Search Criteria: Research Area is "Cardiovascular Research: Vascular Defects"
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 003658 | STOCK Tg(TIE2GFP)287Sato/J | Level 4 |
| This strain expresses Green Fluorescent Protein (GFP) under the direction of the endothelial-specific receptor tyrosine kinase (Tek, formerly, Tie2) promoter. Endothelial cells expressing GFP can be visualized via fluorescent microscopy or purified by FACS. | ||
| 007175 | 129S-Cyp4a14tm1Jhc/J | Repository- Live |
| Mice homozygous for this "Cyp 4a14" mutant allele are viable and fertile. Homozygous deficiency of the targeted gene leads to spontaneous hypertension (more severe in males) that is androgen-sensitive. Homozygotes also exhibit other interrelated metabolic and regulatory effects; increased renal vascular resistance, impaired renal hemodynamics, elevated plasma androgens (5a-dihydrotestosterone (DHT) and testosterone), upregulated Cyp4a12 gene expression, and increased formation of prohypertensive 20-HETE. These "Cyp 4a14" mutant mice may be useful studying kidney function and metabolism, cardiovascular physiology, hypertension, and the relationships between blood pressure, sex hormones, and p450 w-hydroxylases. | ||
| 007205 | 129S-Myo1eGt(ROSA)74Sor/J | Repository- Live |
| Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mice are anemic (low hemoglobin concentration, red blood cell count, hematocrit). These mice also exhibit polychromasia (abnormally high number of immature blood cells). Homozygotes occur at lower than Mendelian ratio (15%). Although homozygotes are fertile, pregnancy is occasionally lethal for homozygous females. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Myo1e-mutant mice may be useful in studying vascular development, hematopoiesis and cellular signaling during development and in 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. | ||
| 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 | ||
| 001649 | A.BY H2bc H2-T18f/SnJ-Dstncorn1/J | Repository- Live |
| Mice homozygous for the recessive Dstncorn1 mutation have abnormally proliferative basal corneal epithelial cells. Focal areas of corneal epithelial hyperplasia are found by one week of age, and neovascularization is found by 14 days of age when the eyes open. This neovascularization, which progresses during the first two months of age, is not found in mice homozygous for the Dstncorn-2J allele (which is a point mutation leading to a change in a single amino acid residue). In both mutants the corneal epithelial cells show increased levels and altered organizational pattern of filamentous actin. The areas of thickened cortical epithelia yield a roughened, opaque corneal surface. At 4 weeks of age in Dstncorn1 homozygotes, expression of keratin 14 and involucrin extend into the suprabasal layer in the areas of hyperplastic corneal epithelia. There is also an increase in the levels of expression of cofilin 1, lumican and kerat
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| 006336 | B6.129-Selplgtm1Rpmc/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 (protein) is detected by flow cytometry analysis of leukocytes. Homozygotes have elevated total leukocyte counts, with increased numbers of neutrophils, lympohcytes and eosinophils. Leukocytes isolated from homozygotes exhibit abnormal tethering and rolling (adhesion and migration) due to impaired attachment. This mutant mouse strain represents a model that may be useful in studies of leukocyte adhesion and migration in the inflammatory response. This strain was transferred from the collection of the Consortium for Functional Glycomics. | ||
| 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. | ||
| 005940 | B6.129S1-Csf2rbtm1Cgb/J | Repository- Live |
| Homozygous mice are viable and fertile with no behavioral abnormalities. In response to GM-CSF, bone marrow and splenocytes from homozygous mice fail to exhibit proliferation, enhanced survival in vitro, or synergistic interaction with M-CSF. They also fail to proliferate in response to IL-5. IL-3 binding and responses are unaffected. Cell composition in thymus, spleen, bone marrow, and lymph node is not significantly altered. Circulating eosinophils are dramatically reduced in blood with lesser reduction in bone marrow and tissues. Homozygous mice develop pulmonary peribronchovascular lymphoid infiltrates and areas resembling pulmonary alveolar proteinosis (PAP). Consistent with this, mutant mice have greatly increased surfactant protein-B and D accumulation in lung/airway tissue, no attenuation of saturated phosphatidylcholine with advancing age, and high levels of GM-CSF in bronchoaveolar lavage fluid. Homozygous mice are resistant to intradermal Leishmania major infection an
..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 002778 | B6.129S2-Alox15tm1Fun/J | Repository- Live |
| Homozygous (12/15-LO-deficient) mutant mice are viable and fertile. 12/15-LO-deficient mice develop a myeloproliferative disorder (MPD) (similar to human chronic myelogenous leukemia (CML)) that progresses to transplantable leukemia. Chronic MPD stage homozygotes exhibit increased activation of the phosphatidylinositol 3–kinase (PI3-K) pathway, hyperphosphorylation/decreased nuclear accumulation of the transcription factor interferon consensus sequence binding protein (ICSBP), and increased expression of the oncoprotein Bcl-2; all of which are reversible upon treatment with a PI3-K inhibitor. The evolution of MPD to leukemia is associated with additional regulation of ICSBP at the RNA level. Peritoneal macrophages have altered arachidonic acid metabolism as well as a diminished ability to oxidize low density lipoprotein (LDL) following stimulation. These mutant mice may be useful in studying myeloproliferative disorders, chronic myelogenous leukemia, and other cancers. | ||
| 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 | ||
| 006243 | B6.129S4-Timp1tm1Pds/J | Repository- Live |
| Homozygous females and hemizygous males (the gene is X-linked) are viable and fertile. No endogenous transcript is detected in lung tissue from affected mice by Northern blot analysis.. Homozygous mice have increased resistance to corneal and pulmonary infection with P. aeruginosa, and have altered immune, hematopoietic, and vascular permeability in bleomycin-induced lung injury trials. Homozygotes also show increased and continued progression of aneurysm formation compared with wild-type mice in induced thoracic aortic aneurysm (TAA) models. Mice with this X-linked targeted mutation may be useful in studies of cornea and pulmonary infection, pulmonary injury and aneurysm, as well as of P. aeruginosa resistance in individuals with unresolved, antibiotic-resistant pulmonary infections, such as those often observed in cystic fibrosis patients.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genet
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| 008039 | B6.129S7-Gja1tm1Dlg/J | Repository- Live |
| Mice homozygous for this Cx43flox conditional allele are viable and fertile, with loxP sites flanking exon 2 of the targeted gene. Presence of the loxP sites has no reported affect on expression of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have exon 2 deleted in the cre-expressing tissue(s). These Cx43flox mutant mice may be useful in generating conditional mutations for studying the role of connexin and gap junctions in various tissues and systems, including the cardiovascular system. | ||
| 006112 | B6.129X1-Ela2tm1Sds/J | Repository- Live |
| Homozygous mice are viable, fertile and phenotypically normal in the absence of inflammatory stress. Homozygotes do not express the targeted gene in bone marrow myeloid cells. Homozygous mice have increased susceptibility to sepsis, morbidity, and mortality following intraperitoneal injection of Gram-negative (e.g. (K. pneumoniae and E. coli), but not Gram-positive (e.g. (S. aureus), bacteria. Despite this, mutant mice are not at increased risk to spontaneous infection. Although neutrophil, T cell, and macrophage migration/recruitment to the site of infection is unaffected in homozygous mutant mice, neutrophils show impaired bactericidal activity. Further, homozygous mice treated with a broad-spectrum inflammatory stimulus (zymosan) have impaired leukocyte firm adhesion and transmigration as well as reduced pro-inflammatory cytokine production. Upon exposure to cigarette smoke, homozygous mice are protected from the accumulation of neutrophils and macrophages in th
..... For more information please see the full phenotype on the strain data sheet | ||
| 000002 | B6.C3-Pde6brd1 Hps4le/J | Repository- Live |
| 007083 | B6.Cg-Cav1tm1Mls/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile and do not display any gross physical abnormalities. Mutant mice exhibit exercise intolerance when challenged and are slightly hyperphagic. No gene product (protein) is detected by Western blot analysis in adipose, lung and heart tissues or in cultured mouse embryonic fibroblasts (MEFs). A decrease in the level of co-expressed caveolin-2 protein is immunodetected. At age 4-5 months, mutant mice are often smaller than their wildtype littermates. By one year of age, mutant mice weigh 5 to 7 grams less than wildtype, and are resistant to diet-induced obesity. Progressive adipose pathology results in reduced white adipose tissue with abnormally small adipocytes and enlarged, hyperplastic brown adipose tissue. Homozygotes display lipid metabolism and uptake disruption with elevated serum triglycerides and free fatty acid levels, and reduced leptin levels. Isolated aortic tissue segments have a diminished vasoconstriction
..... For more information please see the full phenotype on the strain data sheet | ||
| 006137 | B6.Cg-Tg(Cdh5-cre)7Mlia/J | Repository- Live |
| Hemizygotes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. In the differentiated endothelium transgene expression is observed as early as E7.5 and progresses to almost full penetrance by E14.5. In adult mice, uniform cre expression is observed in the endothelium of developing and quiescent vessels of all organs examined, as well as within a subset of hematopoietic cells. When bred with any mouse containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the flanked genome. These mice may be useful in studies of the cardiovascular system, including angiogenesis, and endothelial and hematopoietic cell lineages. | ||
| 004659 | B6.Cg-Tg(TIE2GFP)287Sato/1J | Repository- Live |
| This strain expresses Green Fluorescent Protein (GFP) under the direction of the endothelial-specific receptor tyrosine kinase (Tek, formerly, Tie2) promoter. Endothelial cells expressing GFP can be visualized via fluorescent microscopy or purified by FACS. 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. | ||
| 004669 | B6;129S2-Itgb3tm1Hyn/J | Repository- Live |
| Mice that are homozygous for this targeted allele are viable and fertile. No gene product (protein) is detected on the surface of platelets. Significant (50%) embryonic lethality attributed to fetal hemorrhaging and placental defects is observed. Until three weeks of age, additional pup loss may occur due to hemorrhaging in the skin and gastrointestinal tract. Gastrointestinal tract bleeding is commonly observed in adults and is frequently associated with an enlarged spleen. Erythrocyte number, hemoglobin, hematocrits and thrombus formation are all reduced while bleeding time is prolonged. Varying degrees of liver and kidney necrosis are also observed. Although increased numbers of osteoclasts are observed (3.5 fold over that seen in heterozygotes) they appear to be dysfunctional, having a reduced ability to resorb whale dentin in vitro. Mice are osteosclerotic and hypocalcemic. Enhanced tumor angiogenesis and vascular endothelial growth factor-induced blood vessel growth are observed.
..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 007202 | B6;129S4-5830428H23RikGt(ROSA)76Sor/J | Repository- Live |
| At age E11.5 to E18.5, homozygous embryos exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mice are anemic (low hemoglobin concentration, red blood cell count, hematocrit). These mice also exhibit polychromasia (abnormally high number of immature blood cells); kidney defects (abnormally high blood urea nitrogen level, kidney size smaller than wildtype, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells in glomeruli); abnormalities in palate bone fusion and abnormal neural crest derived and thoracic skeleton development. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes occur at lower than Mendelian ratio (18%) and 8% die by age 1 week. Surviving homozygotes and heterozygotes are viable and fertile. These 5830428H23Rik (BC055757)-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases
..... For more information please see the full phenotype on the strain data sheet | ||
| 006238 | B6;129S4-Thbs2tm1Bst/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile. Multiple analyses has confirmed the absence of protein in embryonic and adult tissue of homozygous mice. Homozygotes exhibit skin disorders (abnormal collagen fiber patterns, reduced tensile strength, increased fragility) and skin fibroblasts have attachment defects. Mice also exhibit an increase in total density/cortical thickness of the long bones, abnormally long bleeding times, and a significant increase in blood vessel density. Homozygous mice exhibit accelerated wound healing after biopsy and accelerated/increased tumor formation following chemically-induced skin carcinogenesis. Mutant mice may be useful in studies of collagen fibrillogenesis in skin and tendons, angiogenesis and vascular pathophysiology, wound healing, chemically-induced tumor progression, and as a potential model for Ehlers Danlos syndrome. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are fre
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| 007206 | B6;129S4-TiparpGt(ROSA)79Sor/J | Repository- Live |
| Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mice are anemic (low hemoglobin concentration, red blood cell count, hematocrit). These mice also 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, degraded glomeruli are often observed, increased number of vascular smooth muscle cells partially filling the glomeruli space); and abnormalities in palate bone fusion. Homozygotes occur at lower than Mendelian ratio (22%), and 32% die by age 2 week. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Tiparp-mutant mice may be useful in studying kidney development, vascular development, hematopoiesis and cellular signaling during development and in adult mice; specifically receptor tyrosine
..... For more information please see the full phenotype on the strain data sheet | ||
| 006028 | B6;129S6-Epha2tm1Jrui/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile with no overt developmental or behavioral abnormalities. The Jackson Laboratory is distributing these mice on their original C57BL/6;129S6 mixed background. The published phenotype of these mutant mice is described below. In mutant mice of a mixed BALB/c, C57BL/6, and 129S6 background, murine pulmonary microvascular endothelial cells (MPMEC) isolated from homozygotes express no endogenous protein. MPMEC show impaired ephrin-A1-induced vascular assembly and defective migration both in vitro and in vivo. In addition, MPMEC from homozygous mice exhibit decreased angiogenesis and fail to activate Rac1 in response to ephrin-A1 in vivo. Mutant mice crossed to BALB/c for 7 generations are protected from tumor progression, angiogenesis and metastasis following metastatic mammary adenocarcinoma cell transplantation. These mutant mice may be useful in studies of postnatal angiogenesis (endothelial cell migra
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| 006044 | B6;129S7-Ephb4tm1And/J | Repository- Live |
| Mice homozygous for this targeted mutation show growth retardation and lack of blood flow by embryonic day 9.5-10 (E9.5-10), with lethality occurring around this time. Expression of lacZ occurs exclusively in embryonic vascular endothelial cells and is preferentially expressed on veins. Homozygous embryos show defective angiogenic remodeling at the capillary plexus stage in both yolk sac and head. Arrested cardiac morphogenesis and defective myocardial trabecular extensions are also observed. Heterozygous mice are viable, fertile, exhibit no behavioral defects, and have identical lacZ expression patterns. 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. The developmental abnormalities in homozygous mice closely resemble those observed for mutant mice bearing a lacZ-expressing null mutation
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| 006070 | CBy.129S6(B6)-Epha2tm1Jrui/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable, fertile, and display no overt developmental or behavioral abnormalities. In mutant mice of a mixed BALB/c, C57BL/6, and 129S6 background, murine pulmonary microvascular endothelial cells (MPMECs) isolated from homozygotes express no endogenous protein. MPMECs from Epha2-deficient mice show impaired ephrin-A1-induced vascular assembly and defective migration both in vitro and in vivo. In addition, MPMECs from homozygous Epha2 mice exhibit decreased angiogenesis and fail to activate Rac1 in response to ephrin-A1 in vivo. Mutant mice on a BALB/c background that were transplanted with metastatic mammary adenocarcinoma cells showed impaired tumor progression, angiogenesis and metastasis to the lung, compared with wildtype littermate controls. These mutant mice may be useful in studies of postnatal angiogenesis (endothelial cell migration, assembly into new tubules, and cytoskeletal regulation), or as a
..... For more information please see the full phenotype on the strain data sheet | ||
| 006125 | FVB-Tg(H2-D-Il15)3304Clgr/J | Repository- Live |
| Mice hemizygous for this transgene are viable and fertile. The transgene was designed to optimize the overexpression of secreted, mature interleukin-15. Transgenic IL-15 expression has a similar tissue distribution as the endogenous gene, but at a significantly higher level. IL-15 protein is detectable in the serum from most mutant, but not from wildtype, mice. Mutant mice develop a progressive alopecia by as early as 5-6 weeks of age, with skin lesions appearing over time. While all transgenic mice exhibit early polyclonal/benign expansion of natural killer and memory CD8+ T lymphocytes (T/NK), two distinct phenotypes emerge over time: approximately 70% of the transgenic mice will exhibit polyclonal T/NK progression in multiple tissues, while the remaining 30% are characterized by T/NK clonal expansion in multiple tissues and acute lymphoblastic leukemia (T/NK ALL). Both T/NK phenotypes are fatal within the first year of life. Mice harboring this transgene may be useful in
..... For more information please see the full phenotype on the strain data sheet | ||
| 004585 | STOCK Cav1tm1Mls/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile and do not display any gross physical abnormalities. Mutant mice exhibit exercise intolerance when challenged and are slightly hyperphagic. No gene product (protein) is detected by Western blot analysis in adipose, lung and heart tissues or in cultured mouse embryonic fibroblasts (MEFs). A decrease in the level of co-expressed caveolin-2 protein is immunodetected. At age 4-5 months, mutant mice are often smaller than their wildtype littermates. By one year of age, mutant mice weigh 5 to 7 grams less than wildtype, and are resistant to diet-induced obesity. Progressive adipose pathology results in reduced white adipose tissue with abnormally small adipocytes and enlarged, hyperplastic brown adipose tissue. Homozygotes display lipid metabolism and uptake disruption with elevated serum triglycerides and free fatty acid levels, and reduced leptin levels. Isolated aortic tissue segments have a diminished vasoconstriction
..... 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. | ||
| 006203 | B6.129(FVB)-Ahrtm3.1Bra/J | Repository-Cryopreserved |
| These mice possess loxP sites on either side of exon 2 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Hepatic protein expression of the conditional allele (before exon 2 excision) is equivalent to wildtype by Western blot analysis. This strain may be useful in generating tissue-specific mutants of the floxed allele for use in studies including teratogenesis and xenobiotic metabolism (including dioxin and PCB), Per-Arnt-Sim transcription factors, and fetal vascular development such as ductus venosus closure.
When bred to a strain expressing Cre recombinase in hepatocytes (see Stock No. 003574 for example), this mutant mouse strain may be useful in studies of toxicology. When bred to a strain expressing Cre recombinase in endothelial cells (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 003178 | B6.129-Arnttm1Mcs/J | Repository-Cryopreserved |
| Arnt-/- embryonic stem cells fail to activate genes that normally respond to low oxygen tension. They also fail to respond to a decrease in glucose concentration, indicating that ARNT is crucial in the response to hypoxia and to hypoglycaemia. Arnt-/- embryos were not viable past embryonic day 10.5 and showed defective angiogenesis of the yolk sac and branchial arches, stunted development and embryo wasting. The defect in blood vessel formation in Arnt-/- yolk sacs is similar to the angiogenic abnormalities reported for mice deficient in vascular endothelial growth factor or tissue factor. | ||
| 002938 | B6.129-Kdrtm1Jrt/J | Repository-Cryopreserved |
| Mice homozygous for the Kdrtm1Jrt targeted mutation (formerly called Flk1) die at ~E8.5-E9.5 due to defects in hematopoietic and endothelial development. Embryos lack blood islands at E7.5 and fail to form organized blood vessels. There is severe reduction in hematopoietic progenitor cells. | ||
| 005617 | B6.129P-Psen2tm1Bdes/J | Repository-Cryopreserved |
| 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 or Western blot analysis. Alveolar wall thickening, fibrotic deposits, hemorahages in alveoli and airways are observed by histological analysis of lung tissue from homozygotes 3 months of age and older. This mutant mouse strain may be useful in studies of Alzheimer's disease. | ||
| 004159 | B6.129P2-Adra1btm1Cta/J | Repository-Cryopreserved |
| Mice that are homozygous null for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Adra1b transcripts are detected. The amount of alpha 1 adrenergic recptor binding activity as measured by radioligand assays is dramatically decreased in homozygous liver, heart and cerebral cortex. The blood pressure response induced by increasing doses of phenylephrine is reduced by 45% in comparison to wild type mice. Similarly, phenylephrine-induced contraction of aortic tissue is diminished 25%. This mutant mouse strain represents a model that may be useful in studies related to blood pressure regulation. | ||
| 002681 | B6.129P2-Agttm1Unc/J | Repository-Cryopreserved |
| Newborn homozygotes for the targeted disruption of Agt have no obvious pathological defects although only a few survive to adulthood. There are pathological changes in adult kidney and blood vessels. The effect of gene copy number was examined using these mice and C57BL/6J-TgH(Agtdup)1Unc (002690). Plasma angiotensinogen levels increase progressively, although not linearly, from zero in zero-copy (Agttm1Unc/Agttm1Unc) mice to 145% of normal in four-copy (Agtdup/Agtdup) mice. Mice of all genotypes are normal at birth, but most zero-copy animals show pathological changes as adults, the kidneys are normal in the other genotypes. The blood pressures of the one-copy through four-copy animals show significant and almost linear increases of approximately 8mmHg per gene copy despite their normal compensatory mechanisms being intact. | ||
| 002690 | B6.129P2-Agttm2Unc/J | Repository-Cryopreserved |
| The entire agiotensinogen gene (Agt) was duplicated by homologous recombination allowing the examination of the effects of gene copy number on normal AGT function. Homozygous mice (Agtdup/Agtdup) are viable and fertile. They show blood pressure levels ~16 mmHg higher than normal wildtype siblings (two copies of Agt gene). Hemizygous mice (Agtdup/+) show blood pressure levels ~8 mmHg higher than normal wildtype siblings. This transgenic demonstrates the causality between genotypes at the angiotensinogen locus and blood pressures. Blood pressures of one-copy (Agttm1Unc/+) through four-copy (Agtdup/Agtdup) animals show significant and almost linear increases of approximately 8mmHg per gene copy despite their normal compensatory mechanisms being intact. | ||
| 002830 | B6.129P2-Plgtm1Jld/J | Repository-Cryopreserved |
| Mice homozygous for the Plgtm1 targeted mutation are viable and fertile. They show a progressive multi-organ pathology and die around 6 months of age. The pathology is characterized by wasting, rectal prolapse, impaired skin wound healing, gastointestinal ulceration, and thrombosis. No details of mammary gland morphology have been provided. | ||
| 006184 | B6.129P2-Tbxas1tm1Swl/J | Repository-Cryopreserved |
| Homozygotes are viable and fertile with no gross physical or behavioral abnormalities. Northern blot show absence of a full length transcript in homozygous spleen and thymus. Homozygous mice exhibit prolonged bleeding time, defective platelet aggregation, and are protected from arachidonic acid induced-shock. These mice may be useful in studies of vascular biology, including hemostasis and thrombosis, as well as human TXAS-deficiency. | ||
| 002270 | B6.129S-Fn1tm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for the Fn1tm1Hyn targeted mutation die during early embryonic development. Blastocyst development and implantation of homozygotes is normal. Gastrulation is initiated and appears normal, including extensive mesodermal movement. From embryonic day 8 onwards homozygous mutant embryos deteriorate through the 10th and 11th days of gestation. Homozygous mutant embryos have a shortened anterior-posterior axes, fail to develop a notochord or somites, and have abnormal development of the heart, blood vessels, and yolk sac indicating a general deficiency in mesodermally derived tissues. Heterozygous mice are viable for at least 2 years and appear healthy and approximately the same size as wild-type littermates. Plasma levels of fibronectin in heterozygotes are 50% lower than normal wildtype siblings. | ||
| 002463 | B6.129S-Itga4tm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for the Itga4tm1Hyn targeted mutation die during embryonic development. Homozygous mutant embryos fail to fuse the allantois with the chorion during placentation. There is a defect in the epicardium and coronary vessels results in in utero cardiac hemorrhage; also known as CD49D, VLA-4. | ||
| 002274 | B6.129S-Itga5tm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for the Itga5tm1Hyn targeted mutation die during embryonic development. Homozygous mutant embryos exhibit defects in the vasculature of the yolk sac and the embyro as well as severe defects in posterior and extraembryonic mesoderm. Implantation and initiation of gastrulation and neurulation is normal. There is normal development of notochord, somite and considerable development of brain, optic and otic anlagen and branchial arches. | ||
| 005669 | B6.129S-Runx1tm1Spe/J | Repository-Cryopreserved |
| Heterozygous mice are viable, fertile, devoid of hemorrhagic lesions, and exhibit mild hematopoietic impairment. Mice that are homozygous for the targeted mutation have an embryonic lethal phenotype; animals are alive at embryonic day 11.5, but start dying at embryonic day 12.5. Embryos exhibit extensive hemorrhagic lesions in the central nervous system including the intraventricular regions and metencephalon as well as segmental bleeds at the VII-VIII cranial nerve complex, cervical, thoracic, and caudal regions. At embryonic day 10.5, symmetrical and bilateral necrosis preceding hemorrhage is observed in homozygotes. Homozygous disruption of the endogenous gene completely blocks definitive erythropoiesis, myelopoiesis, and lymphopoiesis. This mutant may be useful in leukemia studies as disruption of the human homolog of this gene is associated with many different leukemias. | ||
| 005963 | B6.129S1-Csf2rb2tm1Cgb Csf2rbtm1Clsc/J | Repository-Cryopreserved |
| Mice homozygous at both loci are viable and fertile with no behavioral abnormalities. Steady state hematopoiesis is normal. Bone marrow from homozygous mice fail to exhibit any cellular responses to GM-CSF, IL-5, or IL-3. Like the similar strain (Stock No. 005940; Csf2rbtm1Cgb), double homozygous mice exhibit eosinopenia, increased surfactant accumulation in lung tissue and pulmonary alveolar proteinosis (PAP), infection resistance, and attenuated tissue repair after injury. This mutant may be useful in studies of PAP, lung physiology and disease, surfactant homeostasis and metabolism, innate immunity, cytokine signaling, myoproliferative disease, hematopoietic cell populations requiring IL-3, GM-CSF, or IL-5 for development and function, and models of ischemic, traumatic, toxic, and inflammatory injuries. | ||
| 004371 | B6.129S2(D2)-Vtntm1Dgi/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) was immunodetected. Serum from mutant mice has no plasma plasminogen activator inhibitor 1 (PAI-1) binding capacity and can not support cell spreading on tissue culture plastic surface. Thrombosis rate after arterial injury is enhanced and angiogenesis in response to tissue injury is decreased in mutant mice. This mutant mouse strain represents a model that may be useful in studies of the in vivo function of vitronectin. | ||
| 004042 | B6.129S2-Alox12tm1Fun/J | Repository-Cryopreserved |
| Mice that are homozygous null for the Alox12 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Alox12 protein product or enzyme activity is detected in platelets derived from homozygous null animals. Platelets exhibit a hyperresponsiveness to ADP-induced aggregation. Studies examining basal transepidermal water loss indicate that null animals exhibit greater water loss through the skin when compared to control animals. | ||
| 003865 | B6.129S2-Itgavtm1Hyn/J | Repository-Cryopreserved |
| The majority (80%) of homozygous null Itgav mice die during embryonic days 9.5-11.5. These mice are characterized by pericardial edema and retarded growth probably due to placental defects. Mice surviving this period die at birth exhibiting intracranial and intestinal hemorrhaging. Angiogenesis in other tissues is normal. Cleft palate is also observed. | ||
| 006039 | B6.129S7-Efnb2tm1And/J | Repository-Cryopreserved |
| Mice homozygous for this targeted mutation show growth retardation and enlargement of the heart at embryonic day 10 (E10), with 100% lethality occurring around E11. Reporter protein expression patterns are consistent with arterial, but not venous, expression of the endogenous gene; prominent lacZ signal is observed in hindbrain and somites, with lower levels in aorta and heart as early as E8.25. Expression in the yolk sac was first detected at E8.5, and is also observed in nephrogenic mesoderm and branchial arches. Homozygous embryos show defective angiogenic remodeling at the capillary plexus stage in both yolk sac and head. Endothelial vessel support cell differentiation of the yolk sac is also defective. Homozygotes lack myocardial trabecular extensions, and capillary ingrowth into the neural tube does not occur. Heterozygous mice are viable, fertile, exhibit no behavioral defects, and have identical lacZ expression patterns. These mutant mice may be useful in studying
..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 004863 | B6.129X1-Snap25tm1Mcw/J | Repository-Cryopreserved |
| Homozygous mutant mice die at birth from respiratory failure. At embryonic day 17.5 to 18.5 homozygous embryos appear smaller and do not display spontaneous movement or sensorimotor reflexes. Dilated vascular channels in subcutaneous tissues give the embryos an external blotchy appearance. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of brain tissue from homozygous animals. Histological analysis of fetal diaphragm tissue reveals a dispersed pattern of innervation and fewer layers of muscle fibers. Thin, disarrayed intercostal and anterior chestwall muscles are also observed. Spontaneous miniature endplate potential (mEPP) activity is detected in the diaphragm phrenic nerve, but no evoked endplate potentials (EPP), evoked neurotransmitter release or muscle contraction is detected with stimulation of the neuromuscular junction (NMJ). Mutant NMJs exhibit larger endplate diameters and lower levels of acetylcholinesterase. Tetrodotoxin (TTX) resistant m
..... For more information please see the full phenotype on the strain data sheet | ||
| 004202 | B6.C3 Pde6brd1 Hps4le/+ +-Lmx1adr-8J/J | Repository-Cryopreserved |
| 001623 | B6.D2-Car2n/J | Repository-Cryopreserved |
| In human, CAR2 deficiencies can result in osteopetrosis, renal tubular acidosis, impaired growth, cerebral calcification, and mental retardation. Mice homozygous for Car2<n> do not display cerebral calcification or osteopetrosis, although medial calcification of small arteries has been found in several organs, most notably the male genital tract. The phenotype of these mice includes renal tubular acidosis, doubled urine output, increased urine pH and Cl-, decreased blood pH and HCO-3, phosphatemia, lower plasma bicarbonate, and a smaller body size. Despite smaller body weight, the kidneys are of normal size and plasma potassium and creatinine levels are normal. Type A and B intercalated cells of the kidney are severely depleted. Car2n homozygotes have reduced susceptibility to audiogenic and chemogenic seizures and hippocampal slices from homozygotes are more resistant to hypoxia than are those of wild type controls. Increase
..... For more information please see the full phenotype on the strain data sheet | ||
| 002511 | B6;129-Adra2btm1Gsb/J | Repository-Cryopreserved |
| Homozygotes are viable and fertile. They exhibit an absence of alpha2-mediated peripheral vasoconstriction. | ||
| 003807 | B6;129S-Seletm1Hyn Selltm1Hyn Selptm1Hyn/J | Repository-Cryopreserved |
| Mice that are homozygous null for the Sele, Sell and Selp genes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities at birth. As mice mature, however, they become susceptible to mucocutaneous infections that eventually lead to death. No Sele, Sell or Selp gene products (mRNA or protein) are detected. Leukocytes from these mice exhibit a deficiency in the ability to interact with, and roll along, the venular wall endothelium. This deficiency in the crucial first step of leukocyte recruitment to surrounding tissues in response to infection or injury contributes to an elevated leukocyte count in the peripheral blood. Delays in neutrophil and eosinophil recruitment to the peritoneum in response to thioglycollate and ragweed allergen, respectively, have been observed, specifically. These mice are suitable for use in research applications studying leukocyte homeostasis, infectious diseases and inflam
..... For more information please see the full phenotype on the strain data sheet | ||
| 003806 | B6;129S-Seletm1Hyn Selltm1Hyn/J | Repository-Cryopreserved |
| Mice that are homozygous null for the Sele and Sell genes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Sele or Sell gene products (mRNA or protein) are detected. A slightly diminished response in neutrophil recruitment to the peritoneum in response to thioglycollate is observed, as is a diminished ability to interact with the venular endothelium resulting in increased "rolling" along the vessel wall. These mice are suitable for use in research applications studying leukocyte homeostasis, infectious diseases and inflammation. | ||
| 002916 | B6;129S2-Seletm1Hyn Selptm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for both the Seletm1Hyn Selptm1Hyn mutations are viable and fertile. They are characterized by leukocytosis, spontaneous bacterial infections, dermatitis and defective leukocyte recruitment in many models of inflammation. | ||
| 002915 | B6;129S2-Seletm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for the Seletm1Hyn targeted mutation are viable and fertile. Homozygous mutant mice show only subtle defects in leukocyte recruitment, unless P-selectin (Selp) is also ablated or blocked with antibody. | ||
| 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. | ||
| 006182 | B6;129S6-Ptgs1tm1Fun/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Reduced gene product (protein) levels, 10% of wildtype levels, are detected by Western blot analysis of nonstimulated peritoneal macrophages. RT-PCR analysis of stomach and kidney tissue reveals that gene product (mRNA) levels are reduced by 70-73%. This allele is a hypomorph. Mutant mice have a reduced response to arachidonic acid and capsaicin evoked ear inflammation and to carrageenan induced paw edema. Platelet aggregation is impaired as indicated by resistance to arachidonic acid induced thrombosis in vivo, and failure to aggregate in response to arachidonic acid in vitro. Mutant mice exhibit lengthened bleeding time. This mutant mouse strain may be useful in studies related to inflammatory immune response and thrombosis. | ||
| 002637 | B6SJL-Tg(CAMalpha1b)7Wjk/J | Repository-Cryopreserved |
| Mice carrying the CAMalpha1b transgene display stable myocardial specific hypertrophy with ensuing markers of hypertrophy being elevated. In addition, alpha 1 adrenergic receptor signaling through the Gq-phospholipase C-protein kinase C signaling pathway is enhanced. | ||
| 002907 | C.129S4(B6)-Col3a1tm1Jae/J | Repository-Cryopreserved |
| Mice homozygous for the Col3a1tm1Jae targeted mutation exhibit a shorter life span with approximately 10% of homozygous mutant mice surviving to adulthood. The major cause of death of is rupture of the major blood vessels. | ||
| 005057 | FVB.129-Kcnj2tm1Swz/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation have a complete cleft of the secondary palate and die within 12 hours of birth. Heterozygotes 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 analysis of cardiac tissue or Southern blot analysis. Inwardly rectifying potassium ion currents are absent in cerebral artery myocytes and cardiac ventribular myocytes isolated from homozygote neonates. Elevated external potassium ion concentrations do not dilate isolated neonatal cerebral arteries. Homozygotes exhibit altered electrocardiogram profiles indicative of reduced heart rate and bradycardia. This mutant mouse strain may be useful in studies of potassium ion dependent vasodilation, cardiac arrythmia such as Anderson syndrome, cleft palate and developmental bone malformation. | ||
| 005941 | FVB/N-Tg(tetO-Aurkb,lacZ)41Kra/J | Repository-Cryopreserved |
| Hemizygous and homozygous transgenic mice are viable, fertile, normal in size, and do not display any behavioral abnormalities. Expression of the bicistronic transgene is directed by a tetracycline-responsive regulatory element (TRE; tetO). When transgenic mice are bred with another transgenic strain expressing the tetracycline-controlled transactivator protein (tTA) under the regulation of a tissue-specific promoter, both aurora kinase B (Aurkb) and lacZ cistrons are inducibly expressed in the appropriate tissue in the bitransgenic offspring. This mouse was originally designed to be bred with Tg(Pf4-tTA)42Kra transgenic mice, which express tTA from a megakaryocyte-specific promoter. Megakaryocytes and platelet cells derived from the bitransgenic offspring show inducible and reversible beta-galactosidase expression. Further, megakaryocytes inducibly express Aurkb mRNA (but not protein) with a modest effect on megakaryocyte ploidy and no effect on platelet quant
..... | ||
| 003256 | STOCK Fgf2tm1Doe/J | Repository-Cryopreserved |
| Mice homozygous for the Fgf2tm1Doe targeted-mutant allele have low blood pressure, presumably resulting from low vascular tone, increased megakaryocyte colony stimulation activity-induced megakaryocyte colony formation; increased platelet counts, and decreased IL3-induced colony formation. Vessel layer hypertrophy following vessel injury is not altered in the absence of FGF2. Cardiac hypertrophic response to induced high blood pressure is severely blunted in the absence of FGF2. Both sexes of the mutant exhibit no discernible morphologic or behavioral defects and have a normal life span. Both sexes are fertile and fecundity is normal. | ||
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Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.View a Data sheet for New Strains Under Development
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- Strains that will be made available from a live distribution colony at The Jackson Laboratory.
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