JAX Mice Database - Virology Research

Search Criteria: Research Area is "Virology Research"

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

JAX^® Mice Strains

Stock Number	Strain Name Phenotype	Standard Supply
001303	NOD.CB17-Prkdc^scid/J	Level 1
	Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdc^scid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen ..... For more information please see the full phenotype on the strain data sheet
001803	CBySmn.CB17-Prkdc^scid/J	Level 2
	Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdc^scid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen ..... For more information please see the full phenotype on the strain data sheet
001913	B6.CB17-Prkdc^scid/SzJ	Level 3
	Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdc^scid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen ..... For more information please see the full phenotype on the strain data sheet
005557	NOD.Cg-Prkdc^scid Il2rg^tm1Wjl/SzJ	Level 3
	The NOD.Cg-Prkdc^scid Il2rg^tm1Wjl/SzJ mice, commonly known as NOD scid gamma (NSG), do not express the Prkdc gene nor the X-linked Il2rg gene. NSG mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Histological examination of lymphoid tissues reveals absence of lymphoid cells and some cystic structures in the thymus, an absence of follicles in the spleen and markedly diminished celluarity of lymph nodes. NSG mice are deficient in mature lymphocytes, serum Ig is not detectable and natural killer (NK) cell cytotoxic activity is extremely low. These mice are resistant to lymphoma development even after sublethal irradiation treatment. These mutant mice have been shown to readily support engraftment of human CD34⁺ hematopoietic stem cells and represent a superior, long-lived model suitable for studies employing xenotransplantation strategies. Please note that the NSG carries the tr ..... For more information please see the full phenotype on the strain data sheet
002663	B6.129S2-Cd4^tm1Mak/J	Level 4
	Mice homozygous for the Cd4^tm1Mak targeted mutation have a significant block in CD4⁺ T-cell development; 90% of their circulating T-cells are CD8⁺. Cell surface expression of CD4 protein is not detected on thymocytes and lymph node cells from homozygous mice. Homozygous mutant mice also show a Class II restricted deficit in helper T-cell activity and other T-cell responses. This mutant mouse strain may be useful in studies of T cell development, susceptibility to viral infection and inflammation.
001131	C3SnSmn.CB17-Prkdc^scid/J	Level 4
	Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdc^scid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depe ..... For more information please see the full phenotype on the strain data sheet
002570	NOD.Cg-Prkdc^scid B2m^tm1Unc/J	Level 4
	Mice homozygous for both the B2m^tm1Unc and Prkdc^scid (commonly referred to as scid) mutations on the NOD/ShiLtSz background are class I deficient, B and T cell deficient, C-5 deficient (Hc⁰), and have low NK cells. This strain is an ideal model for xenograft transplantation studies and is an excellent source for insulitis-free, MHC class I-negative islets for transplantation studies.
006087	B6.129S4-Cxcl10^tm1Adl/J	Repository- Live
	Homozygous mice are viable, fertile, and have no overt morphological or developmental abnormalities. No endogenous gene expression is observed in bone marrow-derived macrophages before or after IFN-gamma stimulation. Homozygous mice have defective T cell responses, including impaired proliferation and IFN-gamma secretion following antigenic challenge (129Sv background). In experimental models of T helper-1 (Th1)-mediated immune responses, homozygous-deletion leads to diminished immune function; contact hypersensitivity is reduced (129Sv background) and diminished threshold for disease expression in experimental autoimmune encephalomyelitis (EAE, human model of multiple sclerosis) (C57BL/6 background). After injection with a neurotropic coronavirus MHV, null mice (on a B6;129Sv background) exhibit impaired viral clearance, decreased CD4⁺/CD8⁺ infiltration into the brain, and are protected from viral-induced demyelination. Similarly, homozygous mice (on a C57BL/6 ba ..... For more information please see the full phenotype on the strain data sheet
006262	B6.129X1-Fut2^tm1Sdo/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous mice have a chinchilla (gray) coat color, while heterozygotes have the typical black coat color expected for the C57BL/6J genetic background. Alpha (1,2) fucosylated glycans are not detected in the uterine epithelia from homozygotes at estrus. Beta galactosidase staining is detected in endocervial and uterine gland mucus secreting cells, stomach foveolar pit cells and chief cells, and colon goblet cells. The pattern of beta galactosidase activity mimics the endogenous expression pattern of the endogenous gene. This mutant mouse strain represents a model of the nonsecretor ABH histo-blood group antigen, which confers resistance to Norwalk virus infection, and may be useful in studies of reproductive biology, gastrointestinal tract epithelium, and the function of fucosylated glycans. This strain was transferred fr ..... For more information please see the full phenotype on the strain data sheet
006908	B6.Cg-Ikbke^tm1Tman/J	Repository- Live
	Homozygous IKKepsilon mutant mice are viable and fertile. Homozygous deletion results in a complete loss of the endogenous kinase function in lung, spleen, and embryonic fibroblasts. These mice have increased susceptibility to viral infection due to defective inteferon (IFN) signaling. These IKKepsilon mutant mice may be useful in immunological studies involving IFN signaling and host responses to infection.
002936	C.B6-Klra8^Cmv1-r/UwaJ	Repository- Live
	This BALB/c congenic carries C57BL/6 alleles for loci in the natural killer cell gene complex (NKC) on mouse chromosome 6. The region contains Klra (formerly Ly49), Klrb1 (formerly Ly55) and Klra8. This strain is useful in tumor models involving NK cell regulation and the expression of NK1.1 on BALB/c background. It plays a role in elucidating the contribution of the NKC region in controlling infectious agents.
007707	C57BL/6-Itgb7^tm1Mshi/J	Repository- Live
	Mice homozygous for this b₇ (D146A) targeted mutation are viable and fertile. DNA sequencing confirms an aspartate (D) to alanine (A) substitution at position 146 of the targeted b₇ integrin gene. As such, homozygotes have a mutant ADMIDAS (adjacent to metal ion-dependent adhesion site) cation binding/exchange site in the b₇ integrin head (A-domain). The resulting imbalance between the non-adhesive and adhesive states of leukocyte integrins skews toward a persistently adhesive state. Homozygous mutants exhibit impaired leukocyte migration, perturbed lymphocyte trafficking in the gut, and reduced T- and B-cell numbers in small/large bowel and gut-associated lymphoid tissues (less T-cells in Peyer's patches (PP), fewer intraepithelial lymphocyte (IEL) and lamina propria lymphocyte (LPL) compartments in the small intestine; and less B-cells in PP and the large intestine). In a ..... For more information please see the full phenotype on the strain data sheet
007840	NOD.Cg-Prkdc^scid Tg(Ins2-CD86)12B70Flv/FswJ	Repository- Live
	Tg(Ins2-CD86)12B7 mice homozygous for the Prkdc^scid mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Transgenic mice express the human CD86 T cell co-stimulatory protein under the control of the rat insulin promoter (Ins2). RT-PCR analysis detects human CD86 mRNA expression in the pancreas. Very low expression levels are also detected in the kidney and thymus of some but not all transgenic mice. Immunohistochemistry indicates that transgenic CD86 protein expression is restricted to the Islets of Langerhans. Transgenic, Prkdc^scid homozygous mice lack functional T cells and B cells, and do not become diabetic. In the absence of the Prkdc^scid mutation, NOD-Tg(Ins2-CD86), transgenic mice experience accelerated diabetes. Diabetes onset in male and female transgenic NOD-Tg(Ins2-CD86) mice starts at 8 weeks of age and 85-90% of the mice ultimately become d ..... For more information please see the full phenotype on the strain data sheet
006605	NOD.Cg-Prkdc^scid Emv30^b Tg(HLA-A/H2-D/B2M)1Dvs/DvsJ	Repository- Live
	Although NOD mice that carry this transgene (Stock No. 006604) develop diabetes significantly earlier than do NOD/ShiLtDvs (NOD) controls, this transgenic strain harbors the Prkdc^scid mutation (characterized by an absence of functional T cells and B cells), and therefore does not become diabetic. This strain is useful for adoptive transfer experiments, and as a source of insulitis free pancreatic islets.
005053	NOD.Cg-Prkdc^scid Gusb^mps/SndsJ	Repository- Live
	Mice homozygous for the 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. This strain is a model for the human lysomal storage disease, mucopolysaccharidosis type VII. On the NOD-Prkdc^scid background, this strain can be used for xenotransplantation experiments and cell trafficking studies (Hofling et al., 2003).
004166	129-Itgb5^tm1Des/J	Repository-Cryopreserved
	Mice that are homozygous for the Itgb5^tm1Des targeted mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. No Itgb5 gene product (mRNA or protein) is detected. Homozygotes display defects in VEGF-mediated vascular permeability. Cultured keratinocytes derived from homozygous mutant animals display impaired adhesion and migration on vitronectin-coated surfaces.
000212	129P4.Cg-Axin1^Fu/J	Repository-Cryopreserved
	The fused mutation is dominant and generally more severe in homozygotes, but has highly varying penetrance in both the heterozygote and homozygote, to the extent that some homozygotes do not have an abnormal phenotype. Phenotypic traits of mice carrying the Axin1^Fu allele include shortened, bifurcated, or absent tails, kinked tails with fused vertebrae, other asymmetrical fusions of vertebrae, axial duplications, and ribs fused at the proximal ends. Imperforate anus, anemia at birth, waltzing movement, deafness, and missing or abnormal kidneys have also been reported. Both heterozygotes and homozygotes are generally fertile although female carriers transmit with a lower penetrance than males do. (Reed, 1936; Dunn and Gluecksohn-Waelsch, 1954; Theiler and Gluecksohn-Waelsch, 1956.)
002089	AK.B6-H2^b Fv1^b/J	Repository-Cryopreserved

003863	B6.129S6-Tapbp^tm1Luc/J	Repository-Cryopreserved
	Mice that are homozygous null for the Tapbp gene are viable and fertile. No Tapbp gene product is detected. Tapbp is an integral component of the MHC class I peptide loading complex. Expectedly, mice that are homozygous null for tapasin fail to assemble loading complexes. Overall expression of surface MHC class I expression is reduced. Although some class I molecules are able to translocate to the cell surface, they are unable to do so in association with peptide antigen. Antigen presenting cells from null animals had a slightly reduced ability to stimulate CD8⁺ T cells. A more significant defect is observed in the ability to present foreign antigen. CTL responses are differentially affected. Significant defects in positive and negative intrathymic selection are also observed.
004971	B6.FVB-Tg(CD46)2Gsv/J	Repository-Cryopreserved
	These mice carry the YAC-CD46 transgene coding for the human CD46 protein (also known as MCP), which serves as the receptor for the human measles virus, group B adenoviruses, the human herpes simplex VI virus and Neisseria gonorrhoeae. The expression of this transgene is under the direction of the human CD46 promoter. Transgene expression is detected by in situ hybridization examination of whole animal sections, by Northern blot analysis of brain, spleen, lymph nodes, thymus, kidney, liver, gut and lung, and by FACS analysis of CD4⁺/CD8⁺ lymphocytes. Levels of transgenic protein on cell surfaces are similar to levels found in human cells. This line carries 10 to 12 copies of the transgene. Transgenic mice are susceptible to measles virus (MV) infection, expressing MV antigens and releasing infectious viral particles. The spread of the virus throughout the nervous system and the suppression of the immune system mimic the course of MV infection in humans. Tra ..... For more information please see the full phenotype on the strain data sheet
002389	B6.S/Ut-Fv1^b Me1^a Mst1r^Fv2-s/J	Repository-Cryopreserved

000652	BDP/J	Repository-Cryopreserved

002632	BXH2/Ty1BedJ	Repository-Cryopreserved

006134	C.129S4(B6)-Cxcl10^tm1Adl/J	Repository-Cryopreserved
	Homozygous mice are viable, fertile, and have no overt morphological or developmental abnormalities. No endogenous gene expression is observed in bone marrow-derived macrophages before or after IFN-gamma stimulation. Homozygous mice have defective T cell responses, including impaired proliferation and IFN-gamma secretion following antigenic challenge (129Sv background). In experimental models of T helper-1 (Th1)-mediated immune responses, homozygous-deletion leads to diminished immune function; contact hypersensitivity is reduced (129Sv background) and diminished threshold for disease expression in experimental autoimmune encephalomyelitis (EAE, human model of multiple sclerosis) (C57BL/6 background). After injection with a neurotropic coronavirus MHV, null mice (on a B6;129Sv background) exhibit impaired viral clearance, decreased CD4⁺/CD8⁺ infiltration into the brain, and are protected from viral-induced demyelination. Similarly, homozygous mice (on a C57BL/6 ba ..... For more information please see the full phenotype on the strain data sheet
002091	C57BL/6Boy-Fv1ⁿ/J	Repository-Cryopreserved

002226	C57BL/6J-Tg(Alb1HBV)44Bri/J	Repository-Cryopreserved
	This strain is referred to as "50-4" or "Tg(Alb1-HBV)Bri44" in the primary reference.
002456	FVB/N-Tg(CryHIVPR)72Gjj/J	Repository-Cryopreserved
	Mice homozygous for the expression of HIV-1 protease (HIVPr) linked to the lens alphaA-crystallin promoter are viable and fertile. Homozygotes develop bilateral cataracts at 23 - 24 days of age, beginning in the perinuclear region of the lens. Proteolysis begins with the loss of betaB1-, betaB3- and betaA3-crystallins and the appearance of crystallin fragments, accompanied by protein leakage and breakdown of cytoskeletal elements. It appears that the HIV-1 protease works in concert with other endogenous proteases to induce the changes that eventually result in opacification of the lens.
001850	MEV-Q/TyJ	Repository-Cryopreserved
	In 1989 Taylor and Rowe described generating a linkage testing stock homozygous for 11 ecotropic MuLV proviruses on 10 distinct chromosomes. The strain was named MEV/1Ty for Multiple Ecotropic proVirus. These proviral insertions can be identified via Southern blot analysis of PvuII or HindIII digests using the MuLV-specific pEcB4 probe. The first progenitor strain C58/J contributed the following proviruses identified by the PvuII junction fragments indicated in parenthesis: Emv20 (8.2kb), Emv21 (6.6 kb), Emv23 (3.7 kb), Emv24 (3.5 kb), Emv25 (3.4 kb), Emv26 (2.9 kb), and Emv27 (9.4 kb). The second progenitor strain AKXD-14/Ty contributed Emv11 (4.3 kb), Emv13 (3.4 kb), and Emv14 (8.6 kb) from AKR/J and Emv3 (5.2 kb) from DBA/2J. Emv3 is the proviral insertion causing the dilute allele of Myo5a. This strain is also homozygous for nonagouti (a). Further analysis of MEV/1Ty progeny identified subsequent MuLV provirus re-insertions that were used to ..... For more information please see the full phenotype on the strain data sheet
001855	MEV-V/TyJ	Repository-Cryopreserved
	In 1989 Taylor and Rowe described generating a linkage testing stock homozygous for 11 ecotropic MuLV proviruses on 10 distinct chromosomes. The strain was named MEV/1Ty for Multiple Ecotropic proVirus. These proviral insertions can be identified via Southern blot analysis of PvuII or HindIII digests using the MuLV-specific pEcB4 probe. The first progenitor strain C58/J contributed the following proviruses identified by the PvuII junction fragments indicated in parenthesis: Emv20 (8.2kb), Emv21 (6.6 kb), Emv23 (3.7 kb), Emv24 (3.5 kb), Emv25 (3.4 kb), Emv26 (2.9 kb), and Emv27 (9.4 kb). The second progenitor strain AKXD-14/Ty contributed Emv11 (4.3 kb), Emv13 (3.4 kb), and Emv14 (8.6 kb) from AKR/J and Emv3 (5.2 kb) from DBA/2J. Emv3 is the proviral insertion causing the dilute allele of Myo5a. This strain is also homozygous for nonagouti (a). Further analysis of MEV/1Ty progeny identified subsequent MuLV provirus re-insertions that were used to ..... For more information please see the full phenotype on the strain data sheet
001748	NFS.C3Fg-Emv32/J	Repository-Cryopreserved

001736	NFS/N-Fgv2/J	Repository-Cryopreserved

004083	NOD.129(B6)-Prkdc^scid Idua^tm1Clk/J	Repository-Cryopreserved
	At birth, mice that are homozygous null for the Idua gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No alpha-L-iduronidase enzyme activity or mRNA is detected. By three weeks of age, homozygous null mice develop a flattened facial profile and a thickening of digits. Defective bone formation is noticeable by fifteen weeks, characterized by a broadening and thickening of long bones. Evidence of lysosomal storage disorder is apparent in cells of the reticuloendothelial system at four weeks. By eight weeks progressive evidence of lysosomal storage is seen in Kupffer cells, splenic sinusoidal lining cells, chondrocytes, glial and Purkinje cells. This animal model is suitable for use in studies investigating the lysosomal storage disorder mucopolysaccharidosis type I (MPS I).
002571	NOD.Cg Prkdc^scid-B2m^b/Dvs	Repository-Cryopreserved

004644	NOD.Cg Prkdc^scid-Tg(CSF2)2Ygy Tg(IL3)1Ygy Tg(KITLG)3Ygy/YgyJ	Repository-Cryopreserved
	Tg(IL3)1Ygy, Tg(CSF2)2Ygy, and Tg(KITLG)3Ygy encode porcine interleukin 3 (IL3), Porcine granulocyte macrophage-colony stimulating factor (CSF2, commonly designated GM-CSF) and soluble Porcine stem cell factor (KITLG, commonly designated sSCF) respectively. All three are individually driven by the human cytomegalovirus promoter. These three transgenes were co-injected and they co-segregate. RT-PCR detects transgenic expression of porcine IL-3, CSF2 and KITLG in bone marrow and spleen in NOD.Cg Prkdc^scid-Tg(IL3)1Ygy Tg(CSF2)2Ygy Tg(KITLG)3Ygy mice. Porcine IL3, CSF2, and KITLG are present in the serum of these mice in levels that can be detected by ELISA. NOD.Cg Prkdc ^scid-Tg(IL3)1Ygy Tg(CSF2)2Ygy Tg(KITLG)3Ygy/YgyJ not only provide a system in which long-term porcine tissue and stem cell engraftment can be achieved (Abe et al, 2002) but also is a useful tool for evaluating donor-specific tolerance induction by mixed chimerism across xenogeneic ba ..... For more information please see the full phenotype on the strain data sheet
005345	NOD.Cg-Cd38^tm1Lnd Prkdc^scid/LtJ	Repository-Cryopreserved
	CD38 is an ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase. This ubiquitously expressed ectoenzyme is the major NAD hydrolase in mice. NOD/Lt mice homozygous for the Cd38^tm1Lnd targeted allele develop accelerated Type 1 diabetes associated with an ART2 (T cell ADP-ribosyltransferase)-dependent and NAD-mediated loss of regulatory CD4+CD25+ Foxp3+ and CD4+iNKT cells (Chen, J. et al 2006; Chen, Y.G et al 2006). Combining the Prkdc^scid mutation with the Cd38^tm1Lnd targeted allele completely prevents diabetes development. For investigators wishing to study the role of CD38 in beta cell biology, the presence of the Prkdc^scid allele provides insultis-free islets for analysis. Congenic, doubly homozygous NOD.Cd38^tm1Lnd Prkdc^scid mutant mice exhibit no significant difference in glucose tolerance when compared to NOD or NOD. Prkdc^scid, thus not suppor ..... For more information please see the full phenotype on the strain data sheet
006609	NOD.Cg-Prkdc^scid Tg(HLA-A2.1)1Enge/DvsJ	Repository-Cryopreserved
	Although transgenic NOD mice develop diabetes significantly earlier than do NOD/ShiLtDvs (NOD) mice, this transgenic strain harbors the Prkdc^scid mutation (characterized by an absence of functional T cells and B cells) and therefore does not become diabetic. This strain is useful for adoptive transfer experiments and as a source of insulitis free pancreatic islets.
004262	NOD.Cg-Prkdc^scid Tg(HLA-A2.1)1Enge/Dvs	Repository-Cryopreserved

004346	NOD.Cg-Prkdc^scid Tg(Ins2-CD80)3B7Flv/DvsJ	Repository-Cryopreserved
	These mice are characterized by pancreatic beta cells that express a rat insulin promoter (Rip) regulated transgene encoding the human CD80 T cell co-stimulatory molecule. They are an excellent source of MHC class I positive, CD80 transgene-expressing islet cells, a potent antigenic reagent for propagating diabetogenic CD8+ T lymphocytes derived from NOD mice in vitro. The presence of the Prkdc^scid allele eliminates the possibility that isolated islet cells will introduce contaminating T lymphocytes onto cultures.
004230	NOD.Cg-Prkdc^scid Tg(Ins2-E3)1Dvs/DvsJ	Repository-Cryopreserved

003843	NOD.Cg-Prkdc^scid Tg(Ins2-GAD2)1Lt/LtJ	Repository-Cryopreserved
	NOD.Cg-Prkdc^scid Tg(Ins2-GAD2)1Lt/LtJ transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Transgenic mice are homozygous for Prkdc^scid and are free of potential insulitic lymphocytes resulting in diabetes resistance. Similar to the NOD/Lt-Tg(Ins2-GAD2)1Lt (Stock No. 003074) the transgene inserted into Chromosome Y, thus only males are transgenic (Bridgett et al, Diabetes 1998 47:1848-56). This model provides a tool for studying the role of GAD2 as a islet autoantigen in the NOD mouse model of Type 1 diabetes.
003844	NOD.Cg-Prkdc^scid Tg(Ins2-GAD2)2Lt/LtJ	Repository-Cryopreserved
	NOD.Cg-Prkdc^scid Tg(Ins2-GAD2)2Lt/LtJ transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Transgenic mice are homozygous for Prkdc^scid and are free of potential insulitic lymphocytes resulting in diabetes resistance. Delayed diabetes onset is observed when splenic lymphocytes from 5 week old pre-diabetic NOD females are adoptively transferred into NOD transgenic mice homozygote for Prkdc^scid when compared to adoptive transfers into control NOD females. Similar to the NOD/ShiLt(Cg)-Tg(Ins2-GAD2)2Lt/J (Stock No. 005870) homozygous transgenic mice are developmentally lethal due to the transgene insertion site (Bridgett et al, Diabetes 1998 47:1848-56). This model provides a tool for studying the role of GAD2 as an islet autoantigen in the NOD mouse model of Type 1 diabetes.
004606	NOD.Cg-Prkdc^scid H2-Ab1^tm1Doi Tg(HLA-DQA1,HLA-DQB1)1Dv/SzJ	Repository-Cryopreserved
	This strain which is MHC II deficient and has no functional T or B cells expresses a humanized transgenic HLA-DQ8 molecule that has been linked to IDDM development. This model is a valuable genetic tool for identifying the role of HLA-DQ8 in Type 1 Diabetes.
005589	NOD.Cg-Prkdc^scid H2-Ab1^tm1Doi/SzJ	Repository-Cryopreserved
	These mice have no MHC class II expression which makes them useful to facilitate the engraftment of human immune cells.
002380	NOD.Cg-Tg(Ins2-TAg)1Lt Prkdc^scid/DvsJ	Repository-Cryopreserved
	Homozygous NOD/Lt-TgN(RipTag)1Lt-Prkdc^scid mice develop pancreatic beta cell adenomas. They are able to produce 2-3 litters before the insulin secreted from the adenoma makes them too hypoglycemic. Because Prkdc^scid mice lack T-cells the adenomas from this strain are free of the autoimmune T-cells found in the adenomas of NOD/Lt-TgN(RipTag)1Lt mice.
002023	SWR.M-Emv21 Emv22/J	Repository-Cryopreserved
	This strain carries a pair of linked retroviral insertions that occurred simultaneously on Chr 18 in a MEV substrain related to MEV/1Ty. Homozygosity for one of the insertions causes a juvenile lethal wasting condition that results in death at approximately 16 days of age. The proviruses rarely recombine; during development of this incipient congenic strain, a mouse was never found to have Emv21 in the absence of Emv22. There is no evidence that either of these viruses causes germline or somatic infection resulting in integration of new germline copies. (brs per personal communication from B. Taylor)

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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 Phenotype	Standard Supply
002577	B6;CB17-Ghrhr^lit Prkdc^scid/Bm	Research Strain
	Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdc^scid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen ..... For more information please see the full phenotype on the strain data sheet
002038	CB17;HPG-Prkdc^scid Gnrh1^hpg/Bm	Research Strain
	Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdc^scid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen ..... For more information please see the full phenotype on the strain data sheet
004257	NOD.Cg-Prkdc^scid Tg(TcrLCMV)327Sdz/Dvs	Research Strain

002313	NOD.Cg-Prkdc^scid Emv30^b/Dvs	Research Strain
	Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdc^scid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen ..... For more information please see the full phenotype on the strain data sheet

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New Strains Under Development

(See informational text following listing of strains)

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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
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Stock Number	Strain Name Phenotype	Standard Supply
007745	B6.Cg-Mirn155^tm1.1Rsky/J	Under Development for Production
Mice homozygous for this loss-of-function/reporter allele (bic/mir-155-/-) are viable and fertile. The lacZ reporter allows the detection of bic promoter transcriptional activity using fluorescence activated cell sorting (FACS). In homozygotes, miR-155 expression is undetectable in activated splenic B cells. In heterozygotes, approximately 60% of germinal center (GC) B cells express the lacZ reporter whereas the vast majority of the non-GC B cells do not. Homozygous mice exhibit a reduced fraction of GC B cells in the gut-associated lymphoid tissue (GALT; including Peyer's patches (PPs) and mesenteric lymph nodes (mLNs)). In addition, bic/miR-155-/- B cells exhibit deficient tumor necrosis factor (TNF) and lymphotoxin-a (LT-a) cytokine production. Homozygous mice show impaired T cell-dependent antibody responses, and their T cells show a TH2 cytokine bias (an increased percentage of interleukin-4 (IL-4) producing cells and a decreas ..... For more information please see the full phenotype on the strain data sheet
008309	C57BL/6-Rag2^tm1Cgn/J	Under Development for Production
Mice homozygous for the RAG-2^fl allele are viable and fertile, with loxP sites flanking exon 3 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region (coding for the entire RAG-2 protein) deleted in the cre-expressing tissue(s). These RAG-2^fl mice may be useful in generating conditional mutations for studying the role of RAG-2 in B and T cell development (including cancer and toxicology research as a xenograft/transplant host), T and B cell receptor (V(D)J) recombination, hematopoiesis, hematology, immunology, and inflammation research. For example, when bred to a strain with inducible Cre recombinase expression in liver and lymphocytes (see Stock No. 003556), this mutant mouse strain may be useful in studies of B and T cell development.
008158	C57BL/6-Serpinb9^tm1Arp/J	Under Development for Production
Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RT-PCR analysis of myeloid and lymphoid cells. After experimental viral infection, homozygous mice have lower (5 to 9-fold reduction) numbers of virus specific cytotoxic T lymphocytes (CTLs) and increased apoptosis of virus specific CD8 T cells when compared to wildtype controls. Mutant mice have impaired Lymphocytic Choriomeningitis virus (LCMV) infection clearance. Granzyme A and granzyme B specific activity is reduced in cytotoxic granules and increased in CTL cytoplasm. Mutant CTLs have a 3-fold increase in the number of granules lacking granzyme B. This mutant mouse strain may be useful in studies of viral immune response and inflammation, and the exocytosis pathway in CTL apoptosis.
006483	CBy.129S2(B6)-Cd4^tm1Mak/J	Under Development for Production
Mice homozygous for the Cd4^tm1Mak targeted mutation have a significant block in CD4⁺ T-cell development; 90% of their circulating T-cells are CD8⁺. Cell surface expression of CD4 protein is not detected on thymocytes and lymph node cells from homozygous mice. Homozygous mutant mice also show a Class II restricted deficit in helper T-cell activity and other T-cell responses. This mutant mouse strain may be useful in studies of T cell development, susceptibility to viral infection and inflammation. 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.
007225	FVB.129(B6)-Usp18^tm1Dzh/J	Under Development for Production
Homozygous Usp18 (or Ubp43) mutant mice on the FVB/N genetic background are viable and fertile, exhibiting none of the severe neurologic disorders that lead to embryonic lethality or early death reported for Ubp43-deficient mice on a C57BL/6 or mixed B6;129 genetic background. In contrast to wildtype mice, thymi from homozygous mice injected with LPS exhibit no protein from the targeted gene. Expression of the lacZ cassette is observed in both heterozygous and homozygous brain tissues. Homozygous mice are hypersensitive to type I interferon (IFN) and undergo apoptosis upon IFN stimulation. Ubp43-deficiency results in enhanced and prolonged STAT1 phosphorylation, DNA binding, and increased induction of hundreds of interferon stimulated genes (ISGs). Homozygous mice exhibit greater resistance to the cytopathic effects caused by a number of viruses (including lymphocytic choriomeningitis virus (LCMV), vesicular stomatitis virus (VSV), and Sindbis virus (SNV)). Ubp43-defici ..... For more information please see the full phenotype on the strain data sheet

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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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