Search Criteria: Research Area is "Virology Research"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 001303 | NOD.CB17-Prkdcscid/J | Level 1 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, 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-Prkdcscid/J | Level 2 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, 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-Prkdcscid Il2rgtm1Wjl/SzJ | Level 2 |
| The NOD.Cg-Prkdcscid Il2rgtm1Wjl/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 | ||
| 000686 | SJL/J | Level 2 |
| SJL mice display a very high incidence of reticulum cell sarcomas resembling Hodgkin's disease by approximately one year of age. Sarcomas first appear in the Peyer's patches and mesenteric lymph nodes and later in the spleen, liver, thymus and other lymph nodes. Most of the tumors are mixed-cell types classified as type B reticulum cell neoplasms, but a few are type A histiocytomas. This strain is also characterized by extreme aggression in males and its susceptibility to experimental autoimmune encephalomyelitis (EAE) for multiple sclerosis research. SJL/J mice develop a spontaneous myopathy resulting from a splice-site mutation in the Dysferlin gene. This Dysfim allele has been shown to result in decreased levels of dysferlin protein in SJL/J mice and makes this strain a good model for limb girdle muscular dystrophy 2B. This spontaneous myopathy is characterized by a progressive loss of muscle mass and strength corresponding with an increase in muscle pathology incl ..... For more information please see the full phenotype on the strain data sheet | ||
| 001913 | B6.CB17-Prkdcscid/SzJ | Level 3 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, 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 | ||
| 002663 | B6.129S2-Cd4tm1Mak/J | Level 4 |
| Mice homozygous for the Cd4tm1Mak 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-Prkdcscid/J | Level 4 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, 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 | ||
| 013596 | 129S-Batf3tm1Kmm/J | Repository- Live |
| These Batf3-/- knockout mice have a loxP-flanking neomycin (neo) resistance cassette replacing exons 1-2 of the basic leucine zipper transcription factor, ATF-like 3 (Batf3) gene, abolishing gene function. Mice that are homozygous for this allele are viable and fertile. Batf3 is highly expressed in CD11c+ CD8α+ conventional dendritic cells (cDCs), with low to absent expression in other immune cells.The deletion of Batf3 prevents development of splenic CD8α+ cDCs, which are important for cross-presentation during infections. Lymph nodes and thymi of Batf3-/- mice lack CD8α+ DCs, and DCs generated from Batf3-/- bone marrow (BM) and spleens are deficient in Toll-like receptor (TLR) 3-induced interleukin (IL)-12 production. These mice also lack CD103+CD11b- DCs in the lung, intestine, mesenteric lymph nodes (MLNs), dermis, and skin-draini ..... For more information please see the full phenotype on the strain data sheet | ||
| 008449 | B6(Cg)-Rag2tm1.1Cgn/J | Repository- Live |
| These RAG-2del mutant mice harbor a pan deletion of exon 3 of the targeted locus. Homozygotes (RAG-2del/del) are viable and fertile, with pan deletion of the entire RAG-2 protein coding region. Homozygous mice may be expected to have the same knockout phenotype as other RAG-2 null mutants or similarly created RAG-2 exon 3 pan-deleted mutants; with hematopoietic and immune system defects including arrested B cell and T cell development at the pro-B and the pro-T cell stages, respectively. These RAG-2del mice may be useful in studying the role of RAG-2 in B cell 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.
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 ..... | ||
| 010818 | B6.129-Ifnb1tm1Lky/J | Repository- Live |
| The Ifnb1 gene was targeted to introduce an internal ribosomal entry site (IRES) and enhanced yellow fluorescent protein (EYFP) immediately behind the stop codon of the gene. All regulatory elements, including the polyadenylation signal, are left intact and are derived from the endogenous gene. When activated, the targeted gene co-translates EYFP both in vitro and in vivo, leaving cells that have made type 1 interferon-beta readily detectable by flow cytometry or immunohistochemistry. Expression of EYFP faithfully mimics the expression of the targeted gene. | ||
| 013755 | B6.129S(C)-Batf3tm1Kmm/J | Repository- Live |
| These Batf3-/- mutant mice are lacking exons 1-2 of the basic leucine zipper transcription factor, ATF-like 3 (Batf3) gene, abolishing gene function. Mice that are homozygous for this allele are viable and fertile. Batf3 is highly expressed in CD11c+ CD8α+ conventional dendritic cells (cDCs), with low to absent expression in other immune cells.The deletion of Batf3 prevents development of splenic CD8α+ cDCs, which are important for cross-presentation during infections. Lymph nodes and thymi of Batf3-/- mice lack CD8α+ DCs, and DCs generated from Batf3-/- bone marrow (BM) and spleens are deficient in Toll-like receptor (TLR) 3-induced interleukin (IL)-12 production. These mice also lack CD103+CD11b- DCs in the lung, intestine, mesenteric lymph nodes (MLNs), dermis, and skin-draining lymph nodes. Exhibiting defects in CD8+T cell r ..... For more information please see the full phenotype on the strain data sheet | ||
| 008380 | B6.129S1-Tlr7tm1Flv/J | Repository- Live |
| These toll-like receptor 7 targeted mutation mice may be useful in studies of viral immunity. Homozygotes demonstrate reduced responses to in vivo infection with vesicular stomatitis virus. This emphasizes the roll of the gene in viral recognition by plasmacytoid dendritic cells and B cells which activate costimulatory molecules and produce cytokines. No RNA expression is detected in bone marrow-derived macrophages by Northern blot analysis. The lacZ reporter introduced under the gene's promoter shows that within mesenteric lymph nodes, expression is normally confined to the perifollicular regions. Homozygotes are viable, fertile, have no obvious developmental problems, but are poor breeders for unknown reasons. | ||
| 006087 | B6.129S4-Cxcl10tm1Adl/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 | ||
| 008881 | B6.129S6-Cd1d1/Cd1d2tm1Spb/J | Repository- Live |
| Homozygous (CD1-deficient) mice are viable and fertile, with no protein expression from the targeted locus observed on antigen presenting cells (APC) by FACS analysis. Natural killer T (NKT) cells are restricted by MHC class I-like CD1 molecules expressed on APC, and because the CD1 molecule is also required for the development of NKT cells, these CD1-deficient mice selectively lack NKT cells. Because activated NKT cells normally produce interleukin-4 (IL-4), interferon-gamma, granulocyte-macrophage colony-stimulating factor, IL-2 and TNF-alpha, CD1-deficient mice may exhibit abnormal immune responses dependent upon such cytokines/chemokines. These CD1-deficient mice may be useful in studying NKT cell immunology; including Th1- and Th2-responses, antiviral and antitumor responses, asthma, various inflammatory responses, autoimmunity and peripheral tolerance. | ||
| 004919 | B6.Cg-Fcgrttm1Dcr Tg(CAG-FCGRT)276Dcr/DcrJ | Repository- Live |
| These FcRn-/- hFcRn (276) Tg mice harbor a null mutation of the FcRn α-chain (Fcgrttm1Dcr) and also express a human FcRn α-chain cDNA (FCGRT) under the control the human cytomegalovirus immediate early promoter enhancer with chicken beta-actin/rabbit beta-globin hybrid promoter (CAG).
Mice homozygous for the FcRn α-chain null allele lack FcRn α-chain mRNA or protein expression, fail to transport IgG across the neonatal gut, degrade IgG at an accelerated rate, are functionally IgG deficient, and also exhibit plasma albumin deficiency. While hFcRn (276) transgene expression corrects the relative albumin deficiency caused by the FcRn α-chain knockout, expression of the hFcRn (276) transgene is unable to bind and protect murine IgG from degradation in FcRn α-chain null mice. However, hFcRn (276) transgene expression corrects the rapid decay rate of infused human IgG in FcRn-/- hFcRn (276) Tg mice. Furthermore, human antibodies ..... For more information please see the full phenotype on the strain data sheet | ||
| 014565 | B6.Cg-Fcgrttm1Dcr Tg(FCGRT)32Dcr/DcrJ | Repository- Live |
| These mFcRn-/- hFcRn (32) Tg mice are homozygous for the null mutation of the FcRn α-chain (Fcgrttm1Dcr) and express a human FcRn α-chain (FCGRT) transgene. Founder line 32 is more efficient in prolonging the serum half-life of hIgG compared with founder line 276 (see STOCK no. 004919). In Petkova et al.(2006), it is shown that the antibody half life of Hu4D5-IgG1 antibodies in mFcRn-/- hFcRn (32) Tg/0 is similar to those observed in mFcRn-/- hFcRn (276) Tg/Tg mice (see STOCK no. 004919). (Hu4D5-IgG1 human antibodies are directed against human epidermal growth factor receptor 2). In studies by Petkova et al. (2006), mice were pre-treated with human IgG to partially saturate the human FcRn. Since human FcRn does not bind mouse IgG, these mice have low levels of mouse IgG. These humanized FcRn mice may be useful in studying the quantitati ..... For more information please see the full phenotype on the strain data sheet | ||
| 006908 | B6.Cg-Ikbketm1Tman/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. | ||
| 007745 | B6.Cg-Mir155tm1.1Rsky/J | Repository- Live |
| 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-α (LT-α) 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 decreased percentage of interferon-γ (IFN-& ..... For more information please see the full phenotype on the strain data sheet | ||
| 008634 | B6;129-Mavstm1Zjc/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. Loss of MAVS (mitochondrial antiviral signaling) protein expression abolishes viral induction of interferons and prevents the activation of NFΚB (Rela, v-rel reticuloendotheliosis viral oncogene homolog A (avian)) and IRF3 (interferon regulatory factor 3) in multiple cell types, except plasmacytoid dendritic cells (pDCs). The protein is not required for interferon induction by cytosolic DNA or by Listeria monocytogenes. Mice lacking the protein fail to induce interferons in response to poly(I:C) stimulation and are severely compromised in immune defense against viral infection. Experimental results provide in vivo evidence that the cytosolic viral signaling pathway through the targeted gene is specifically required for innate immune responses against viral infection. | ||
| 013756 | C.129S-Batf3tm1Kmm/J | Repository- Live |
| These Batf3-/- mutant mice are lacking exons 1-2 of the basic leucine zipper transcription factor, ATF-like 3 (Batf3) gene, abolishing gene function. Mice that are homozygous for this allele are viable and fertile. Batf3 is highly expressed in CD11c+ CD8α+ conventional dendritic cells (cDCs), with low to absent expression in other immune cells.The deletion of Batf3 prevents development of splenic CD8α+ cDCs, which are important for cross-presentation during infections. Lymph nodes and thymi of Batf3-/- mice lack CD8α+ DCs, and DCs generated from Batf3-/- bone marrow (BM) and spleens are deficient in Toll-like receptor (TLR) 3-induced interleukin (IL)-12 production. These mice also lack CD103+CD11b- DCs in the lung, intestine, mesenteric lymph nodes (MLNs), dermis, and skin-draining lymph nodes. Exhibiting defects in CD8+T cell r ..... For more information please see the full phenotype on the strain data sheet | ||
| 008309 | C57BL/6-Rag2tm1Cgn/J | Repository- Live |
| Mice homozygous for the RAG-2fl 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-2fl 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. | ||
| 000674 | I/LnJ | Repository- Live |
| I/LnJ mice were originally derived by Dr. LC Strong in 1926 from an unpedigreed stock of mice. A high proportion of mice from this strain lack a corpus callosum. This absence is associated with slow growth of the medial septum subadjacent to the cavum septi. I/LnJ mice are resistant to mmtv induced mammary tumor development and generate neutralizing antibodies to mmtv and MuLv virions that effectively block viral transmission. Due to a frameshift mutation in alpha 1 phosphorylase kinase these mice have increased glycogen content in resting skeletal muscle. The reproductive performance of I/LnJ mice is very poor. Further analysis indicates that oocytes from I/LnJ mice display retarded kinetics of meiotic maturation and a high frequency of metaphase I arrest. Some oocytes fail to resume meiosis. Oocytes have many very small centrosomes with an absence of microtubules. I/LnJ mice, in addition to carrying several other coat color alleles, are homozygous for the piebald mutation (Ednrb<> ..... For more information please see the full phenotype on the strain data sheet | ||
| 010636 | NOD.Cg-B2mtm1Unc Prkdcscid Il2rgtm1Wjl/SzJ | Repository- Live |
| The NOD.Cg-Prkdcscid B2mtm1Unc Il2rgtm1Wjl/SzJ mice, commonly known as NOD-scid Il2rynull B2m null (NSG-B2m), do not express the Prkdc gene, the X-linked Il2rg gene nor the B2m gene. Triple mutant mice are viable, normal in size and do not display any gross physical or behavioral abnormalities, but can be poor breeders. Mutant mice combine the features of the NOD/ShiLtJ background, the severe combined immune deficiency mutation (scid), IL2 receptor gamma chain deficiency and the MHC class I molecule, beta-2 microglobulin, deficiency and are relatively resistant to graft versus host disease (GVHD). The mean survival time (MST) of NOD-scid Il2rynull B2mnull irradiated with 2 Gy and injected with 5 x 106 human peripheral blood mononuclear cells (PBMC) is 44 days compared to the MST of 21 days in the NOD-scid Il2rynull treated similarly. The bl ..... For more information please see the full phenotype on the strain data sheet | ||
| 012478 | NOD.Cg-Prkdcscid Tg(HLA-DRA*0101,HLA-DRB1*0101)1Dmz/GckJ | 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. NOD.CB17-Prkdcscid mice with the DR1 transgene survive to 14 months as compared to 8.5 months without the transgene. Physiological parameters in this strain are similar to NOD.CB17-Prkdcscid mice. Engraftment of human hematopoietic cells occurs regardless of DR1 genotype and is enhanced by intrahepatic engraftment using neonatal mice. Following injection, 15-20% human CD45+ cells are detected in peripheral blood. Short-term engrafted cord blood mononuclear cells can mount an immune response to tumor-associated antigen. This mutant mouse strain may be useful for xenotransplantation and vaccine development. | ||
| 009617 | NOD.Cg-Prkdcscid Il2rgtm1Wjl Tg(HLA-A2.1)1Enge/SzJ | Repository- Live |
| The NOD.Cg-Prkdcscid Il2rgtm1Wjl Tg(HLA-A2.1)1Enge/SzJ mice, commonly known as NOD scid gamma, HLA-A2.1 (NSG-A2), express human class I MHC Ag HLA-A2.1 , but do not express the Prkdc gene nor the X-linked Il2rg gene. Triple mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. NSG mice, carrying the HLA-A2.1 transgene (homozygous or hemizygous), overcome one of the limitations of immune response seen in the NSG model (Stock No. 005557), in that they develop protective T cell responses against human viral infections, specifically Epstein-Barr virus, exhibiting traits similar to those seen in humans. This model may be useful for studying response to human antigens and represent a unique preclinical model for vaccine development.
Please note that this strain carries the true null interleukin-2 receptor gamma chain mutation and ..... | ||
| 014570 | NOD.Cg-Prkdcscid Il2rgtm1Wjl Tg(HLA-A/H2-D/B2M)1Dvs/SzJ | Repository- Live |
| Mice that are homozygous for the Prkdcscid and Il2rgtm1Wjl alleles (males are hemizygous for the Il2rgtm1Wjl allele) Tg(HLA-A2/H2-D/B2m)1Dvs/SzJ are immunodeficient and express human HLA class 1 heavy and light chains. HLA-A2 and B2M proteins are detected on the surface of NSG-HLA-A2/HHD splenocytes by flow cytometry analysis. Transplantation of purified human hematopoietic stem cells into newborn NSG-HLA-A2/HHD mice establishes a humanized immune microenvironment allowing functional maturation of human hematopoietic cells. Epstein-Barr virus (EBV) infection results in EBV-associated B cell proliferation and HLA-restricted EBV antigen-specific effector memory CTLs. | ||
| 012479 | NOD.Cg-Prkdcscid Il2rgtm1Wjl Tg(HLA-DRA*0101,HLA-DRB1*0101)1Dmz/GckRolyJ | Repository- Live |
| Mice that are homozygous for the targeted transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mutant mice combine the features of the NOD/ShiLtJ background, the severe combined immune deficiency mutation (scid), IL2 receptor gamma chain deficiency and a human/mouse chimeric MHC Class II transgene (Tg(HLA-DRB1*01)1Dmz). This mutant mouse strain is expected to be useful for xenotransplantation and vaccine development. | ||
| 012480 | NOD.Cg-Prkdcscid Il2rgtm1Wjl Hprtb-m3/EshJ | Repository- Live |
| Mice that are homozygous/hemizygous for these alleles are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mutant mice combine the following characteristics: NK cell deficiency (NOD/ShiLtJ background), T and B cell deficiency (Prkdcscid), reduced numbers of lymphocytes and myeloid dendritic cells (Il2rgtm1Wjl) and biochemically defective stromal cells (Hprtbm-3). These mice can be used for transplantation of human primary cancers. During tumor growth, Hprt-defective murine fibroblast and stromal cells replace human stromal cells. In culture, the addition of HAT selection media eliminates murine fibroblasts and other stromal cells and facilitates the isolation of human cancer cells. These mice may be used to generate patient-specific low passage cell lines from primary cancers for use in chemosensitivity profiling and other applications. | ||
| 013062 | NOD.Cg-Prkdcscid Il2rgtm1Wjl Tg(CMV-IL3,CSF2,KITLG)1Eav/MloySzJ | Repository- Live |
| These mice contain three coinjected transgenes, human interleukin-3 (IL-3), human granulocyte/macrophage-stimulating factor (GM-CSF), and human Steel factor (SF) gene, each driven by a human cytomegalovirus promoter/enhancer sequence. These mice are maintained on the NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ mice (Stock No. 005557) background. These mice constitutively produce 2-4 ng/ml serum levels of human IL-3, GM-CSF, and SF. The Il2rg-/- specific NOD.SCID background supports human and murine hematopoietic cell engraftment, and suppresses human erythropoiesis, enhances human myelopoiesis, and reduces human B-lymphopoiesis in mice after transplant of human bone marrow or fetal liver cells. | ||
| 011066 | NOD.Cg-Prkdcscid Il2rgtm1Wjl Tg(CSF2)2Ygy Tg(IL3)1Ygy Tg(KITLG)3Ygy/YgyJGckRolyJ | Repository- Live |
| These mutant mice carry the Prkdcscid and Il2rgtm1Wjl alleles and the Tg(IL3)1Ygy, Tg(CSF2)2Ygy and Tg(KITLG)3Ygy transgenes. The Tg(CSF2)2Ygy transgene contains the porcine colony stimulating factor 2 (granulocyte-macrophage) sequence (CSF2) under the control of the human cytomegalovirus promoter. The Tg(IL3)1Ygy transgene contains the porcine interleukin 3 sequence under the control of the human cytomegalovirus promoter. The Tg(KITLG)3Ygy transgene contains the porcine kit ligand (KITL) under the control of the human cytomegalovirus promoter. The 3 transgenes were coinjected together in the original transgenic strain used to generate this mutant strain. | ||
| 014543 | STOCK Hgftm1.1(HGF)Aveo Prkdcscid/J | Repository- Live |
| Mice homozygous for both the hHGFki and Prkdcscid alleles, also called immunocompromised hHGFki mice, are viable and fertile.
The hHGFki allele is a "humanized" knock-in mutation that replaces the mouse hepatocyte growth factor (HGF) coding region downstream of the signal sequence with the human HGF cDNA sequence. As a result, the endogenous mouse promoter drives expression of human HGF. While the human HGF activates both the human and murine form of its tyrosine kinase receptor (met proto-oncogene (MET; c-Met)), the murine HGF is unable to activate human MET. Mice homozygous for hHGFki express only the human form of HGF. In homozygous hHGFki mice, HGF expression from the knock-in allele is observed in developing embryo, as well as adult liver, kidney and lung. hHGFki homozygous mice exhibit an increase in serum HGF after clotting. Mice homozygous for the Prkdcscid mutation exhibit T- and B-cell deficiency. | ||
| 004257 | NOD.Cg-Prkdcscid Tg(TcrLCMV)327Sdz/Dvs | Research Strain |
| These mice do not develop diabetes; The presence of the T cell receptor expressing transgene does not alter the resistance to type 1 diabetes conferred to the NOD background by homozygosity for the scid mutation. | ||
| 002313 | NOD.Cg-Prkdcscid Emv30b/Dvs | Research Strain |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, 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 | ||
| 004166 | 129-Itgb5tm1Des/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the Itgb5tm1Des 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-Axin1Fu/J | Cryopreserved - Ready for recovery |
| 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 Axin1Fu 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-H2b Fv1b/J | Cryopreserved - Ready for recovery |
| 010486 | B6.129P2-Isg15tm1Kpk/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this allele are viable and fertile and possess a loxP site flanked neomycin resistance cassette disrupting exon 2 of the targeted gene. Composition of the major cell populations of the immune system in spleen, bone marrow, lymph nodes and thymus is not affected by the mutation. Homozygous mice have an increased susceptibility to influenza A/B, HSV-1 and Sinbis virus, however, response to VSV and LCMV is unaltered from control mice. These mice may be useful in studying interferon-induced antiviral responses and differing susceptibilities to viral infection. | ||
| 003863 | B6.129S6-Tapbptm1Luc/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 006262 | B6.129X1-Fut2tm1Sdo/J | Cryopreserved - Ready for recovery |
| 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 | ||
| 008633 | B6.BXD8-Klra8Cmv1-del/WumJ | Cryopreserved - Ready for recovery |
| Animals lacking Ly49H (Klra8, killer cell lectin-like receptor, subfamily A, member 8) expression on natural killer cells were selected from progeny of BXD8 recombinant inbred mice backcrossed to C57BL/6 for ten generations. A number of other intact killer cell lectin-like receptors and integrin alpha M (Mac1) are still effectively expressed on natural killer cells. Natural killer cell functions (e.g. upregulation of IFN-gamma after activation via NK1.1, and cellular proliferation) are unaffected by this mutation. Compared to the parental C57BL/6 strain, these mutant mice are more susceptible to murine cytomegalovirus (MCMV), but not herpes simplex virus-1 (HSV-1) or ectromelia virus infection. Homozygotes are viable and fertile. | ||
| 009344 | B6.Cg-Tg(tetO-Ifng)184Pop/J | Cryopreserved - Ready for recovery |
| The donating investigator reports that homozygous mice are viable and fertile. These TRE/IFN-γ transgenic mice have expression of mouse interferon-gamma (IFN-γ) regulated by the tetracycline-responsive promoter (tetO [also called tetracycline-responsive element (TRE or tet-operator)] fused to the human cytomegalovirus minimal promoter). When mated to a mutant strain expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), expression of IFN-γ may be regulated with the tetracycline analog doxycycline (dox) in the double mutant offspring. Because interferon-gamma (IFN-γ) is a pleiotropic cytokine secreted by activated T-lymphocytes and natural killer cells, these line 184 TRE/IFN-γ mice may be bred to generate bi-transgenic mutant mice with conditional (inducible/reversible) expression of IFN-γ for studying antiviral responses, immune surveillance, inhibiting cellular prol ..... For more information please see the full phenotype on the strain data sheet | ||
| 004971 | B6.FVB-Tg(CD46)2Gsv/J | Cryopreserved - Ready for recovery |
| 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-Fv1b Me1a Mst1rFv2-s/J | Cryopreserved - Ready for recovery |
| 010816 | B6;C-Ghrhrlit Prkdcscid/BmJ | Cryopreserved - Ready for recovery |
| B6;C-GhrhrlitPrkdcscid/BmJ mice are deficient in growth hormone and IGF1 and are useful for determining endocrine dependence of grafted cells and tissues (Beamer et al., 1993, Cancer Research, v53:3741; Friend et al., 2001 Growth Hormone & IGF Research, v11:84). | ||
| 000652 | BDP/J | Cryopreserved - Ready for recovery |
| 002632 | BXH2/Ty1BedJ | Cryopreserved - Ready for recovery |
| 006134 | C.129S4(B6)-Cxcl10tm1Adl/J | Cryopreserved - Ready for recovery |
| 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 | ||
| 002936 | C.B6-Klra8Cmv1-r/UwaJ | Cryopreserved - Ready for recovery |
| 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. | ||
| 009601 | C3;B6-Tg(AAVS1)A1Xob/J | Cryopreserved - Ready for recovery |
| Hemizygous mice are viable and fertile with no reported phenotypic abnormalities from the insertion of multiple full-length human AAVS1 sites (adeno-associated virus integration site 1) at a single chromosomal locus. The multiple (approximately five) AAVS1 loci within the transgene allow site-specific integration of hybrid vectors containing AAV inverted terminal repeat-flanked genes of interest.
Adeno-associated virus (AAV) is a nonpathogenic parvovirus with a single-stranded DNA genome (4.7 kb) containing two genes (rep and cap) flanked by 145-base inverted terminal repeats (ITRs). Efficient replication of the AAV genome occurs in the presence of a helper virus, either adenovirus or herpes simplex virus. In the absence of a helper virus, ITRs and Rep proteins are sufficient to mediate the integration of AAV sequences into a specific AAVS1 site in the host cell genome and thereby establish a latent infection. In addition, low levels of helper-independent AAV replic ..... | ||
| 007707 | C57BL/6-Itgb7tm1Mshi/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this β7 (D146A) targeted mutation are viable and fertile. DNA sequencing confirms an aspartate (D) to alanine (A) substitution at position 146 of the targeted β7 integrin gene. As such, homozygotes have a mutant ADMIDAS (adjacent to metal ion-dependent adhesion site) cation binding/exchange site in the β7 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 addition, CD4+CD45RBhigh T cells isolated fro ..... For more information please see the full phenotype on the strain data sheet | ||
| 008158 | C57BL/6-Serpinb9tm1Arp/J | Cryopreserved - Ready for recovery |
| 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 (five to nine-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 three-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. | ||
| 002091 | C57BL/6Boy-Fv1n/J | Cryopreserved - Ready for recovery |
| 002226 | C57BL/6J-Tg(Alb1HBV)44Bri/J | Cryopreserved - Ready for recovery |
| This strain is referred to as "50-4" or "Tg(Alb1-HBV)Bri44" in the primary reference. | ||
| 006483 | CBy.129S2(B6)-Cd4tm1Mak/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Cd4tm1Mak 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. | ||
| 008338 | CByJ.B6(Cg)-Rag2tm1Cgn/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the RAG-2fl 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-2fl 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. In an attempt to offer alleles on well-characterized or multiple genetic background ..... | ||
| 007225 | FVB.129(B6)-Usp18tm1Dzh/J | Cryopreserved - Ready for recovery |
| 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 | ||
| 002456 | FVB/N-Tg(CryHIVPR)72Gjj/J | Cryopreserved - Ready for recovery |
| 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 | Cryopreserved - Ready for recovery |
| 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 | Cryopreserved - Ready for recovery |
| 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 | ||
| 001736 | NFS/N-Fgv2/J | Cryopreserved - Ready for recovery |
| 004083 | NOD.129(B6)-Prkdcscid Iduatm1Clk/J | Cryopreserved - Ready for recovery |
| 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 Prkdcscid-B2mb/Dvs | Cryopreserved - Ready for recovery |
| 004644 | NOD.Cg Prkdcscid-Tg(CSF2)2Ygy Tg(IL3)1Ygy Tg(KITLG)3Ygy/YgyJ | Cryopreserved - Ready for recovery |
| 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-Cd38tm1Lnd Prkdcscid/LtJ | Cryopreserved - Ready for recovery |
| 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 Cd38tm1Lnd 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 Prkdcscid mutation with the Cd38tm1Lnd targeted allele completely prevents diabetes development. For investigators wishing to study the role of CD38 in beta cell biology, the presence of the Prkdcscid allele provides insultis-free islets for analysis. Congenic, doubly homozygous NOD.Cd38tm1Lnd Prkdcscid mutant mice exhibit no significant difference in glucose tolerance when compared to NOD or NOD. Prkdcscid, thus not suppor ..... For more information please see the full phenotype on the strain data sheet | ||
| 004262 | NOD.Cg-Prkdcscid Tg(HLA-A2.1)1Enge/Dvs | Cryopreserved - Ready for recovery |
| 004346 | NOD.Cg-Prkdcscid Tg(Ins2-CD80)3B7Flv/DvsJ | Cryopreserved - Ready for recovery |
| 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 Prkdcscid allele eliminates the possibility that isolated islet cells will introduce contaminating T lymphocytes onto cultures. | ||
| 004230 | NOD.Cg-Prkdcscid Tg(Ins2-E3)1Dvs/DvsJ | Cryopreserved - Ready for recovery |
| 003843 | NOD.Cg-Prkdcscid Tg(Ins2-GAD2)1Lt/LtJ | Cryopreserved - Ready for recovery |
| NOD.Cg-Prkdcscid 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 Prkdcscid 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-Prkdcscid Tg(Ins2-GAD2)2Lt/LtJ | Cryopreserved - Ready for recovery |
| NOD.Cg-Prkdcscid 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 Prkdcscid 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 Prkdcscid 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. | ||
| 016148 | NOD.Cg-Prkdcscid Alox15tm1Fun/NadlJ | Cryopreserved - Ready for recovery |
| Mice homozygous for Alox15tm1Fun and Prkdcscid, commonly referred to as NOD.scid12LOKO, are viable and fertile. NOD.scid12LOKO mice injected with NOD/ShiLtJ, Stock No. 001976, splenocytes do not develop diabetes. This strain may be useful in adoptive transfer studies. | ||
| 002570 | NOD.Cg-Prkdcscid B2mtm1Unc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for both the B2mtm1Unc and Prkdcscid (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. | ||
| 006605 | NOD.Cg-Prkdcscid Emv30b Tg(HLA-A/H2-D/B2M)1Dvs/DvsJ | Cryopreserved - Ready for recovery |
| 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 Prkdcscid 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-Prkdcscid Gusbmps/SndsJ | Cryopreserved - Ready for recovery |
| 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-Prkdcscid background, this strain can be used for xenotransplantation experiments and cell trafficking studies (Hofling et al., 2003). | ||
| 005589 | NOD.Cg-Prkdcscid H2-Ab1tm1Doi/SzJ | Cryopreserved - Ready for recovery |
| These mice have no MHC class II expression which makes them useful to facilitate the engraftment of human immune cells. | ||
| 006609 | NOD.Cg-Prkdcscid Tg(HLA-A2.1)1Enge/DvsJ | Cryopreserved - Ready for recovery |
| Although transgenic NOD mice develop diabetes significantly earlier than do NOD/ShiLtDvs (NOD) mice, this transgenic strain harbors the Prkdcscid 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. | ||
| 007840 | NOD.Cg-Prkdcscid Tg(Ins2-CD86)12B70Flv/FswJ | Cryopreserved - Ready for recovery |
| Tg(Ins2-CD86)12B7 mice homozygous for the Prkdcscid 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, Prkdcscid homozygous mice lack functional T cells and B cells, and do not become diabetic.
In the absence of the Prkdcscid 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 ..... | ||
| 002380 | NOD.Cg-Tg(Ins2-TAg)1Lt Prkdcscid/DvsJ | Cryopreserved - Ready for recovery |
| Homozygous NOD/Lt-TgN(RipTag)1Lt-Prkdcscid 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 Prkdcscid 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. | ||
| 010605 | STOCK Prkdcscid Gnrh1hpg/BmJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, 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 | ||
| 002023 | SWR.M-Emv21 Emv22/J | Cryopreserved - Ready for recovery |
| 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) | ||
| 015812 | B6.Cg-Ifih1tm1.1Cln/J | Under Development - Now Accepting Orders |
| A targeting vector was designed to delete exon1 and 400 bp of upstream sequence of the interferon induced with helicase C domain 1 Ifih1 gene in order to abolish gene function. Homozygous mice are viable and fertile. Ifih1, an intracellular sensor of dsRNA, activates various immune cell types, including NK cells, after viral infection. Ifih1 detects dsRNAs that penetrate into the cytosol of the cell and transmits signal through accessory cells inducing IFN-α and IFN-β production. Homozygous mutant mice exhibit a decrease in NK cell activation and a decrease in IFN-γ production after treatment with Poly (I:C), an analogue of viral dsRNA. These mice may be useful for studying immune responses to viruses and other pathogens. | ||
| 012566 | B6.Cg-Mapk11tm1Jda Mapk14tm1Jda/J | Under Development - Now Accepting Orders |
| Mice homozygous for both polymorphic alleles (p38αβY323F) are viable, fertile and of normal size and weight. Each mutation introduces a tyrosine to phenylalanine at codon 323 (Y323F) within exon 11 of their respective locus; this prevents phosphorylation of residue 323 for each protein. While each polymorphism should have no direct affect on canonical MAPK cascade-induced p38 activation, the T cell receptor (TCR)-mediated alternative activation pathway of p38 activation is abolished in homozygous p38αβY323F mice. Accordingly, activation-induced p38 phosphorylation in p38αβY323F T cells is reduced relative to the respective contribution of each isoform to total T cell p38 activity (p38βY323F > p38αY323F > p38αβY323F). This failure to activate both the p38α and p38β isoforms in T cells via TCR engagement results in impaired T cell proliferation compare ..... For more information please see the full phenotype on the strain data sheet | ||
| 017637 | NOD.Cg-Prkdcscid Il2rgtm1Wjl H2-Ab1tm1Gru Tg(HLA-DRB1)31Dmz/SzJ | Under Development - Now Accepting Orders |
| These NSG-Abo DR4 mice lack expression of the murine Prkdc gene, the X-linked Il2rg gene, and MHC class II, but express the human leukocyte antigen DR4 gene. When maintained as homozygous for all three targeting events, and carrying one copy of the transgene, these mice are viable and fertile. Unlike in the NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ (NSG) mice (Stock No. 005557), the expression of HLA-DR4 in these mice leads to the development of allo-graft-versus-host disease (GVHD) after engraftment of human DR4-negative CD4+ T cells. These mice may be useful for targeting human CD4+ T cells in transplantation studies in the absence of xeno-GVHD. | ||
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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.
New Strains Awaiting TransferThe 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.
- Receive periodic updates on the status of the colony AWAITING TRANSFER
- 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
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.
Send questions to our Technical Support team using the Express Technical Support Form.
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