Search Criteria: Research Area is "Internal/Organ Research: Gastrointestinal Defects"
New Strains Awaiting Transfer from the Donor
Additional Register Interest Strains
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 004326 | C3Bir.129P2(B6)-Il10tm1Cgn/Lt | Level 4 |
| Mice homozygous for the Il10tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet | ||
| 100410 | WBB6F1/J-KitW/KitW-v | Level 4 |
| Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. KitW/KitW-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. KitW/KitW-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment. | ||
| 006050 | 129-Sirt6tm1Fwa/J | Repository- Live |
| Homozygous neonates are smaller than their wildtype and heterozygous littermates. They develop normally until approximately 21 days of age, when they develop an acute and rapid, aging-like degenerative pathology resulting in death by postnatal day 24. Homozygous mutant mice exhibit subcutaneous fat loss, lordokyphosis (hunchbacked spine) with osteopenia (30% loss of bone mineral density), colitis, and severe lymphopenia due to increased lymphocyte apoptosis. At day 12, mice have reduced insulin-like growth factor I (IGF-1) levels in serum, and develop severe hypoglycemia. Mouse embryonic fibroblasts (MEFs) prepared from homozygous embryos exhibit reduced proliferation, defective base excision repair function, as indicated by increased sensitivity to alkylating agents and ionizing radiation, and increased chromosomal aberrations. The donating investigators report that no gene product (mRNA or protein) is detected by RT-PCR or immuoblot analysis of tissues, MEFs or embryonic stem cells f ..... For more information please see the full phenotype on the strain data sheet | ||
| 008355 | B6.129(Cg)-Slc6a4tm1Kpl/J | Repository- Live |
| Mice that are homozygous for the serotonin transporter targeted mutation (SERT-/- or 5-HTT-/-) are viable and fertile with a superficially unremarkable behavioral phenotype through early adulthood. Serotonin uptake is completely absent in homozygous mice. SERT-deficiency is pleiotropic (many different phenotypic traits). Homozygotes and, to a lesser extent, heterozygotes exhibit diminished responses to serotonin receptor agonists and other classes of drugs (including MDMA, SSRIs, 8-OH-DPAT, and DOI). SERT-mutant mice are also reported to have increased anxiety-like behaviors, altered neuroendocrine and sympathoadrenal responses to even minor stress, diminished aggression, altered emotional learning, substantially increased rapid eye movement (REM) sleep time, reduced brain excitability, increased body temperature, increased colonic motility, reduced spinal reflex to injury, reduced bladder response to stretching, blood pressure responses, diminished bone and muscl ..... For more information please see the full phenotype on the strain data sheet | ||
| 008195 | B6.129-Adipoqtm1Chan/J | Repository- Live |
| Homozygous mice are viable and fertile, with absence of targeted allele expression confirmed in adipose tissue (mRNA) and plasma (adiponectin protein). While homozygous mice have normal glucose tolerance and insulin resistance, beta-oxidation activity is significantly increased in muscle and liver. Homozygotes also have endothelial dysfunction (increased leukocyte rolling and leukocyte adhesion), are protected from DSS-induced colitis, and are more susceptible to myocardial ischemia/reperfusion. When fed a high fat diet, obese homozygotes are significantly heavier with increased insulin levels and altered insulin resistance. These adiponectin-deficient (Adipoq-/- or Adipo-/-) mice may be useful in studying obesity, diabetes, insulin resistance, metabolism, inflammation, leukocyte-endothelium interactions, and colitis. | ||
| 009106 | B6.129-Cyp27a1tm1Elt/J | Repository- Live |
| These mice harbor a targeted mutation of the Cyp27a1 (cytochrome P450, family 27, subfamily a, polypeptide 1) locus that abolishes endogenous gene expression. Homozygous mice (also called Cyp27a1-/-, cyp27-/-, or sterol 27-hydroxylase-deficient mice) are viable and fertile, with no RNA or protein expression from the targeted gene detected in liver tissue. Both formation of bile acids and excretion of fecal bile acids are decreased in homozygous mice. Compensatory up-regulation of hepatic enzymes that convert cholesterol to bile acids (bile acid synthesis) is also observed. Cyp27a1-/- mice exhibit a dramatic increase in cytochrome P450 3A (Cyp3a11) which catalyzes side-chain hydroxylations of bile acid intermediates subsequently facilitating their excretion in the bile and urine. Homozygous mice also have increased expression of other nuclear xenobiotic receptor PXR (pregnane X receptor) target genes. | ||
| 007572 | B6.129P2(Cg)-Rorctm2Litt/J | Repository- Live |
| Mice homozygous for this Rorc(γtGFP (or RORγt)GFP) mutant allele are viable and fertile. While Rorcγ mRNA is detected in liver in Rorc(γ)tGFP homozygotes, mRNA and protein for the thymus-specific isoform (Rorcγt) encoded by the targeted allele are not detected in the thymus. EGFP expression reports Rorc(γt) transcription in the thymi of adult Rorc(γt)GFP mice. Homozygous mice exhibit abnormal lymph node, Peyer's patch, and lymphoid tissue inducer (LTi) cell development. Mice with Rorcγt-deficient T cells lack tissue-infiltrating proinflammatory T-helper cells (Th17 cells), and are protected from induced autoimmune disease (EAE) on this genetic background. The donating investigator also reports increased thymoma incidence with age in homozygotes. These RorcγtGFP mutant mice may be useful in studying immune system homeostasis, T cell repertoire selection, CD4/CD8 double positive (CD4+/CD8 For more information please see the full phenotype on the strain data sheet | ||
| 008875 | B6.129P2-Lgr5tm1(cre/ERT2)Cle/J | Repository- Live |
| While homozygous mice are not viable, heterozygous Lgr5-EGFP-IRES-CreERT2 mice are viable and fertile; harboring a Lgr5-EGFP-IRES-creERT2 "knock-in" allele that both abolishes Lgr5 (Gpr49) gene function and expresses EGFP and CreERT2 fusion protein from the Lgr5 promoter/enhancer elements. EGFP fluorescence is observed in crypt base columnar cells in small intestine (aka stem cells of the small intestine) and colon. Cre-ERT2 fusion gene activity is inducible; observed in the same cells only following tamoxifen administration. EGFP or inducible CreERT2 expression may also be observed in other Lgr5-expressing cell types (including pre-malignant mouse adenomas, colon cancer cells, epithelial stem cells of the stomach gland, basal epithelial layer stem cells of the mammary glands, and hair follicle stem cells).
The donating investigator reports variegated expression of the Lgr5-EGFP-IRES-CreERT2 transgene in the small intestine and colon (something which may h ..... | ||
| 004781 | B6.129P2-Lyz2tm1(cre)Ifo/J | Repository- Live |
| This strain expresses Cre recombinase from the endogenous Lyzs locus. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in deletion of the targeted gene in the myeloid cell lineage, including monocytes, mature macrophages, and granulocytes. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This strain represents an effective tool for generating myeloid cell-specific targeted mutants.
View cre expression characterization. | ||
| 008377 | B6.129S1-Tlr5tm1Flv/J | Repository- Live |
| The toll-like receptor gene targeted in this strain is a sensor for monomeric flagellin, a component of bacterial flagella known to be a virulence factor. These mice have been used to investigate the mechanism of flagellin detection and signalling in antibacterial immune responses to Salmonella typhimurium and Pseudomonas aeruginosa. The gene has been found to be essential for the recognition of bacterial flagellin both in vivo and ex vivo. Mice that are homozygous for this targeted deletion are viable and fertile. Transcripts of this gene are absent from bone marrow-derived macrophages in homozygotes. Relative to controls, homozygotes have increased fat mass throughout the body, particularly in visceral fat, a substantial increase in serum triglyceride and cholesterol levels, increased blood pressure, and higher than normal production of pro-inflammatory cytokines interferon gamma and interleukin 1 beta in adipose tissue. Basal insulin levels and i ..... For more information please see the full phenotype on the strain data sheet | ||
| 006144 | B6.129S2(C)-Itgaetm1Cmp/J | Repository- Live |
| Mice that are homozygous for this targeted mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. No endogenous gene expression is detected in intraepithelial lymphocytes by FACS analysis or on TGF-beta1-treated splenocytes by immunoprecipitation. Homozygous null mice exhibit reduced numbers of intestinal intraepithelial lymphocytes and lamina propria lymphocytes. These mice may be useful in studies of the immune system, including T cell function. 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. | ||
| 008117 | B6.129S4(129S6)-Ssttm1Ute/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. No gene product (mRNA or protein) is detected by Northern blot, in situ hybridization or radioimmunoassay analysis of brain tissue. Homozygotes exhibit increased baseline plasma growth hormone, corticosterone and total ghrelin levels compared to wildtype. Mutant mice have impaired motor performance ability. Somatostatin-deficient mice have enlarged stomachs with an increased number of parietal cells and hyperchlorhydria. Hippocampal neprilysin activity is diminished. Compared to wildtype controls, amyloid beta 42 peptides levels are elevated in the hippocampus. This mutant mouse strain may be useful in studies of gastric homeostasis, learning and memory and endocrinology. | ||
| 006133 | B6.129S4-Vdrtm1Mbd/J | Repository- Live |
| Heterozygous mice are phenotypically indistinguishable from wildtype siblings. As originally characterized on a mixed B6;129 genetic background, homozygous mice are viable and fertile with normal survival until approximately 14 months. RNA isolated from the intestine and kidney show a truncated deletion of the second zinc finger coding region followed by a premature termination codon, resulting in the absence of receptor protein. Homozygous mice exhibit an identical phenotype as the human disease hereditary vitamin D-dependent rickets type II (HVDDR). As early as 21 days of age, mutant mice demonstrate hypocalcemia, hypophosphatemia, hyperparathyroidism, increased serum parathyroid hormone, abnormal blood mineral levels, and growth retardation. In addition, renin and plasma angiotensin II levels are increased. Homozygous mice are hypertensive and exhibit cardiachypertrophy. At 4 weeks of age, homozygous mice exhibit perioral and periorbital alopecia that progresses over the entire bod ..... For more information please see the full phenotype on the strain data sheet | ||
| 013061 | B6.129S6-Ccr6tm1(EGFP)Irw/J | Repository- Live |
| Homozygous Ccr6-EGFP mice are viable and fertile; harboring an enhanced green fluorescent protein (EGFP) allele that both abolishes endogenous Ccr6 gene function and expresses EGFP from the Ccr6 promoter/enhancer elements. As such, robust EGFP fluorescence is directed to all mature B cells, subpopulations of splenic CD4+ and CD8+ T cells, CD4+ and CD4- myeloid dendritic cells (DC), some CD11c+ DC, and most CD11b+ myeloid DC. Fluorescence is detected at lower levels in epidermal Langerhans cells (LC). These mice exhibit abnormalities in Peyer's patches, decreased isolated lymphoid follicle development in the intestine, and reduced numbers of intestinal M cells. | ||
| 009598 | B6.129S6-Plac8tm1Bhk/J | Repository- Live |
| Homozygous (Onzin-/-) mice are viable and fertile with a loxP-flanked pgk-neo cassette disrupting exon 4 of the Plac8 (placenta-specific 8 or Onzin) locus. Tissues from homozygous mice have no RNA (full-length/isoforms/altered splice variants) or protein expression from the targeted allele. Histological and peripheral blood analysis of homozygous mice is indistinguishable from wild-type mice. Similarly, leukocyte populations in the thymus, spleen, and lymph nodes exhibit no gross changes in the development of T cell, B cell, or macrophage populations associated with Onzin-deficiency. Compared to wild-type mice, Onzin-deficient mice exhibit impaired host defense; when given intraperitoneal injection of Klebsiella pneumonia, homozygotes develop acute peritonitis and heightened innate immune response consistent with an increased bacterial burden. Neutrophils isolated from homozygous mice exhibit normal phagocytosis but less effective killing of bacteria. Be ..... For more information please see the full phenotype on the strain data sheet | ||
| 008691 | B6.129X1-Ebi3tm1Rsb/J | Repository- Live |
| Mice homozygous for this Ebi3-mutant allele are viable and fertile with the donating investigator reporting no overt autoimmunity or inflammatory disease associated with the mutation. No RNA from the targeted gene is observed in splenocytes isolated from homozygotes. Ebi3-deficiency leads to impaired Treg activity with failure to control homeostatic proliferation. Homozygotes exhibit decreased numbers and function of invariant natural killer T cells (iNKT); stimulated iNKT cells show impaired IL-4 production both in vivo and in vitro. Homozygotes are resistant to oxazolone-induced colitis (mediated primarily by T helper (Th) 2-type cytokine production by iNKT cells), whereas Ebi3-deficiency shows no affect on trinitrobenzene sulfonic acid-induced colitis (a predominantly Th1-mediated colitis model). These Ebi3-mutant strains may be useful in studying Treg function, IL12 heterodimeric cytokines (such as IL-35 and IL-27),IFNgamma production, and Th1/Th ..... For more information please see the full phenotype on the strain data sheet | ||
| 000528 | B6.Cg-PhexHyp/J | Repository- Live |
| Hypophosphatemia (PhexHyp) is an X-linked semidominant mutation that causes defects in phospate metabolism. It is allelic with the gyro mutation (PhexGy) but hypophosphatemia mutant mice do not circle. Hemizygous males and heterozygous females can be recognized at 20 to 30 days of age by their shortened hindlimbs and tail. They have reduced body size which persists throughout life, and skeletal changes resembling rickets. Hemizygous males are more affected than heterozygous females. Viability is normal in both sexes, but heterozygous females show better fertility than hemizygous males. | ||
| 009350 | B6.Cg-Tg(CDX2-cre)101Erf/J | Repository- Live |
| Mice hemizygous for the CDX2P9.5-NLSCre transgene are viable and fertile, with a 9.5 kb human caudal type homeo box 2 (CDX2) promoter/enhancer sequence directing expression of a nuclear-localized Cre recombinase predominantly to colonic epithelium during late gestation and in adult tissues. Specifically, Cre recombinase expression is observed in epithelium from the distal ileum and cecum, and throughout the colon from the crypt base to the luminal surface. Cre recombinase expression is also observed throughout the caudal region of the embryo during early development. When these transgenic mice are bred with mice containing a loxP-flanked sequence, Cre-mediated recombination is expected to result in deletion of the floxed sequences in the Cre recombinase-expressing tissues of the offspring. | ||
| 005698 | B6.Cg-Tg(Gfap-TK)7.1Mvs/J | Repository- Live |
| Mice hemizygous for the transgenic insert are viable, normal in size, and do not display any behavioral abnormalities. Transgenic males are infertile. Proliferating cells that express the herpes simplex virus thymidine kinase (HSV-TK) transgene will metabolize ganciclovir (GCV) to toxic nucleotide analogues and undergo cell death. Transgene-derived HSV-TK is present exclusively in cells expressing endogenous Gfap. This coexpression occurs in brain astrocytes and adult neural stem cells, enteric glia, hepatic stellate cells, and unknown cells in heart, lung, kidney, adrenal, and spleen. Chronic GCV treatment for 21 days depletes GFAP-positive adult neural stem cells from forebrain proliferative zones. GCV treatment eliminated growth of primary multipotent neurospheres cultured from the germinal zones of postnatal and adult, but not early embryonic, transgenic mice. Notably, the same treatment prevented growth of secondary multipotent neurospheres from all three developmental stag ..... For more information please see the full phenotype on the strain data sheet | ||
| 013038 | B6;129S7-Smad5tm1Zuk/J | Repository- Live |
| In this strain, the allele replaces exon 2 of the endogenous MAD homolog 5 (Smad5) gene with a PGK-hprt selection cassette, abolishing gene function. Mice homozygous for the Smad5 allele have an embryonic lethal phenotype and do not survive past E11.5. Heterozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous embryos lack ectopic vasculogenesis and hematopoiesis in the amnion, lack both a foregut pocket and entrance to the hindgut diverticulum, and are absent of primordial germ cells. The allantois is fused to the chorion and is not elongated. These embryos also exhibit a defect in heart looping and embryonic turning associated with Left-right asymmetry. At later stages, mutant embryos have craniofacial and neural tube abnormalities, are edematous, and after E9.0 the yolk sacs contain red blood cells but still lack well organized vasculature. These mice may be useful for studying ventrolateral morpho ..... For more information please see the full phenotype on the strain data sheet | ||
| 004333 | C.129P2(B6)-Il10tm1Cgn/J | Repository- Live |
| Mice homozygous for the Il10tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet | ||
| 008701 | C.129X1(B6)-Ebi3tm1Rsb/J | Repository- Live |
| Mice homozygous for this Ebi3-mutant allele are viable and fertile with the donating investigator reporting no overt autoimmunity or inflammatory disease associated with the mutation. No RNA from the targeted gene is observed in splenocytes isolated from homozygotes. Ebi3-deficiency leads to impaired Treg activity with failure to control homeostatic proliferation. Homozygotes exhibit decreased numbers and function of invariant natural killer T cells (iNKT); stimulated iNKT cells show impaired IL-4 production both in vivo and in vitro. Homozygotes are resistant to oxazolone-induced colitis (mediated primarily by T helper (Th) 2-type cytokine production by iNKT cells), whereas Ebi3-deficiency shows no affect on trinitrobenzene sulfonic acid-induced colitis (a predominantly Th1-mediated colitis model). These Ebi3-mutant strains may be useful in studying Treg function, IL12 heterodimeric cytokines (such as IL-35 and IL-27) and IFNgamma production, and Th ..... For more information please see the full phenotype on the strain data sheet | ||
| 010710 | FVB;129S6-Sncatm1Nbm Tg(SNCA)1Nbm/J | Repository- Live |
| These PAC-Tg(SNCAWT);Snca-/- mice are viable and fertile, harboring a Snca knockout allele and a transgene encoding the human α-synuclein. As homozygotes, expression of endogenous mouse α-synuclein is abolished and replaced by human α-synuclein from the two total insertions of the PAC-Tg(SNCAWT). While brain RNA expression of SNCAWT is more than 50-fold greater compared to normal endogenous mouse α-synuclein, protein levels are only 1 to 1.5-fold greater. In colon however, both RNA and protein expression of SNCAWT are ~100-fold greater than normal endogenous mouse α-synuclein. PAC-Tg(SNCAWT);Snca-/- mice do not show any enteric nervous system abnormalities or widespread α-synuclein aggregation in brain or colon. No detectable motor behavior impairments, autonomic abnormalities, olfactory dysfunction, dopaminergic deficits, Lewy body inclusions or neurodegeneration are ..... For more information please see the full phenotype on the strain data sheet | ||
| 010799 | FVB;129S6-Sncatm1Nbm Tg(SNCA*A53T)1Nbm Tg(SNCA*A53T)2Nbm/J | Repository- Live |
| These double transgenic homozygous mice (dbl-PAC-Tg(SNCAA53T);Snca-/- mice) are viable and fertile, harboring a Snca knockout allele and two independently inserted transgenes encoding the human A53T-mutant α-synuclein associated with autosomal dominant Parkinson's disease. As homozygotes, expression of endogenous mouse α-synuclein is abolished and replaced by α-synuclein*A53T from the four total insertions of the PAC-Tg(SNCAA53T). While brain RNA expression of SNCAA53T is ~10-fold greater compared to normal endogenous mouse α-synuclein, protein levels are only 1 to 1.5-fold greater. In colon however, both RNA and protein expression of SNCAA53T are ~80-fold greater than normal endogenous mouse α-synuclein. By three months of age, dbl-PAC-Tg(SNCAA53T);Snca-/- mice show robust abnormalities in enteric nervous system function (impaired colonic motility [males only] and prolonge ..... For more information please see the full phenotype on the strain data sheet | ||
| 009355 | SAMP1/YitFcsJ | Repository- Live |
| SAMP1/YitFcs (also called SAMP1/YitFc or SAMP1/Fc) mice develop a spontaneous ileitis that is similar in many features to human Crohn's disease. Development of ileitis is accelerated by the presence of luminal bacteria and is characterized by discontinuous segmental inflammation involving the ileum while sparing the proximal small intestine and colon. The histopathologic features of SAMP1/Fc ileitis include transmural inflammation, crypt abscesses, and epithelial changes including loss of villi, crypt elongation, and crypt branching. SAMP1/Fc mice were originally distinguished from the strain from which they were derived (SAMP1/Yit) by spontaneous onset of ileum inflammation by 10 weeks of age at nearly 100% penetrance and the emergence of a perianal fistulizing disease not reported in the parental strain. Other distinguishing characteristics of the SAMP1/Fc substrain include incidence of skin lesions inversely correlated with the occurrence of intestinal inflammation, chronic ileitis ..... For more information please see the full phenotype on the strain data sheet | ||
| 017523 | 129S6.Cg-Tg(Gfap-TK)7.1Mvs/RhnJ | Under Development - Now Accepting Orders |
| Mice hemizygous for the transgenic insert are viable, normal in size, and do not display any behavioral abnormalities. Transgenic males are infertile. Proliferating cells that express the herpes simplex virus thymidine kinase (HSV-TK) transgene will metabolize ganciclovir (GCV) to toxic nucleotide analogues and undergo cell death. Transgene-derived HSV-TK is present exclusively in cells expressing endogenous Gfap. This coexpression occurs in brain astrocytes and adult neural stem cells, enteric glia, hepatic stellate cells, and unknown cells in heart, lung, kidney, adrenal, and spleen. Chronic GCV treatment for 21 days depletes GFAP-positive adult neural stem cells from forebrain proliferative zones. GCV treatment eliminated growth of primary multipotent neurospheres cultured from the germinal zones of postnatal and adult, but not early embryonic, transgenic mice. Notably, the same treatment prevented growth of secondary multipotent neurospheres from all three developmental stag ..... For more information please see the full phenotype on the strain data sheet | ||
| 006369 | 129-Cckbrtm1Kpn/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 receptor function was detected in competition binding assay of brain (cerebral plasma) membranes. When compared to wildtype, gastric pH in homozygotes is higher, pH 5.2, after overnight fast. Histological analysis reveals diminished parietal cell, enterochromaffin-like cell (ECL) and antral comatostatin-producing D cell densities. An increase in the number of gastrin-producing G cells is observed. There is an increased number of H+, K+ -ATPase immunoreactive negative cells and abnormal distribution of parietal cells in oxyntic glands. Circulating gastrin levels are 10-fold higher in homozygotes. Gastric mucosal histamine levels are greatly reduced and histamine-immunoreactive ECL cells are absent. This mutant mouse strain may be useful in studies of hypochlorhydria, hypergastinemia, gastric antral endocrine regulation, and ..... For more information please see the full phenotype on the strain data sheet | ||
| 003451 | 129-Smad3tm1Par/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted mutation are viable. Although fertile, they produce litters at reduced efficacy compared to wild type or heterozygous mice. Null mutants are approximately 20%-30% smaller than heterozygous or wildtype litter mates, with males exhibiting a more pronounced size reduction. Reporter lacZ expression is observed in many developing embryonic tissues with highest levels in mesenchymal derivatives. Expression in adult mutant mice is observed in the colon, with highest levels in the muscularis propria and submucosa with lower levels in the epithelium. At approximately 4-6 months of age, they develop gastric tumors. The donating investigator originally described spontaneous, deeply invasive colorectal adenocarcinomas that penetrate through all layers of the intestinal wall and metastasize to lymph nodes. Colorectal adenocarcinomas are not a component of the phenotype observed in this strain at The Jackson Laboratory. However, the gastric epithelium was fo ..... For more information please see the full phenotype on the strain data sheet | ||
| 008243 | 129;B6-Tff3tm1Dkpy/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this intestinal trefoil factor (ITF or Tff3) mutant allele are viable and fertile with no RNA or protein expression of the targeted gene in the gastrointestinal tract. Homozygous mice exhibit impaired physiological migration of intestinal epithelium to the mucosal surface, have impaired mucosal healing and increased susceptibility to dextran sulfate sodium (DSS)- induced colitis, and are more susceptible to chemotherapy and radiation-induced mucositis. These intestinal trefoil factor (ITF or Tff3) mutant mice may be useful in studying gastrointestinal tract injury (including inflammatory bowel diseases), maintenance of the mucosal barrier, migration and turnover of the intestinal epithelium, and therapies for colon cancer. | ||
| 009085 | 129S/Sv-Rettm1Cos/J | Cryopreserved - Ready for recovery |
| The Ret- allele (also called ret-k-, ret-k minus, or c-ret-) disrupts the region of the ret proto-oncogene (Ret; also called ret-k or c-ret) locus harboring the invariant lysine codon required for Ret kinase activity. Homozygous mice die around 16-24 hours after birth, exhibiting abnormalities in kidney/urinary (renal agenesis/hypodysplasia) and peripheral nervous system development (including sympathetic, parasympathetic, and enteric ganglia), as well as abnormal enteric neural crest cell migration. Because homozygous mice lack enteric ganglia from the hindgut, these mice are also a model of Hirschsprung's Disease. | ||
| 003292 | 129S6/SvEvTac-Wastm1Sbs/J | Cryopreserved - Ready for recovery |
| WAS-deficient mice are viable and fertile. Mutant mice show normal lymphocyte development, serum immunoglobulin (Ig) levels and antibody responses. However, peripheral blood lymphocyte counts and platelet numbers are reduced in these mice. Development of chronic colitis is also observed. In vitro, WAS-deficient T cells show markedly impaired proliferative responses to anti-CD3e mediated stimulation. The Was gene is X-linked, so hemizygous males are WAS deficient. | ||
| 000202 | AEJ/Gn-bd/J | Cryopreserved - Ready for recovery |
| 008884 | B6.129(Cg)-Pnliptm1Dyh/J | Cryopreserved - Ready for recovery |
| These mice harbor a null mutation of the Pnlip (pancreatic lipase [also called pancreatic triglyceride lipase or PTL]) gene. Homozygous (PTL-/-) mice are viable and fertile, with no protein expression from the targeted allele observed in pancreatic tissue extracts. Homozygotes exhibit mildly delayed triglyceride (also called triacylglycerol or TAG) absorption after low fat diet feeding, but significantly delayed TAG absorption on a high fat/high cholesterol diet. Homozygous mice have a significant decrease in the rate/amount of cholesterol absorption; attributed to PTL-deficiency delaying dietary fat absorption to the distal small intestine (ileum) where intestinal cholesterol uptake is less efficient. Because PLT-/- mice retain endogenous Cel (carboxyl ester lipase [also called cholesterol esterase]) expression, pancreatic extracts from PTL-/- mice retain robust TAG hydrolytic activity (albeit at lower levels than wildtype mice). This TAG hydrolytic ..... For more information please see the full phenotype on the strain data sheet | ||
| 004603 | B6.129-P2rx2tm1Ckn/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 or protein) is detected by RT-PCR of intestinal tissue or Western blot analysis of dorsal root and trigeminal ganglia. No immunoreactive staining was detected in ileum by immunohistochemical analysis. Myenteric neurons exhibit altered intracellular electrophysiological action potentials. Fast excitatory postsynaptic potentials (fEPSPs) from mutant S neurons (myenteric plexus interneurons and motorneurons) are inhibited by the nicotinic cholinergic receptor antagonist, mecamylamine. ATP-induced depolarization of isolated mutant S neurons is abolished. Peristalsis is impaired in the ileum. Mutant mice ventilatory response to hypoxia is diminished, as determined by in vitro carotid sinus nerve preparation. ATP and ATP analog (alpha,beta-methyleneATP) elicits a faster discharge (afferent activity) in mutant sinus ner ..... For more information please see the full phenotype on the strain data sheet | ||
| 008313 | B6.129P2-Hlxtm1Rph/J | Cryopreserved - Ready for recovery |
| Homozygous null mice have an embryonic lethal phenotype. Homozygous mice on the C57BL/6 and B6;129 mixed background fail to develop past embryonic days 15.5 due to impaired fetal hematopoiesis (anemia, hypoplastic and abnormal development of the liver, hypoplastic gut). Homozygous mice on the FVB/N background survive through embryonic day 18.5 and dead homozygote newborn pups are observed. Late gestation homozygous embryos on the FVB/N background are smaller than wildtype littermates, pale, hydropic (subcutaneous fluid ballooning skin), and have impaired neural crest cell and enteric neuron migration from the stomach to intestine. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Naive CD4 T cells from heterozygotes exhibit increased responsiveness to IL-4, resulting in differentiation of more Th2 cells. This mutant mouse strain may be useful in studies of liver and gastrointe ..... For more information please see the full phenotype on the strain data sheet | ||
| 006221 | B6.129S1-Lyve1tm1Lhua/J | Cryopreserved - Ready for recovery |
| Homozygotes are viable and fertile, and produce normal-sized litter. No gross phenotypic or behavioral abnormalities have been reported, even in older (2 year old) mice. Homozygous mutants express neither endogenous RNA or protein in liver tissue. Lymphatic capillary vessel morphology in the liver and intestines of homozygous mice is abnormal, with vessels having distended or rounded lumens in contrast to the smaller, typically collapsed, irregular shapes observed in wildtype controls. Intradermal interstitial-lymphatic flow also is increased. Syngenic tumor cell transplants into grow more rapidly and robustly in homozygous mutant mice compared with transplants into wildtype mice, and develop porous interstitial spaces. These mutant mice may be useful in studies of structural and functional characteristics of the lymphatic system, cell-surface retention sequence (CRS) motif-containing growth factor secretion, autocrine and paracrine regulation of cell growth, as well as of cancer and t ..... For more information please see the full phenotype on the strain data sheet | ||
| 009640 | B6.129S4-Viptm1Clw/J | Cryopreserved - Ready for recovery |
| Mice that are heterozygous for the targeted mutation are viable and fertile. No gene product (protein) is detected by immunohistochemical analysis of homozygotes. Homozygous females are subfertile, 15-20% of homozygous females can have litters. Homozygotes exhibit impaired circadian rhythm generation, muscle weakness, increased motor activity and increased induced airway hyperresponsiveness and inflammation. In constant darkness, homozygotes initially display shortened circadian period. Some homozygotes develop arrhythmic circadian periods after extended darkness. Heterozygotes also display abnormal circadian rhythm. Homozygotes have both gross and microscopic anatomical abnormalities of the gastrointestinal tract. 10-15% of homozygotes die of stenosis of the gut before one year of age. Male homozygotes exhibit moderate right ventricular (RV) hypertension, RV hypertrophy, thickened and remodeled pulmonary arteries, perivascular inflammation of smaller pulmonary vessels and airways, red ..... For more information please see the full phenotype on the strain data sheet | ||
| 009082 | B6.129S6-Ostatm1Pda/J | Cryopreserved - Ready for recovery |
| Homozygous (Osta-/-) mice are viable and fertile, with no mRNA or protein expression from the targeted allele. Homozygotes exhibit a small growth deficit that is ameliorated after weaning, partial impairment of intestinal bile acid absorption (impaired basolateral transport of bile acids out of the ileal epithelial cell), altered regulation of bile acid synthesis, a significantly reduced bile acid pool, intestinal lengthening and intestinal hypertrophy. Homozygous mice also have reduced hepatic Cyp7a1 expression that is inversely correlated with ileal expression of fibroblast growth factor 15 (FGF15). These mutant mice may be useful in studying cholesterol metabolism, intestinal drug absorption, intestinal bile acid absorption, bile acid synthesis, and cholesterol and bile acid homeostasis.
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 ..... | ||
| 004366 | B6.129X1-Brs3tm1Jfb/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, normal in size at birth and do not display any gross physical or behavioral abnormalities. This targeted mutation is X-linked; males bearing the targeted allele display a mutant phenotype. At 15 to 16 weeks of age male mice heterozygous for the mutant allele display increased body weight as compared to wildtype littermates. This mutant mouse strain represents a model that may be useful in studies related to energy metabolism and obesity. | ||
| 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 | ||
| 005912 | B6.Cg-Il10tm1Cgn (D3Mit49-D3Mit348)/Lt | Cryopreserved - Ready for recovery |
| Homozygous mice are IL10-deficient and develop spontaneous colitic lesions in the cecum and large intestine as early as 6-8 weeks of age. The severity and age of onset of colitis varies with the donor type and location of the cytokine deficiency colitis susceptibility 1 (Cdcs1) interval. Generally, the C3H/HeJBir region encompassed by D3Mit348 through D3Mit254 (127.7-132.5 megabases) confers increased colitis susceptibility on the B6.129P2-Il10tm1Cgn background (Beckwith J, et al., 2005). Mice on the B6.129P2-Il10tm1Cgn background are prone to rectal prolapse particularly when carrying susceptibility alleles from Chromosome 3. Granulocyte populations in peripheral blood increase upon lesion development and provide a robust non-lethal assessment of colitis severity. | ||
| 009352 | B6.Cg-Tg(CDX2-cre*)189Erf/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the CDX2P9.5-G22Cre transgene are viable and fertile. The 9.5 kb human caudal type homeo box 2 (CDX2) promoter/enhancer sequence is prevented from driving nuclear-localized Cre recombinase expression as a 22 guanine nucleotide repeat tract between initiating methionine (ATG) codon and the remainder of the coding region alters the cre reading frame. Presumably, following a somatic mutation that results in some frameshift mutation(s) in the guanine nucleotide tract in a subset of somatic cells, resultant expression of a functional Cre recombinase is observed predominantly in colonic epithelium during late gestation and in adult tissues. Specifically, mosaic Cre recombinase expression would be observed in epithelium from the distal ileum and cecum, and mainly the proximal and distal colon from the crypt base to the luminal surface. Cre recombinase expression may also be observed in a few caudal-derived cells during early development. When these transgenic ..... For more information please see the full phenotype on the strain data sheet | ||
| 012823 | B6;129-Fzd4tm1Nat/J | Cryopreserved - Ready for recovery |
| Homozygous Fzd4 (frizzled homolog 4 (Drosophila)) mice have a congenital retinal hypovascularization, a progressive inner ear vascular atrophy, a defect in the blood brain barrier in the cerebellum, and a progressive cerebellar degeneration associated with severe ataxia. Mice also show an absence of a skeletal muscle sheath around the lower esophagus associated with progressive esophageal distension. | ||
| 007613 | B6;129-Smad1tm2Sor/J | Cryopreserved - Ready for recovery |
| Homozygotes for the Smad1tm2Sor (also called Smad1L) allele are viable and fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mice carry a mutation in exon 3, which effects MAPK-mediated phosphorylation of the protein. Western blot analysis of MEFs from homozygotes showed that similar protein levels compared to wildtype. Homozygous embryos have fewer primordial germ cells than wildtype controls. Homozygous mice display abnormal gastric mucosa cell population ratios with fewer zymogenic cells and more parietal cells. The cytoskeleton of MEFs from homozygotes exhibit a loss of adhesion zippers, decreased stress fibers, and an accumulation of actin in the cortical regions with an increase in beta-catenin immunostaining localized to the cell membranes. This mutant mouse strain may be useful in studies of stomach development, gastic mucosal homeostasis and BMP and MAPK signaling pathways during development and in the adult. | ||
| 006404 | B6;129S4-Apoa4tm1Bres/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and fertile with no protein detectable in plasma, liver, or intestinal tissues. Homozygotes have decreased plasma levels of cholesterol, free fatty acids, and high density (HDL) and very low density lipoprotein (VLDL). These mice may be useful in studies of lipid metabolism, atherosclerosis, heart disease, appetite regulation, intestinal lipid absorption, or inflammatory bowel disease. | ||
| 000209 | B6C3Fe a/a-Dh/J | Cryopreserved - Ready for recovery |
| A spontaneous mutation on chromosome 1 of the dominant hemimelia gene, Dh, causes a defect in the embryonic splanchnic mesoderm and induces congenital absence of the spleen and widespread visceral and skeletal abnormalities. Mice homozygous for the Dh mutation die shortly after birth. Heterozygotes may exhibit tibial hemimelia, polydactyly, and extra fused toes. Rear leg(s) may be held at an odd angle with bent rear ankles. Heterozygotes have enlarged lymph nodes and elevated numbers of circulating lymphocytes, granulocytes and thrombocytes. They show reduced serum IgM and IgG2 and impaired humoral antibody response as well as decreased numbers of lymph node mast cells. The Pde6brd1 allele contributed to this strain by C3FeLe.B6-a causes blindness and is segregating in this strain. | ||
| 005972 | C3H/HeJBirLtJ | Cryopreserved - Ready for recovery |
| Under conventional housing conditions, C3H/HeJBirLtJ mice develop spontaneous colitis. It should be noted that the phenotype of cecocolitis in this strain requires an interaction with an as yet undefined component of the enteric flora. Inflammation is present mainly in the cecum and right colon. Colitis develops early in life and resolves by three months of age. The colitis is characterized by acute and chronic inflammation, ulcerations, crypt abscesses, regenerative hyperplasia and submucosal scarring. A mild recurrence of the disease can occur after one year. Small lesions at the anorectal junction are common throughout life. | ||
| 008711 | C57BL/6-H2-T3tm1Luc/J | Cryopreserved - Ready for recovery |
| The mouse thymus leukemia (TL) antigen is a nonclassical MHC class I molecule encoded by a locus within the MHC complex harboring two genes; H2-T3 and H2-T18. TL binds with high affinity to the CD8αα molecule expressed on the vast majority of intraepithelial lymphocytes (IEL), and the interaction of CD8αα with TL is important for lymphocyte regulation in the intestine. The C57BL/6 genetic background normally has the functional H2-T3d allele and a mutant H2-T18b allele known to result in no expression on the surface of intestinal epithelial cells (IEC). Because these mutant mice harbor a targeted mutation of the H2-T3 gene that abolishes gene function, expression of TL protein (antibody staining) and RNA (RT-PCR) from either locus is absent in IEC and small/large intestine, respectively. These TL-deficient mice may be useful in studying thymus leukemia (TL) antigen-deficiency on CD8αα intraepith ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 001723 | CByJ.A-Ttc7fsn/J | Cryopreserved - Ready for recovery |
| Homozygous fsn mice suffer from hypochromic and normocytic anemia at birth which becomes more severe with age. The anemia makes the homozygous mice distinguishable as pups because of the pale color of ears and eyes. At 2 weeks of age focal epidermal hyperplasia and inflammation is evident with psoriasiform skin lesions becoming confluent and diffuse in 3-4 week old weanlings. The skin lesions progress to generalized alopecia and shedding of thick white scales. The gross lesions are accompanied by thickening and keratinization of the skin. A progressive paplosquamous disease ensues which is a model for some forms of psoriasis. fsn/fsn mice show hematocrit levels and red blood cell counts that are significantly decreased from birth through adulthood. Consequently the heart, liver and spleen become enlarged but the thymus weight is less than half normal. As the spleen enlarges, the mice also develop a potbellied appearance aiding in homozygous fsn identification. G ..... For more information please see the full phenotype on the strain data sheet | ||
| 012563 | FVB.129(Cg)-Slc9a3tm1Ges/J | Cryopreserved - Ready for recovery |
| These mice harbor a targeted mutation of the Na+/H+ exchanger isoform 3 locus (Nhe3 or Slc9a3) that abolishes endogenous gene expression. While no full-length mRNA is detected in kidney or intestine of homozygous mice, a truncated mutant mRNA lacking codons 320-831 (encoding sequences required for Na+/H+ exchange) is observed but expected to impart no dominant negative effects. When maintained as congenic on the FVB/N genetic background, homozygous mice exhibit a high mortality rate beginning just after weaning, with ~30% surviving to adulthood. Homozygous females are fertile, but homozygous males are infertile.
Homozygous (Nhe3-null) mice lack Na+/H+ exchanger isoform 3 function, and exhibit impaired intestinal absorption; resulting in severe diarrhea, altered salt and water homeostasis, and increased luminal fluid throughout the intestinal tract. Nhe3-null mice have increased PCNA-positive cells in the cryp ..... For more information please see the full phenotype on the strain data sheet | ||
| 008315 | FVB.129P2(Cg)-Hlxtm1Rph/J | Cryopreserved - Ready for recovery |
| Homozygous null mice have an embryonic lethal phenotype. Homozygous mice on the C57BL/6 and B6;129 mixed background fail to develop past embryonic days 15.5 due to impaired fetal hematopoiesis (anemia, hypoplastic and abnormal development of the liver, hypoplastic gut). Homozygous mice on the FVB/N background survive through embryonic day 18.5 and dead homozygote newborn pups are observed. Late gestation homozygous embryos on the FVB/N background are smaller than wild-type littermates, pale, hydropic (subcutaneous fluid ballooning skin), and have impaired neural crest cell and enteric neuron migration from the stomach to intestine. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Naive CD4 T cells from heterozygotes exhibit increased responsiveness to IL-4, resulting in differentiation of more Th2 cells. This mutant mouse strain may be useful in studies of liver and gastrointestin ..... For more information please see the full phenotype on the strain data sheet | ||
| 008660 | FVB.129S2(B6)-Hmox2tm1Poss/J | Cryopreserved - Ready for recovery |
| Homozygotes have reduced total heme oxygenase activity in brain and testes, diminished inflammatory pain response and are more susceptible to hyperoxia with attenuated hypoxic ventilatory response. Cultured neurons from homozygotes exhibit increased neurotoxicity and cell death. Neuronal and endothelial cell damage due to transient focal ischemia and glutamate induced cytotoxicity is increased. Olfactory epithelial neurons have decreased proliferation of neuronal precursors and increased apoptosis. Mutant pulmonary venous myocardium is hypertrophic. After hyperoxic exposure, total lung iron content increased 3.5 fold in homozygotes compared to wild-type. Homozygotes have a slower overall gastrointestinal transit time than wild-type. Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Although homozygous male animals exhibit ejaculatory abnormalities, both male and female homozygotes are fertile ..... For more information please see the full phenotype on the strain data sheet | ||
| 010788 | FVB;129S6-Sncatm1Nbm Tg(SNCA*A30P)1Nbm Tg(SNCA*A30P)2Nbm/J | Cryopreserved - Ready for recovery |
| These double transgenic homozygous mice (dbl-PAC-Tg(SNCAA30P);Snca-/- mice) are viable and fertile, harboring a Snca knockout allele and two independently inserted transgenes encoding the human A30P-mutant α-synuclein associated with autosomal dominant Parkinson's disease. As homozygotes, expression of endogenous mouse α-synuclein is abolished and replaced by α-synuclein*A30P from the PAC-Tg(SNCAA30P). Because PAC-Tg(SNCAA30P) line 1 inserted on the X chromosome and line 2 inserted on a somatic chromosome, homozygous females have four total insertions and homozygous males have three total insertions. While brain RNA expression of SNCAA30P is more than 10-fold greater compared to normal endogenous mouse α-synuclein, protein levels are only 1 to 1.5-fold greater. In colon however, both RNA and protein expression of SNCAA30P are ~80-fold greater than normal endogenous mouse α-synuclein. ..... For more information please see the full phenotype on the strain data sheet | ||
| 005346 | NOD.Cg-Il10tm1Cgn Casp1tm1Sesh/LtJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Il10 and Casp1 targeted mutations are viable and fertile when housed under SPF conditions. NOD/Lt mice deficient for both of these genes develop type 1 diabetes at a rate equivalent to the parental strains. The Il10 targeted mutation also renders this NOD/Lt stock susceptible to colitis (although not as severe as other strains of Il10 deficient mice) when maintained under standard housing conditions. | ||
| 004266 | NOD.Cg-Il10tm1Cgn/DvsJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Il10tm1Cgn targeted mutation are viable and fertile when housed under SPF conditions. This mutant develops type 1 diabetes at the same rate as the NOD/Lt parental strain. The Il10 tm1Cgn mutation also renders this NOD/Lt stock susceptible to colitis (although not as severe as other strains of Il10 deficient mice) when maintained under standard housing conditions. | ||
| 006956 | NOD.Cg-Vdrtm1Ska/CmatJ | Cryopreserved - Ready for recovery |
| Heterozygous mice are viable, fertile, and phenotypically indistinguishable from wildtype siblings. Homozygous mutant mice are viable but infertile. No VDR mRNA is detected by RT-PCR in samples from the intestine or kidney or from homozygous mutant embryo. Increased expression of CTP27B1 and reduced expression of CYP24A1 and calbindin-D9k is detected by RT-PCR in samples from VDR-deficient kidneys. Although mice homozygous for this targeted mutation are viable, shortly after weaning they exhibit dysmorphic features including a flat face and short nose, alopecia, growth retardation, and skeletal defects including hypocalcaemia, decreased bone mineral density, widened growth plates with hypomineralization, less trabeculae and thicker osteo seams. Homozygous mutant mice exhibit metabolic imbalances including abnormally high and low levels of 1,25(OH),2D3 and 25(OH)D3, respectively and abnormal cytokine and chemokine profiles.
Homozygous mice exhibit normal pancreatic islet archite ..... | ||
| 010828 | STOCK Tmpotm1.1Foi/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 LAP2α gene product (mRNA or protein) is detected by Northern or Western blot analysis of primary fibroblasts from neonates. Expression of other TMPO isoforms was not significantly affected. A-type lamin localization is abnormal with decreased lamin in the nucleoplasm. Primary fibroblasts isolated from homozygotes exhibit delayed contact-mediated cell cycle arrest and attain a 1.5 fold increased density before cell cycle arrest compared to wildtype. Homozygotes display thickened plantar paw epidermis due to a twofold increase in proliferating cells. Hematocrit levels are increased. Mutants have a fourfold increased number of erythroid progenitor cells in the spleen and a smaller increase in erythroid progenitor cells in bone marrow. Large intestine crypts are lengthened in mutant mice. The colon epithelium has 20% mor ..... For more information please see the full phenotype on the strain data sheet | ||
| 001788 | STOCK Tg(Fabp1-GH1)10Bir/J | Cryopreserved - Ready for recovery |
| 001400 | STOCK Tg(Fabp1-GH1)5Bir/J | Cryopreserved - Ready for recovery |
| 001515 | STOCK Tg(Fabp1-GH1)7Bir/J | Cryopreserved - Ready for recovery |
| 001878 | STOCK Tg(IFABP-GH)11Bir/J | Cryopreserved - Ready for recovery |
| 001879 | STOCK Tg(IFABP-GH)12Bir/J | Cryopreserved - Ready for recovery |
| 001909 | STOCK Tg(IFABP-GH)15Bir/J | Cryopreserved - Ready for recovery |
| Obligate hemizygous F1 offspring from founder 54 carried approximately 60 copies of the transgene in tandem head-to-tail arrangement in a single insertion site. Expression of the reporter gene, human growth hormone, is appropriately restricted to the intestine where the duodenum and proximal jejunum show expression levels normal for intestinal fatty acid binding protein, but the distal small intestine shows reduced expression. Resultant serum human growth hormone levels were 6-38 ng/ml which is approximately 1000 times lower than in mice carrying a transgene with an extended I-FABP promoter which includes nucleotides -1178 to +28. Use of the extended (-1178 to +28) promoter also results in a more normal expression in the distal small intestine. (Sweetser et al., 1988.) | ||
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