Search Criteria: Research Area is "Research Tools: Internal/Organ Research"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 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 | ||
| 007005 | 129S-Scg5tm1Led/J | Repository- Live |
| The following text reflects the phenotype reported by the donating investigator on a "129Sv" genetic background (probably "Taconic Sv129" (129S6/SvEvJ)). While heterozygotes are viable and fertile, mice homozygous for this mutation (7B2-null) die in prepubertal or pubertal ages (5 weeks) with severe cardio-respiratory failure, convulsions, and hypothermia. No transcripts are detected in brain tissue from the targeted gene. 7B2 null mice are unable to make an active form of prohormone convertase 2 (PC2) and have high circulating corticosterone. Homozygotes on the 129S genetic background exhibit Cushing's-like disease pathologies of liver, pancreas, and pituitary; including pituitary-dependent hyperadrenocorticosteronism, severe hypoglycemia, hyperproinsulinemia, adrenal hypertrophy, pituitary hypotrophy, and altered islet cell morphology. 7B2-null mice develop the disease from intermediate lobe ACTH hypersecretion (rather than from pituitary adenomas). Other abnormalities include thinni
..... For more information please see the full phenotype on the strain data sheet | ||
| 007199 | 129S-Sgpl1Gt(ROSA)78Sor/J | Repository- Live |
| Mice homozygous for this mutant allele have reduced size and weight gains after birth and do not survive past 8 weeks of age. Homozygotes occur at a lower than Mendelian ratio (19%) from heterozygote X heterozygote crosses. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Beta-galactosidase staining pattern mimics the endogenous gene expression pattern in adult intestinal epithelial cells. Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mutant mice are anemic (low hemoglobin concentration, reduced red blood cell count, low hematocrit). Mutants exhibit polychromasia (abnormally high number of immature blood cells), kidney defects (blood urea nitrogen level abnormally high, kidney size smaller than wildtype, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells) and abnormalities in palate bone fusion. Homozygotes are infertile. Heterozygote
..... For more information please see the full phenotype on the strain data sheet | ||
| 005704 | B6.129-Fbn1tm2Rmz/J | Repository- Live |
| Both heterozygous and homozygous "mgR" mutant mice are viable with no phenotypic abnormalities at birth. The protein expressed from this mutant allele is the same size as wild-type. Skin tissues show an intermediate reduction in transcript levels compared to wild-type and the mg-delta null allele. Thus the "mgR" mutation does not completely ablate gene function (resulting in rapid death). Instead, expression is hypomorphic and conducive to studying the clinical stages precursive to animal lethality. Homozygotes develop medial calcification, the inflammatory-fibroproliferative response, and inflammation-mediated elastolysis in the natural history of dissecting aneurysm and die between 2-6 month of age with Marfan syndrome (MFS)-like manifestations. | ||
| 006879 | B6.129-Scd2tm1Myz/J | Repository- Live |
| While heterozygous mice are viable and fertile, mice homozygous for this targeted allele die within 24 hours of birth. Brain tissues from homozygous mice show no expression from the targeted gene. Homozygotes exhibit neonatal lethality with 100% penetrance on this genetic background (less penetrant on 129SvEv genetic background) likely due to severe skin permeability barrier abnormalities. Null mice also have abnormal epidermal morphology and abnormal lipid homeostasis in the skin and liver. These mutant mice may be useful in studying monounsaturated fatty acid synthesis, lipid biosynthesis and metabolism, cholesterol homeostasis, and skin disease, as well as obesity and diabetes. | ||
| 005960 | B6.129S-Pecam1Gt(VICTR20)12Lex/J | Repository- Live |
| Mice that are homozygous for the gene-trapped allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by immunofluorescence in aorta endothelium from homozygotes, and endothelial nitric oxide synthase isoform (eNOS) is not detected in cell to cell junctions between aorta endothelial cells in these mice. Isolated skeletal muscle arterioles from homozygous mutant mice exhibit reduced vessel dilation and no significant change in wall shear stress responses when intraluminar flow is increased. This mutant mouse strain may be useful in studies of cellular adhesion, vascular integrity and physiology. | ||
| 006221 | B6.129S1-Lyve1tm1Lhua/J | Repository- Live |
| 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 | ||
| 006141 | B6.129S2-Thbs1tm1Hyn/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile, with an approximate 20% decrease in embryo/neonate viability and a mild and variable lordotic curvature of the spine apparent from birth. Homozygous mice have an abnormal, but no full length transcript in multiple tissues. Western analysis confirmed the absence of the protein in platelets. Homozygotes exhibit an increase in the number of circulating white blood cells. During the first four to ten weeks of life, homozygotes exhibit patches of acute and organizing pneumonia. At later time points, there is considerable hyperplasia of the various epithelial cell lineages. Mutant mice also have an increased number of retinal endothelial cells and inappropriate remodeling and maturation of retinal vasculature following injury. On the FVB/N background, spontaneous tumor growth and vasculature are significantly increased compared to wildtype. Mutant mice may be useful in studies of inflammatory responses in the lungs, eye, and
..... For more information please see the full phenotype on the strain data sheet | ||
| 007682 | B6.129X1-Apobtm1.1Zc/J | Repository- Live |
| Mice homozygous for this apoB38.9 allele (apoB38.9/38.9) are viable with impaired fertility, bearing a premature stop codon at residue 1767 of the targeted gene. As a result, homozygous plasma shows a truncated apoB38.9 as the sole apoB protein. Plasma from heterozygous (apoB+/38.9) mice have reduced apoB100 and apoB48 compared to wildtype, with apoB38.9 representing 20% of total circulating apoB. This apoB38.9 truncation affects both apoB100 and apoB48 metabolism in mice, and mimics human Familial Hypobetalipoproteinemia (FHBL). Homozygous and, to a lesser extent, heterozygous mice exhibit symptoms of FHBL due to impaired lipoprotein export system/VLDL secretion, including elevated hepatic triglyceride (TG), cholesterol and free fatty acids (FFA), with decreased plasma TG and cholesterol. Because plasma and liver lipid profiles range from mild to severe in populations of heterozygous apoB38.9 mice on a mixed (C57BL/6J;129X1/SvJ) genetic background, apoB+/38
..... For more information please see the full phenotype on the strain data sheet | ||
| 005085 | B6.Cg-Cd44tm1Hbg/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. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms. 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 f
..... | ||
| 006183 | B6.Cg-Col4a5tm1Yseg/J | Repository- Live |
| Heterozygous females and hemizygous males for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Immunofluorescence analysis of kidney tissue from mutant male mice does not detect gene product (protein), but in kidney from mutant female mice a mosaic pattern of gene product (protein) is detected (due to X-inactivation). RNase protection assay analysis of kidney tissue from mutant male mice detects a significantly lower level than wildtype. Hemizygous male and heterozygous female mice develop progressive kidney disease. By 7 weeks of age, 97% of mutant male mice and 78% of heterozygous female mice exhibit proteinuria. Histological analysis of kidneys from mutant male mice at 4 weeks of age reveals thickened capillary walls and mesangial hypercellularity. The pathology progresses to interstitial inflammation, glomerular abnormalities, and focal sclerosis. Electron microscopic examination of glomerular basement memb
..... For more information please see the full phenotype on the strain data sheet | ||
| 006881 | B6.Cg-Tg(Aqp2-cre)1Dek/J | Repository- Live |
| Mice hemizygous for this AQP2-Cre transgene are viable and fertile. Transgenic cre activity, directed by the mouse aquaporin 2 promoter, is observed in kidney cells (collecting duct) and testes (sperm). When bred with mice containing a loxP-flanked sequence of interest, cre-mediated recombination will result in deletion of the flanked sequence. In such breedings, maternal inheritance of the transgene is recommended for kidney-specific recombinase activity as males express cre in sperm as well as kidney tissues. These AQP2-Cre mice may be used to generate conditional mutations in the renal collecting duct for studying nephrology, physiology, metabolism, or type II diabetes. In addition, cre expression in sperm may be useful in generating conditional mutations in multiple or all tissues in the resulting offspring. | ||
| 006235 | B6.Cg-Tg(SFTPC-rtTA)5Jaw/J | Repository- Live |
| Mice that are hemizygous for this transgenic insert are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the human SFTPC, surfactant, pulmonary-associated protein C, promoter. In situ hybridization detects rtTA gene product (mRNA) in lung peripheral epithelial cells from adult mice and 15 postconception day aged embryos from doxycycline treated dams. Induction of transgene expression is detected as early as postconception day 12.5 when the pregnant female is treated with doxycycline. When mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (tetO), expression of the target gene may be regulated by the tetracycline analog, doxycycline (dox); in the presence of dox, transcription of the target gene is induced in cells where rtTA is
..... For more information please see the full phenotype on the strain data sheet | ||
| 006232 | B6.Cg-Tg(Scgb1a1-rtTA)1Jaw/J | Repository- Live |
| Mice hemizygous for the CCSP-rtTA transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the rat Scgb1a1, secretoglobin, family 1A, member 1 (uteroglobin), gene promoter. rtTA activity detected in bronchial and type II epithelial cells of lung tissue from adult transgenic mice and in embryos from pregnant females treated with the tetracycline analog doxycycline (dox). In the latter, rtTA-induced expression of a luciferase reporter under the regulation of a tetracycline-responsive promoter (TRE; tetO) has been detected as early as embryonic day 12.5. When hemizygotes are mated to a second transgenic strain carrying a gene of interest under the regulatory control of a TRE, expression of the target gene in the bitransgenic offspring can be regulated by dox; in the presence of dox, transcription of the target
..... For more information please see the full phenotype on the strain data sheet | ||
| 006470 | B6;129S-Hopxtm1Eno/J | Repository- Live |
| Homozygous mice are viable and fertile on this mixed genetic background. Absence of the targeted protein is confirmed in heart and brain tissues from homozygotes. The lacZ expression pattern is similar to that of the endogenous gene. Homozygous heart tissues show altered serum response factor (SRF)-associated gene expression. Mice homozygous for this null allele segregate into two phenotypic classes characterized by an excess or deficiency of cardiac myocytes. These mutant mice may be useful in studying cardiac growth and development. | ||
| 007204 | B6;129S4-2610005L07RikGt(ROSA)73Sor/J | Repository- Live |
| Mice homozygous for this mutant allele (called BC058969 in the primary publication) are viable and fertile, with greater than 50% embryonic lethality observed in homozygous embryos. Homozygotes occur at a lower than Mendelian ratio (9%) from heterozygote x heterozygote crosses. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes exhibit defects that affect the same cell types and processes as those controlled by the platelet-derived growth factor (PDGF) pathway, including vasculature, kidney, and skeletal defects (sternum and calvarial bones). Notably, 100% incidence of calvarial bones defects is reported. Additionally, homozygotes are reported to have low b-galactosidase activity; in situ hybridization or other sensitive methods may be necessary to detect expression of the lacZ-neo reporter fusion gene. These BC058969-mutant (2610005L07Rik-mutant) mice may be useful in st
..... For more information please see the full phenotype on the strain data sheet | ||
| 007678 | B6;SJL-Tg(KRT14-rtTA)208Jek/J | Repository- Live |
| Homozygous females and hemizygous males carrying this X-linked K14-rtTA transgene (K14-rtTetA(X) or rtTAX) are viable and fertile. These mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the human keratin 14 promoter. As the transgene is located on the X chromosome, random inactivation of the X chromosome may result in mosaic rtTA expression patterns in female mice. When mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE or tetO), expression of the target gene in the basal cells of the squamous epithelia and in the outer root sheath of the hair follicles is induced with administration of the tetracycline analog, doxycycline (dox). These K14-rtTA mice provide a Tet-On tool that allows the inducible expression of genes in skin cells. | ||
| 006245 | C.Cg-Tg(SFTPC-rtTA)5Jaw/J | Repository- Live |
| Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the human SFTPC, surfactant, pulmonary-associated protein C, promoter. rtTA activity is detected in lung peripheral epithelial cells from adult mice and in embryos from pregnant females treated with the tetracycline analog, doxycycline (dox). In the latter, rtTA-induced expression of a luciferase reporter under the regulation of a tetracycline-responsive promoter (TRE; tetO) has been detected as early as embryonic day 10.5. When hemizygotes are mated to a second transgenic strain carrying a gene of interest under the regulatory control of a TRE, expression of the target gene in the bitransgenic offspring may be regulated by dox; in the presence of dox, transcription of the target gene is induced in cells where rtTA is expressed. This
..... For more information please see the full phenotype on the strain data sheet | ||
| 006242 | C.Cg-Tg(Scgb1a1-rtTA)1Jaw/J | Repository- Live |
| Mice hemizygous for the CCSP-rtTA transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the rat Scgb1a1, secretoglobin, family 1A, member 1 (uteroglobin), gene promoter. In situ hybridization detects rtTA gene product (mRNA) in bronchial and type II epithelial cells of lung tissue from adult transgenic mice treated with doxycycline for 7 days. Induction of transgene expression is detected as early as postconception day 14 when the pregnant female is treated with doxycycline. When mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (tetO), expression of the target gene may be regulated by the tetracycline analog, doxycycline (dox); in the presence of dox, transcription of the target gene is induced in cells where rtTA is
..... For more information please see the full phenotype on the strain data sheet | ||
| 007683 | CByJ.129X1(Cg)-Apobtm1.1Zc/J | Repository- Live |
| Mice homozygous for this apoB38.9 allele (apoB38.9/38.9) are viable with impaired fertility, bearing a premature stop codon at residue 1767 of the targeted gene. As a result, homozygous plasma shows a truncated apoB38.9 as the sole apoB protein. Plasma from heterozygous (apoB+/38.9) mice have reduced apoB100 and apoB48 compared to wild-type, with apoB38.9 representing 20% of total circulating apoB. This apoB38.9 truncation affects both apoB100 and apoB48 metabolism in mice, and mimics human Familial Hypobetalipoproteinemia (FHBL). Homozygous and, to a lesser extent, heterozygous mice exhibit symptoms of FHBL due to impaired lipoprotein export system/VLDL secretion, including elevated hepatic triglyceride (TG), cholesterol and free fatty acids (FFA), with decreased plasma TG and cholesterol. These BALB/cByJ-apoB38.9 mice are also heterozygous for the BALB/cByJ-derived SCAD deletion (Acadsdel-J). While BALB/cByJ inbred mice have elevated liver TG f
..... For more information please see the full phenotype on the strain data sheet | ||
| 006206 | FVB.129S6-Gt(ROSA)26Sortm1(HIF1A/luc)Kael/J | Repository- Live |
| Mice heterozygous for this "ODD-luc" knock-in are viable and fertile with no gross phenotypic or behavioral abnormalities. These mice have the C-terminal portion of the hypoxia-inducible factor 1 alpha (HIF1A) oxygen-dependent degradation domain (ODD) fused to the firefly luciferase (luc) gene. This region of the ODD also contains a proline residue (amino acid 564) that, when hydroxylated, will serve as a binding site for von Hippel-Lindau tumor suppressor protein (pVHL). Under normal oxygen concentrations, prolyl hydroxylation by egg-laying-defective nine (EGLN) proteins leads to pVHL-dependent polyubiquitylation and proteasomal degradation (thus, little or no luciferase fluorescence). Under hypoxia, proline hydroxylation is impaired and ubiquitination is attenuated, resulting in stabilization of the fusion protein and high levels of luciferase fluorescence in the hypoxic tissue(s). These "ODD-Luc" bioluminescent reporter mice may be useful in researching transcriptional
..... For more information please see the full phenotype on the strain data sheet | ||
| 006875 | FVB/N-Tg(Tagln-rtTA)E1Jwst/J | Repository- Live |
| Transgenic SM22-rtTA mice are viable and fertile. These mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the murine SM22-alpha (SM22a or transgelin) promoter. When hemizygotes are mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE; tetO), expression of the target gene in the bitransgenic offspring is inducible in smooth muscle cells with administration of the tetracycline analog, doxycycline. These SM22-rtTA mice provide a "Tet-On" tool that allows the inducible expression of genes in smooth muscle cells. | ||
| 005878 | NOD.Cg-Cd44tm1Hbg/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. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms. 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 f
..... | ||
| 003899 | STOCK Cd44tm1Hbg/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. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms. | ||
| 007674 | STOCK Esrrbtm1.1Nat/J | Repository- Live |
| Mice homozygous for this Nr3b2CKO allele possess loxP sites flanking exon 2 of the targeted gene and are viable and fertile. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have the exon containing the initiator methionine codon and encoding the N-terminal 132 amino acids (including part of the DNA-binding domain) deleted in the cre-expressing tissue(s). Of note, if the conditional Nr3b2CKO is deleted by Cre recombinase in the placenta and embryo, embryonic lethality will result (placental defect). If the conditional Nr3b2CKO is deleted by Cre recombinase only in the embryo, the resulting mice exhibit an inner ear defect (decreased endolymph production) resulting in deafness and defective balance. These Nr3b2CKO mutant mice may be useful in generating conditional mutations to study disorders of hearing and balance, inner ear development (such as endolymph-producing epithelia withi
..... For more information please see the full phenotype on the strain data sheet | ||
| 006473 | STOCK Smyd1tm1Dsr/J | Repository- Live |
| Mice heterozygous for this targeted mutation are viable and fertile. Mice homozygous for this targeted allele, however, die between embryonic day (E) 9.5 and 10.5 due to cardiomyocyte maturation defects, including an enlarged heart, single left-side ventricular chamber with tremendous extra cellular matrix expansion between the myocardial and endocardial layers, and defective Hand2 expression. No mRNA transcripts from the targeted mutant gene are detected in cardiac tissue from E9.5 homozygotes. These mutant mice may be useful in studying cardiomyocyte differentiation and cardiac morphogenesis. 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. | ||
| 007679 | SWR.129X1(B6)-Apobtm1.1Zc/J | Repository- Live |
| Mice homozygous for this apoB38.9 allele (apoB38.9/38.9) are viable with impaired fertility, bearing a premature stop codon at residue 1767 of the targeted gene. As a result, homozygous plasma shows a truncated apoB38.9 as the sole apoB protein. Plasma from heterozygous (apoB+/38.9) mice have reduced apoB100 and apoB48 compared to wildtype, with apoB38.9 representing 20% of total circulating apoB. This apoB38.9 truncation affects both apoB100 and apoB48 metabolism in mice, and mimics human Familial Hypobetalipoproteinemia (FHBL). Homozygous and, to a lesser extent, heterozygous mice exhibit symptoms of FHBL due to impaired lipoprotein export system/VLDL secretion, including elevated hepatic triglyceride (TG), cholesterol and free fatty acids (FFA), with decreased plasma TG and cholesterol. Because plasma and liver lipid profiles range from mild to severe in populations of heterozygous apoB38.9 mice on a mixed (C57BL/6J;129X1/SvJ) genetic background, apoB+/38.
..... For more information please see the full phenotype on the strain data sheet | ||
| 004166 | 129-Itgb5tm1Des/J | Repository-Cryopreserved |
| 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. | ||
| 006187 | B6.129S2-Nr4a1tm1Jmi/J | Repository-Cryopreserved |
| Mice homozygous for this targeted mutation are viable and fertile, with no gross anatomical or behavioral abnormalities. No transcript is detectable in thymus. Following acute neuroleptic administration with dopamine D2 receptor antagonists (haloperidol and/or raclopride), homozygous mice exhibit reduced catalepsy and disrupted neuropeptide responses in the brain. In homozygotes, adrenal expression of Nr4a2 (also called Nurr1) is increased threefold following LPS challenge. Mutant mice may be useful in studies of antipsychotic drug/neuroleptic therapies, schizophrenia, neurobiology, nuclear receptor family transcription pathways, adrenal gland, and steroidogenesis. | ||
| 006142 | B6.129S4-Ppargtm1Rev/J | Repository-Cryopreserved |
| All mice homozygous for this targeted mutation die after gestational day 9.5 from severe placental defects and myocardial thinning. Heterozygotes are viable and fertile. White adipose tissue from heterozygous mice display approximately half the mRNA expression compared to wildtype. Tracer-determined glucose disposal rates and hepatic glucose production show that peripheral tissues and livers from heterozygotes are more sensitive to the effects of insulin than wildtype. This mutation eliminates both DNA-binding and ligand-binding functions of the endogenous gene, concomitantly generating a lacZ reporter that faithfully recapitulates the endogenous expression pattern. Heterozygous mice or homozygous embryo-derived cells may be useful in studies of embryo and placental development, diabetes, atherosclerosis, inflammation, and for beta-galactosidase reporter function of the endogenous gene. | ||
| 004125 | B6.129S6-Abcb11tm1Wng/J | Repository-Cryopreserved |
| Mice that are homozygous null for the Abcb11 gene suffer from lowered rates of viability and fertility. No Abcb11 gene product (mRNA or protein) is detected in liver tissue. Homozygotes display growth retardation with body weights being 80% that of wildtype littermates at weaning. Lower body weights persist throughout life. Ultrastructural changes are noted in the hepatic canaliculi (lumen dilation, microvilli loss, and accumulation of biliary material). Hepatocytes exhibit increased numbers of peroxisomes, lysosomes and lipid droplets with a concomitant decrease in stored glycogen. Although average bile flow is not significantly reduced, secretion of major hydrophobic bile salts is clearly impaired. An increase in the secretion of tetra-hydroxylated bile acids, cholesterol and phospholipids is observed. These mice provide a model for studying intrahepatic cholestasis and the mechanisims associated with lipid homeostasis. | ||
| 006042 | B6.129S7-Efnb2tm2And/J | Repository-Cryopreserved |
| Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice with a cre recombinase gene under the control of a promoter of interest, exon 1 of the targeted gene is deleted in the tissue of interest. These mutant mice may be useful in studying the cellular and molecular mechanisms underlying vasculogenesis and angiogenesis, the topography of neovascularization, and adult neovascularization, including tumor angiogenesis. To test the effectiveness of this model, these mutant mice were bred to an endothelial-specific Cre-expressing transgenic mice, Tg(Tek-cre)12Flv (Stock No. 004128) . Offspring homozygous for the Cre-mediated exon 1 deletion show angiogenic remodeling defects and embryonic death identical to homozygous Efnb2tm1And mice (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 004161 | B6;129-Fgf7tm1Efu/J | Repository-Cryopreserved |
| Mice homozygous for this targeted allele are viable, fertile and normal in size. No Fgf7 transcript is detected. By 2 months of age, the hair coat takes on a matted/greasy appearance that becomes more prominent with age. Homozygote kidneys are markedly smaller and posses structural anomalies. Morphometric analyses indicate a reduction (~30% of wildtype) in the total number of nephrons present. Kidney development appears to be effected as early as embryonic day 16.5. This mutant mouse strain represents a model that may be useful in studies related to kidney disease. | ||
| 007208 | B6;129S4-Axud1Gt(ROSA)80Sor/J | Repository-Cryopreserved |
| Mice homozygous for this Axud1-mutant allele are viable and fertile, with some incidence of perinatal lethality before 2 weeks of age (the Donating Investigator reports 18% of homozygotes die by 2 weeks of age). Homozygotes have abnormalities in palate bone fusion. Homozygotes exhibit defects that affect the same cell types and processes as those controlled by the platelet-derived growth factor (PDGF) pathway, including vasculature, kidney, and skeletal defects. These Axud1-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 007207 | B6;129S4-Zfp640Gt(ROSA)81Sor/J | Repository-Cryopreserved |
| Mice homozygous for this Zfp640-mutant allele are viable and fertile, with abnormalities in palate bone fusion and increased weight gain observed only in males after adolescence. Homozygotes exhibit defects that affect the same cell types and processes as those controlled by the platelet-derived growth factor (PDGF) pathway, including vasculature, kidney, and skeletal defects. Additionally, homozygotes are reported to have low b-galactosidase activity; in situ hybridization or other sensitive methods may be necessary to detect expression of the lacZ-neo reporter fusion gene. These Zfp640-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 004670 | B6;129S6-Abcg5/Abcg8tm1Hobb/J | Repository-Cryopreserved |
| Mice that are homozygous for this targeted allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected in liver or jejunum. A 2 to 3 fold increase in fractional absorption of dietary plant sterols results in plasma sitosterol levels that are elevated 30 fold compared to wildtype levels. Biliary cholesterol levels are low, as are plasma and liver cholesterol levels. Plasma and liver cholesterol levels increase rapidly (2.4 and 18 fold, respectively) following cholesterol feeding. This mutant mouse strain represents a model that may be useful in studies related to sitosterolemia and cholesterol homeostasis. | ||
| 004583 | B6SJL-Tg(ABCG5/ABCG8)14-2Hobb/J | Repository-Cryopreserved |
| These transgenic mice over-express the human ABCG5 and ABCG8 genes under the direction of their endogenous regulatory sequences. Copy number of the transgene was estimated using Southern blot analysis to compare transgenic mouse genomic DNA to human genomic DNA. These transgenic mice have approximately ten copies of the transgene. Northern blot analysis revealed the human transgene is expressed in the liver and small intestine. RT-PCR showed trace levels of transgene transcript in ovary tissue. Absorption of dietary cholesterol in transgenic mice is reduced by 50%. Mean fasting plasma cholesterol levels are significantly lower in female transgenic mice. Excretion of neutral sterols in feces is elevated to three times higher above normal in male transgenic mice and six times higher in female transgenic mice. Bile from transgenic animals is opaque as compared to the clear bile of wildtype animals. Cholesterol in the bile is elevated to levels five times higher than normal in male transge
..... For more information please see the full phenotype on the strain data sheet | ||
| 006768 | D2.Cg-Tg(Myh6-Zfpm2)1Sho/EiJ | Repository-Cryopreserved |
| 006225 | FVB.Cg-Tg(SFTPC-rtTA)5Jaw/J | Repository-Cryopreserved |
| Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The donating investigator reports that homozygous transgenic mice are not viable. These transgenic mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the human SFTPC, surfactant, pulmonary-associated protein C, promoter. rtTA activity is detected in lung peripheral epithelial cells from adult mice and in embryos from pregnant females treated with the tetracycline analog doxycycline (dox). In the latter, rtTA-induced expression of a luciferase reporter under the regulation of a tetracycline-responsive promoter (TRE; tetO) has been detected as early as embryonic day 10.5. When hemizygotes are mated to a second transgenic strain carrying a gene of interest under the regulatory control of a TRE, expression of the target gene in the bitransgenic offspring can be regulated by dox; in the presence of dox, tra
..... For more information please see the full phenotype on the strain data sheet | ||
| 006222 | FVB.Cg-Tg(Scgb1a1-rtTA)1Jaw/J | Repository-Cryopreserved |
| Mice hemizygous for the CCSP-rtTA transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the rat Scgb1a1, secretoglobin, family 1A, member 1 (uteroglobin), gene promoter. rtTA activity is detected in bronchial and type II epithelial cells of lung tissue from adult transgenic mice and in embryos from pregnant females treated with the tetracycline analog doxycycline (dox). In the latter, rtTA-induced expression of a luciferase reporter under the regulation of a tetracycline-responsive promoter (TRE; tetO) has been detected as early as embryonic day 12.5. When hemizygotes are mated to a second transgenic strain carrying a gene of interest under the regulatory control of a TRE, expression of the target gene in the bitransgenic offspring can be regulated by dox; in the presence of dox, transcription of the targ
..... For more information please see the full phenotype on the strain data sheet | ||
| 004222 | NOD.129P2(B6)-Il4tm1Cgn/DvsJ | Repository-Cryopreserved |
| Complete Freund's adjuvant (CFA) induced suppression of diabetes in NOD mice has been associated with a shift to Th2 cytokine production. NOD mice deficient in IL4 were created to investigate the role of IL4 in this shift. Mice homozygous for the Il4tm1Cgn targeted mutation are viable and fertile. T and B cell development is normal but IgG1and IgE levels and the ability of homozygous mutant mice to produce Th2-derived cytokines are significantly reduced. IL4 deficient NOD mice develop IDDM with the same incidence as standard NOD/Lt controls, and there is no change between IL4 deficient and wildtype NOD in disease protection conferred by treatment of bacillus Calmette-Guerin vaccine (BCG) or CFA. Both IL4 deficient and wildtype NOD mice are significantly protected from insulitis by treatment of CFA but not by treatment of BCG. (Serreze et al 2001) | ||
| 004266 | NOD.Cg-Il10tm1Cgn/DvsJ | Repository-Cryopreserved |
| 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. | ||
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IMPORTANT NOTE: Price information is on the strain data sheet which can be viewed by clicking on the strain name.
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 002574 | NOD.129P2(B6)-Il4tm1Cgn/Dvs | Research Strain |
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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 Under Development
Select the strain name to link to the strain data sheet.
New Strains Under DevelopmentThe Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.
- Receive periodic updates on the status of the colony UNDER DEVELOPMENT
- Obtain advance notification of strain availability and opportunity to order prior to the strain being published as available
- Provide input affecting speed and quantity of availability
It is VERY IMPORTANT that you register interest in strains Under Development. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain Under Development. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.
- Strains that will be made available from a live distribution colony at The Jackson Laboratory.
These strains are designated as: "Under Development for Distribution Colony"- Strains that will be made available through the Cryopreservation Repository.
These strains are designated as: "Under Development for Cryopreservation Repository"
Send questions to our Technical Support team using the Express Technical Support Form.
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