	The Qa2 or Ped complex includes four similar genes. The functional (Qa2^positive) and null (Qa2^negative) alleles correlate with the rate of preimplantation embryo development such that Qa2^positive mice are characterized by the fast Ped phenotype and Qa2^negative mice, which do not express the QA2 antigen, are characterized by the slow Ped phenotype. This strain, commonly known as B6.K2, is fast Ped or Qa2^positive. B6.K2 mice were developed to provide a control for B6.K1 mice (Stock No. 007958). (Warner CM, 1993; Watkins A, 2006)
001952	C.B10-H2^b/LilMcdJ	Repository- Live

001951	C.C3-H2^k/LilMcdJ	Repository- Live

002591	NOD.B10Sn-H2^b/J	Repository- Live
	This congenic strain serves as a diabetes-resistant control for comparison to the NOD/LtJ strain (Stock No. 001976). The diabetes resistant MHC H2^b haplotype was transferred from C57BL/10J mice to the NOD/Lt strain. These mice exhibit some but not all of the immune dysfunctions of NOD/LtJ mice. They are useful in dissecting the role of MHC versus non-MHC genes in producing aberrant immunophenotypes.
002032	NOD.SW-H2^q/J	Repository- Live
	This congenic strain carries the diabetes-resistant MHC from the from SWR/J (Stock No. 000689) and is used as a comparison to the NOD/ShiLtJ (Stock No. 001976). These mice exhibit some but not all of the immune dysfunctions of NOD/ShiLtJ mice. These mice are useful for dissecting the role of MHC versus non-MHC genes in producing aberrant immunophenotypes.
000472	A.CA-H2^f H2-T18^a/SnJ	Repository-Cryopreserved

001066	A.TH-H2^t2/SfDvEgMobJ	Repository-Cryopreserved

001067	A.TL-H2^t1/SfDvEgMobJ	Repository-Cryopreserved

002089	AK.B6-H2^b Fv1^b/J	Repository-Cryopreserved

002090	AK.B6-H2^b/J	Repository-Cryopreserved

001094	AK.L-H2^b/1CyTyJ	Repository-Cryopreserved

001095	AK.L-H2^oz2/CyJ	Repository-Cryopreserved

001096	AK.L-H2^oz3/CyJ	Repository-Cryopreserved

000470	AK.M-H2^m H2-T18^a/nSnJ	Repository-Cryopreserved

004941	ALR.NOD-(D17Mit61-H2-D)/Lt	Repository-Cryopreserved
	This congenic strain carries the H2 major histocompatibility complex from NOD/Lt on a background that is otherwise, statistically, 99.9% of ALR/Lt origin. The most proximal marker within the NOD/Lt-derived chromosomal segment of this strain is D17Mit61, at 16.4 cM just 3.6 cM from the most proximal gene of the H2 complex, and the most distal is H2-D. The H2 ^g7 haplotype of NOD/Lt differs from the ALR/Lt H2^gx haplotype only at the H2-D locus.
001150	B10.A-H2^h4/(4R)SgDvEgJ	Repository-Cryopreserved

001149	B10.A-H2ⁱ³/(3R)SgDvEgJ	Repository-Cryopreserved

000467	B10.A-H2ⁱ⁵ H2-T18^a/(5R)SgSnJ	Repository-Cryopreserved

000466	B10.AKM-H2^m H2-T18^a/SnJ	Repository-Cryopreserved

001954	B10.AQR-H2^y1/KljMcdJ	Repository-Cryopreserved

005308	B10.Cg-H2^d Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ	Repository-Cryopreserved
	Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities.The TCR expressed from this transgene is specific for influenza virus A/PR/8 hemagglutinin (HA) in the context of the MHC class I molecule H2-K^d. Both thymic and peripheral T-cell populations are skewed toward CD8+ cells. The majority of thymocytes and virtually all CD8+ T cells in lymph nodes express the transgenic TCR beta chain. About 40% of peripheral blood CD8+ T cells react with the HA peptide presented by H2-K^d. When mated with Tg(Ins2-HA)165Bri, double transgenic neonates have similar levels of V-beta 8 and total number of thymocytes as Tg(TcraCl4,TcrbCl4) mice however the double transgenics become spontaneously diabetic after birth and die within 10 days. This transgenic model is useful in the study of T-cell activation, cross presentation of antigens, process of thymic selection, peripheral tolerance and ..... For more information please see the full phenotype on the strain data sheet
005534	B10.Cg-H2^d Tg(Ins2-HA)165Bri/ShrmJ	Repository-Cryopreserved
	Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. Mice homozygote for the transgene have silver grey fur color. Hemizygous and wildtype mice are black. Immunohistochemistry reveals pancreatic islet cell expression of the transgene and no expression in the spleen, kidney or thymus. Isolated islets stain normally for insulin and are morphologically indistinguishable from control islets. Additional functional studies found no expression in bone marrow. Histology revealed no insulitis and the single transgenic mice do not become diabetic. T-cell proliferation assays, Cytotoxic Lymphocyte (CTL) assays, and adoptive transfer studies performed using transgenic mice indicate significantly reduced class 1 and class II T-cell responses compared to controls. Hemagglutination inhibition assays of sera from HA primed transgenic mice indicate antibody titers slightly lower but nearly equivalent to HA primed control m ..... For more information please see the full phenotype on the strain data sheet
005895	B10.Cg-Thy1^a H2^d Tg(TcraCl1,TcrbCl1)1Shrm/J	Repository-Cryopreserved
	Male mice that are hemizygous for the Clone-1 TCR (also called Clone 1 Thy1.1 TCR or Cl.1 TCR) transgene are viable, fertile, and normal in size. Females are very weak and have low fecundity. The donating investigator reports that all transgenic mice are prone to tumor development by 5-6 months of age. The transgene encodes a rearranged low avidity T cell receptor that recognizes an influenza virus hemagglutinin epitope (HA_518-526) restricted by MHC class I H-2K^d. Flow cytometric analysis shows appropriate skewing towards the CD8⁺ T cell compartment in thymocytes and peripheral lymphocytes. Both naive and activated clone 1 T cells exhibit decreased responsiveness when presented with their cognate antigen in vitro and when transferred into mice expressing HA on pancreatic beta cells. CD8⁺ T cells can be induced to exhibit both effector function and antitumor activity. This mouse is further modified with the Thy1.1 allele, rather than th ..... For more information please see the full phenotype on the strain data sheet
001163	B10.D2-H2^bm23/EgJ	Repository-Cryopreserved
	The H2^bm23 mutant allele causes an increase in the percentage of the CD8 T cells bearing Valpha3.2 both in peripheral T cells and CD8 single positive thymocytes. (sim et al, 1997.)
000462	B10.D2-H2^d/n2SnJ	Repository-Cryopreserved

001164	B10.D2-H2^dm1/EgJ	Repository-Cryopreserved

001151	B10.D2-H2^g3/(103R)EgJ	Repository-Cryopreserved

001153	B10.D2-H2ⁱ⁷/(107R)EgJ	Repository-Cryopreserved

001152	B10.D2-H2^ia/(106R)EgJ	Repository-Cryopreserved

000460	B10.D2-Hc⁰ H2^d H2-T18^c/o2SnJ	Repository-Cryopreserved
	This congenic strain carries the H2^d haplotype from DBA/2J following six generations of backcrossing to C57BL/10Sn. This strain still carries the Hc⁰ allele from DBA/2J, making them serum C5 deficient. Mice have increased susceptibility to certain pathogens and impaired chemotactic responses of neutrophils. Allograft rejection is prolonged. The following inbred strains are also homozygous for the Hc⁰ allele: A/HeJ (Stock No. 000645), AKR/J (Stock No. 000648), DBA/2J (Stock No. 000671), NOD/LtJ (Stock No. 001976), NZB/BlNJ (Stock No. 000684), and SWR/J (Stock No. 000689).
003147	B10.D2-Hc¹ H2^d H2-T18^c/nSnJ-Tg(DO11.10)10Dlo/J	Repository-Cryopreserved
	Clonal deletion of autoreactive T cells in vivo was studied using a peptide antigen to induce deletion of antigen-reactive thymocytes. Mice transgenic for a T cell receptor that reacts to this peptide (Tg(DO11.10)10Loh) contain thymocytes that progress from the immature to the mature phenotype. Intraperitoneal administration of the peptide antigen to transgenic mice results in a rapid deletion of the immature CD4⁺ CD8⁺ TCR^lo thymocytes. Apoptosis of cortical thymocytes can be seen within 20 hours of treatment. These results provide direct evidence for the in vivo role of apoptosis in the development of antigen-induced tolerance.
000464	B10.DA-H2^qp1 H2-T18^b/(80NS)SnJ	Repository-Cryopreserved

001823	B10.F-H2^bp5/(14R)J	Repository-Cryopreserved

001818	B10.F-H2^pb1/(13R)J	Repository-Cryopreserved

001012	B10.HTG-H2^g/2CyJ	Repository-Cryopreserved

001894	B10.LG-H2^ar1/J	Repository-Cryopreserved

000459	B10.M-H2^f H2-T18^a^?/SnJ	Repository-Cryopreserved
	This congenic strain carries H2^f derived from the non-inbred stock M (see development field). This strain also carries the Pgk2^b allele and the Tla^d allele. (Snell GD, 1958; Snell GD, 1978; Eicher et al., 1978; Flaherty et al., 1977).
002225	B10.M-H2^f/nMob Fmn1^ld-2J/J	Repository-Cryopreserved

001068	B10.M-H2^f/nMobJ	Repository-Cryopreserved

000739	B10.M-H2^fm2/MobJ	Repository-Cryopreserved

001154	B10.MBR-H2^bq1/SxEgJ	Repository-Cryopreserved

001790	B10.MBR/SxJ	Repository-Cryopreserved

001825	B10.P-H2^kp1/(10R)SgJ	Repository-Cryopreserved

003199	B10.PL-H2^u H2-T18^a/(73NS)Sn-Tg(TCRA)B1Jg/J	Repository-Cryopreserved
	TCR-transgenic mice exhibit the generation of an unusual population of CD4^-CD8^-TCR⁺ thymocytes and the absence of gamma delta cells. Transgenic TCR alpha chain causes thymocytes to differentiate into a CD4^-CD8^-TCR⁺ lineage at an early developmental stage, depleting the number of thymocytes that differentiate into the alpha-beta lineage. This transgene is also associated with the development of T cell lymphosarcoma. In combination with the transgenic strain TCR beta, it can be used as a model for Multiple Sclerosis.
003200	B10.PL-H2^u H2-T18^a/(73NS)Sn-Tg(TCRB)C14Jg/J	Repository-Cryopreserved
	TCR-transgenic mice exhibit the generation of an unusual population of CD4^-CD8^-TCR⁺ thymocytes and the absence of gama delta cells. Transgenic TCR beta chain causes immature T cells to accelerate differentiation into the alpha-beta lineage and thus inhibits the generation of gamma-delta cells. In combination with the transgenic strain TCR alpha, it can be used as a model for Multiple Sclerosis.
001069	B10.RIII-H2^r/(71NS)nMobJ	Repository-Cryopreserved
	The B10.RIII(71NS)/SnJ congenic strain develop chronic and relapsing experimental autoimmune encephalomyelitis (EAE) after immunization with the myelin basic protein (MBP). Susceptibility is associated with the major histocompatibility complex (MHC)(V beta 8<+>, H2<r>) and other non MHC loci. This strain is also susceptible to induction of collagen-induced arthritis.
001760	B10.S-H2^as1/(8R)/J	Repository-Cryopreserved

001817	B10.S-H2^sm1/(12R)SgJ	Repository-Cryopreserved

001650	B10.S-H2^t4/(9R)/J	Repository-Cryopreserved

000456	B10.SM H2^v H2-T18^b/(70NS)Sn-cw/J	Repository-Cryopreserved

001155	B10.T-H2^y2/(6R)SgDvEgJ	Repository-Cryopreserved

000445	B10.WB-H2^j H2-T18^b/SnJ	Repository-Cryopreserved

000444	B10.Y-H2^pa H2-T18^c/SnJ	Repository-Cryopreserved

003483	B6 x B10.D1-H2^q/SgJ-Nox3^het-2J/J	Repository-Cryopreserved

003561	B6 x B10.PL-H2^u/(73NS)Sn-Hxl/J	Repository-Cryopreserved

002995	B6 x C.B10-H2^b/LiMcdJ-Fbn2^fp-2J/J	Repository-Cryopreserved
	Mice homozygous for the recessive fused phalanges 2 Jackson mutation (Fbn2^fp-2J) have syndactyly of the second, third, and/or the fourth digits of the hindlimbs with <20% showing involvement of all three digits. This syndactyly likely results from defective mesenchyme differentiation rather than failed interdigital apoptosis (Arteaga-Solis et al., 2001). This mutant has a less severe phenotype than other Fbn2 mutants do, and shows no involvement of the digits of the forelimbs. Whether this is due to the allele or the genetic background has not been determined. (Chaudhry et al., 2001.)
001737	B6.A-H2-T18^a.HRS-Hr^hr/J	Repository-Cryopreserved
	Mice homozygous for the hr mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of statified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. In an attempt to offer alleles on ..... For more information please see the full phenotype on the strain data sheet
001166	B6.A-H2-T18^a/BoyEgJ	Repository-Cryopreserved

001896	B6.AK-H2-T18^a Ce2^b/J	Repository-Cryopreserved

001895	B6.AK-H2^k/J	Repository-Cryopreserved

001160	B6.C-H2^bm10/KhEgJ	Repository-Cryopreserved

001161	B6.C-H2^bm11/KhEgJ	Repository-Cryopreserved

000368	B6.C-H2^bm1/By	Repository-Cryopreserved

000256	B6.C-H2^bm1/ByBir-Gusb^mps/J	Repository-Cryopreserved
	Mice homozygous for the Gusb^mps 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.
000364	B6.C-H2^bm2/ByJ	Repository-Cryopreserved

000369	B6.C-H2^bm4/ByJ	Repository-Cryopreserved

001158	B6.C-H2^bm7/KhEgJ	Repository-Cryopreserved

000360	B6.C-H2^d Mdmg1^BALB/cBy/aByJ	Repository-Cryopreserved

001429	B6.C-H2^g6/J	Repository-Cryopreserved

005715	B6.Cg H2^g7-Tg(Ins2-CD80)3B7Flv/LwnJ	Repository-Cryopreserved
	Transgenic mice are characterized by pancreatic beta cells that express a rat insulin promoter (Ins2) regulated transgene encoding the human CD80 T cell co-stimulatory molecule. These mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Better than 70% of the B6.H2^g7 transgenic mice become diabetic by 30 weeks of age compared the control B6.H2^g7 which does not develop insulitis or diabetes. Spleens of diabetic B6.H2^g7 transgenic mice used in adoptive transfer experiments transfer diabetes to NOD.scid/RIP-B7.1 and irradiated non-diabetic B6.Cg H2^g7-Tg(Ins2-CD80)3B7Flv/LwnJ mice, yet failed to transfer disease to NOD.scid, B6.scid, CB17.scid, or irradiated B6/RIP-B7.1. B6.Cg H2^g7-Tg(Ins2-CD80)3B7Flv/LwnJ provides a tool for studying mechanisms of loss of tolerance in potentially diabetogenic CD8 T-cells.
006558	B6.Cg-H2^bm1 Tg(GUSB)4Sly/SndsJ	Repository-Cryopreserved
	Mice that are homozygous for this transgene and the Gusb^mps 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 Gusb^mps allele do not exhibit an accumulation of undegraded glycosaminoglycans. These transgenic mice do not carry the Gusb^mps 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).
000944	B6.SJL-H2^b C3^c/2CyJ	Repository-Cryopreserved

000966	B6.SJL-H2^s C3^c/1CyJ	Repository-Cryopreserved

003240	B6;B10.A-H2^a-Tg(H2KmPCC)2939Stoe/J	Repository-Cryopreserved
	PCC transgenic mice are viable and fertile. Pigeon cytochrome c was engineered for expression in lymphoid tissues of transgenic mice in two forms: one in which it is expressed as a type II plasma membrane protein (mPCC), and a second in which it was targeted to the mitochondria after cytoplasmic synthesis (ePCC). This strain carries the mPCC construct. (For mice carrying the ePCC construct, see strain 003221.) PCC is expressed in thymus, spleen and LPS stimulated B cells in both strains of mice. mRNA expression levels are higher in mPCC mice than in ePCC mice. However, tolerance is induced in the thymus of both strains, regardless of antigen compartmentation.
002432	B6J x B6.C-H2^bm1/ByJ-Cdh23^v-J/J	Repository-Cryopreserved
	Mice homozygous for the waltzer Jackson spontaneous mutation (Cdh23^v-J) exhibit the circling, head-tossing, deafness, and hyperactivity typical of circling mutants. Homozygous mutant mice are very similar to other waltzer mutants (Cdh23^v and Cdh23^v-2J). Most homozygotes are deaf from birth. Abnormalities of the inner ear include degeneration of the organ of Corti, spiral ganglion, stria vascularis, and saccular macula. Double heterozygotes with shaker-1 (Cdh23^v/+ Myo7a^sh1/+) become deaf by 3 to 6 months of age. Double heterozygotes show degeneration in the organ of Corti, stria vascularis, and spiral ganglion similar to that of Cdh23^v-J homozygotes, but less severe and with much later onset. Viability and breeding ability are somewhat reduced.
002844	BALB.5R-H2ⁱ⁵/LilJ	Repository-Cryopreserved

001041	BKS.B6-H2^b/J	Repository-Cryopreserved

001892	BRVR.B10-H2^b/J	Repository-Cryopreserved

001893	BRVR.D2-H2^d/J	Repository-Cryopreserved

000443	C3.HTG-H2^g H2-T18^b^?/SnJ	Repository-Cryopreserved

000441	C3.JK-H2^j H2-T18^b/SnJ	Repository-Cryopreserved

000440	C3.LG-H2^ar1/CkcCyJ	Repository-Cryopreserved

000439	C3.NB-H2^p H2-T18^c^?/SnJ	Repository-Cryopreserved

000473	C3H-H2^o2 C4b^b/SfSnJ	Repository-Cryopreserved

000437	D1.C-H2^d H2-T18^c/SnJ	Repository-Cryopreserved

000436	D1.DA-H2^qp1/SnJ	Repository-Cryopreserved

000435	D1.LP-H2^b H2-T18^b^?/SnJ	Repository-Cryopreserved

000434	LP.RIII-H2^r H2-T18^b/SnJ	Repository-Cryopreserved

001383	LT.MA-Glo1^b H2^k/J	Repository-Cryopreserved

004308	NOD.ALR-(D17Mit16-H2-D)/LtJ	Repository-Cryopreserved
	This allelic congenic strain commonly called D.R2, carries a defined segment of Chr 17 that includes the ALR H2^gx complex and insulin dependent diabetes susceptibility locus 16, Idd16a^ALR. At 35 weeks of age diabetes incidence in this NOD.ALR strain is significantly suppressed with 50% of the females and almost 15% the males diabetic as compared to NOD/ShiLt in which 100% of the females and nearly 70% of the males were diabetic. Similar to Stock No. 004309 pancreatic histological examination of pre-diabetic 8-week old males show lower mean insulitis scores than controls. This strain is useful for identifying candidate genes and dissecting the role of Idd16a in autoimmune diabetes.
004447	NOD.Cg-H2^h4/DilTacUmmJ	Repository-Cryopreserved
	NOD.Cg-H2^h4/DilTacUmm mice are completely protected from diabetes; however, a low incidence of perivascular and periductal insulitis is detected (20-30%). Protection from diabetes is complete even upon treatment with cyclophosphamide. These mice do, however, develop spontaneous thyroiditis and produce IgG autoantibodies when treated with 0.05% NaI in water (100% incidence in both sexes 6-8 week post treatment or by 4 months of age). Without treatment, thyroiditis is delayed and incomplete (60-70% incidence in 7-10 month old mice). This strain is an excellent model for autoimmune thyroiditis.
001626	NOD.NON-H2^nb1/LtJ	Repository-Cryopreserved
	This congenic strain carries the diabetes-resistant MHC from the NON/LtJ strain (Stock No. 002423) and is used as a comparison to the NOD/LtJ (Stock No. 001976). These mice exhibit some but not all of the immune dysfunctions of NOD/LtJ mice. These mice are useful for dissecting the role of MHC versus non-MHC genes in producing aberrant immunophenotypes.
003153	WLC.C-H2^d.GR-Mtv2/MorJ	Repository-Cryopreserved
	The GR strain carries five endogenous proviral copies of mouse mammary tumor virus (MMTV) including Mtv2. In GR, Mtv2 causes mammary carcinomas in 100% of breeding females prior to one year of age. Mtv2 deletes T cells carrying V beta 14 in the presence of MHC class II I-E (Ferrick 1992). This double congenic carries the GR Mtv2 locus in an exogenous and endogenous MMTV-free genetic background (WLC/MorJ, Stock No. 002600) and in an H2^d background. This congenic represents a model for studying MMTV-induced mammary tumorigenesis in the absence of multiple endogenous proviruses (Morris 1986). Mammary tumor incidence has not been confirmed at The Jackson Laboratory.

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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
003599	B10.RIII H2^r H2-T18^b/(71NS)Sn-Ap3b1^pe-11J/J	Research Strain

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New Strains Under Development

(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 Under Development
Select the strain name to link to the strain data sheet.

Stock Number	Strain Name Strain Description	Standard Supply
001627	NON.NOD-H2^g7/LtJ	Under Development for Cryo
This histocompatibility congenic strain carries the diabetogenic MHC from NOD/ShiLtJ mice. These mice exhibit some but not all of the immune dysfunctions of NOD/ShiLtJ mice. These mice are useful for dissecting the role of MHC versus non-MHC genes in producing aberrant immunophenotypes.

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New Strains Under Development
Receive periodic updates on the status of the colony UNDER DEVELOPMENT

Obtain advance notification of strain availability and opportunity to order prior to the strain being published as available

Provide input affecting speed and quantity of availability
The Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.
Strains that will be made available from a live distribution colony at The Jackson Laboratory.
These strains are designated as: "Under Development for Distribution Colony"

Strains that will be made available through the Cryopreservation Repository.
These strains are designated as: "Under Development for Cryopreservation Repository"
It is VERY IMPORTANT that you register interest in strains Under Development. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain Under Development. 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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Send questions to our Technical Support team using the Express Technical Support Form.
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JAX® Mice Strains

Strains from the Research Colonies of Jackson Laboratory Scientists

New Strains Under Development

JAX^® Mice Strains