Search Criteria: Research Area is "Hematological Research: Clotting Defects"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 002508 | B6.129S2-Plattm1Mlg/J | Repository- Live |
| Homozygotes develop normally, are fertile and have a normal life span. There are no histological abnormalities. Pulmonary clot lysis is 21% that of normal wildtype siblings. Endotoxin induced venous thrombosis is increased over that seen in normal wildtype siblings. Fibrin dissolution by PLAT-deficient macrophages is unaffected. | ||
| 004201 | B6.Cg-Selplgtm1Fur/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No targeted allele product (mRNA or protein) is detected by Northern blot or immunoassay. Mutant mice exhibit mild neutrophilia. Impaired early neutrophil migration in thioglycolate-induced peritonitis is followed by a delayed recovery to nearly normal levels. Although early trauma-induced leukocyte adhesion and migration is greatly reduced and in vivo leukocyte rolling (leukocyte-endothelial cell interaction) in postcapillary venules is severely decreased, cytokine-induced/E selectin-mediated leukocyte rolling is only slightly reduced in the mutant mice. This mutant mouse strain represents a model that may be useful in studies of leukocyte adhesion and migration in the inflammatory response. | ||
| 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 descriiption on the strain data sheet | ||
| 004424 | B6;129S4-F8tm1Kaz/J | Repository- Live |
| Mice that are homozygous for the targeted, X chromosome-linked mutant allele are viable and fertile. Homozygous females and carrier males have less than 1% of normal factor VIII activity and exhibit prolonged clotting times. Care should be exercise when obtaining tail clippings for the purpose of genotyping. Clipped tails of affected mice must be cauterized immediately or the mouse will succumb to excessive blood loss within several hours. Only mice that have reached the age of 4 weeks or older should have their tails clipped. Spontaneous bleeding into joints or soft tissues, a trait associated with human patients afflicted with hemophilia A is not observed. No bleeding difficulties are apparent during birth. These mice recapitulate key features of hemophilia A and provide an excellent model for use in exploring gene therapy strategies. | ||
| 000683 | RIIIS/J | Repository- Live |
| RIIIS/J mice have prolonged bleeding times with normal platelet activity and low levels of factor VIII:C and plasma von Willebrand factor antigen, making it a good animal model for human von Willebrand disease. This bleeding tendency is an incomplete dominant, autosomal trait. RIIIS/J mice also produce a low antibody response to several bacterial polysaccharide antigens and are reported to be resistant to collagen induced arthritis. Despite a B cell immunodeficiency, RIIS/J mice develop severe experimental autoimmune myasthenia gravis (EAMG) (Tuzun et al., 2004). RIII/J have a high incidence of mammary tumors and ovarian tumors. RIIIS/J mice carry Mtv8, and Mtv14, but high incidence of tumors has not been reported in these mice. In fact, some studies indicate a resistance to chemically induced tumors. RIIIS/J mice have been reported to develop far fewer lung tumors than A/J or SWR/J mice subsequent to Urethan treatment. BALB/c x RIII F1 males are also highly resistant to
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| 007239 | B6.129-Ggcxtm1Dgi/J | Repository-Cryopreserved |
| Most homozygous embryos die between developmental days E9.5 and E18. Those that suvive gestation die at birth of massive intra-abdominal hemorrhage. Heterozygous mice exhibit normal development and survival with no evidence of hemorrhage and normal functional activity of the vitamin K-dependent clotting factors IX, X, and prothrombin. | ||
| 004303 | B6.129P2-F9tm1Dws/J | Repository-Cryopreserved |
| Mice that are homozygous for this targeted mutation are viable, fertile and normal in size. As this mutation is X-linked, males bearing the targeted allele display a mutant phenotype similar to that seen in homozygous females. Gene product activity, as measured by clotting activity using an activated partial thromboplastin time (APTT) Factor IX assay, was reduced to 8% of normal. Mutant mice experience spontaneous bleeding that can lead to swelling of the top of the feet or the footpads. Sudden death due to massive internal hemorrhaging can occur as a result of normal fighting in the cage. Tail cut wounds must be cauterized to prevent blood loss and death in mutant mice. This mutant mouse strain represents a model that may be useful in studies related to gene therapy methods and function of factor IX mutations. | ||
| 002829 | B6.129P2-Plaurtm1Jld/J | Repository-Cryopreserved |
| Homozygous mice are born and survive to adulthood with no overt phenotypic abnormalities. No Plaur gene product (protein) is detected. In addition, activated peritoneal macrophages collected from homozygous mice fail to promote plasminogen activation in vitro. The loss of the receptor also results in a redistribution of uPA in some tissues but has no impact on pro-PLAU activation in the urogenital tract. Thus, in the absence of other challenging factors such as infection, injury, or other functional deficits, PLAUR deficiency does not compromise fertility, development, or hemostasis. These mice provide a means to test the proposed function of PLAU/PLAUR in wound repair, atherogenesis, and tumor cell invasion in vivo. | ||
| 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. | ||
| 004078 | B6.129S2-F5tm1Dgi/J | Repository-Cryopreserved |
| Approximately half of the mice that are homozygous null for the F5 gene die at embryonic day 9-10. Those that develop beyond this stage continue to develop but suffer from massive intra-abdominal hemorrhages and die within two hours of birth. Also observed are microscopic hemorrhages in a variety of tissues. Blood present in the intra-abdominal cavity is unclotted and completely deficient of factor V activity. | ||
| 004080 | B6.129S2-F5tm2Dgi/J | Repository-Cryopreserved |
| These mice carry the F5 Leiden mutation whereby the arginine at position 504 is replaced by a glutamine disrupting a cleavage site necessary for the inactivation of the factor V protein. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Clotting activity is indistinguishable from that of wildtype mice. Rarely, spontaneous vascular thrombo-embolic events are observed. Analysis of tissue fibrin content indicates increased deposition of fibrin in multiple tissues. When maintained on a mixed B6;129 genetic background, mice homozygous for this allele experience disseminated intravascular thrombosis resulting in increased fetal loss. This loss is not observed on a congenic C57BL/6J genetic background. This mutant mouse strain represents a model useful in research examining the disease aspects of the Leiden mutation and thrombosis in general. | ||
| 002509 | B6.129S2-Plautm1Mlg/J | Repository-Cryopreserved |
| Homozygotes develop normally, have a normal life span, and are poor breeders. Pups often need fostering. Rectal prolapse of a non-infectious origin develops in 9% of homozygotes and/or extensive non-healing ulcerations occur at the eyelids and around the face. Small, focal fibrin deposits are occasionally seen in the intestines and in the sinusoids of the liver, and excessive fibrin deposits are seen in ulcerated skin or prolapsed rectum. Pulmonary clot lysis is comparable to that seen in normal wildtype siblings. Endotoxin induced venous thrombosis is increased over normal wildtype siblings. Fibrin dissolution by PLAU-deficient macrophages is greatly reduced but macrophage invasion into the peritoneal cavity after thioglycollate injection is unaffected. Homozygous knockout mice have increased levels of Abeta42 and Abeta40 in plasma. Brain Abeta levels are not significantly different than controls. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds,
..... For more information please see the full descriiption on the strain data sheet | ||
| 003795 | B6.129S2-Vwftm1Wgr/J | Repository-Cryopreserved |
| Mice that are homozygous null for the Vwf gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Vwf protein product is detected in platelets, plasma, heart or lung endothelium. Null mice exhibit defects in hemostasis characterized by prolonged bleeding times in all mice with spontaneous bleeding events observed in ten percent of neonates. Intravital microscopic analysis indicates a complete absence of thrombus formation following vascular injury. Observed levels of factor VIII are reduced to twenty percent of that seen in wild type mice. Although heterozygous mice carrying a single null allele exhibit no defects in hemostasis, they do have reduced levels of factor VIII (57 percent that of wildtype) making them a suitable model for type 1 von Willebrand disease. Characteristics displayed by homozygous null animals qualify them as an appropriate model for severe (type 3) von Willebrand disease. | ||
| 007238 | B6.Cg-Tg(Alb-PLG)1Dgi/J | Repository-Cryopreserved |
| The level of PLG in the plasma of these mice expressing the human plasminogen gene under the control of a mouse albumin promoter is approximately 16% of the level in control human plasma. Mice exhibit increased susceptibility to group A streptococci (GAS). Although enhanced green fluorescent protein (EGFP) is incorporated in the transgene, it is not expressed. | ||
| 002327 | C.129S2-Plattm1Mlg/J | Repository-Cryopreserved |
| 002328 | C.129S2-Plautm1Mlg/J | Repository-Cryopreserved |
| Homozygotes develop normally, are fertile and have a normal life span. Rectal prolapse of a non-infectious origin develops in 9% of homozygotes and/or extensive non-healing ulcerations occur at the eyelids and around the face. Small, focal fibrin deposits are occasionally seen in the intestines and in the sinusoids of the liver, and excessive fibrin deposits are seen in ulcerated skin or prolapsed rectum. Pulmonary clot lysis is comparable to that seen in normal wildtype siblings. Endotoxin induced venous thrombosis is increased over normal wildtype siblings. Fibrin dissolution by PLAU-deficient macrophages is greatly reduced but macrophage invasion into the peritoneal cavity after thioglycollate injection is unaffected. Homozygous knockout mice have increased levels of Abeta42 and Abeta40 in plasma. Brain Abeta levels are not significantly different than controls. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a
..... For more information please see the full descriiption on the strain data sheet | ||
| 000120 | C3H/HeSn-Rab27aash/J | Repository-Cryopreserved |
| Ashen mice have a lightened coat color that is gray on a non-agouti background similar to that of dilute (Myo5ad) or leaden (ln) mutants. Lane and Womack reported that on an agouti background the yellow pigment is more dilute in ashen mice resulting in a grayer agouti than that found in dilute or leaden mice, but Wu et al. subsequently reported that dilute and ashen mice have identical degrees of coat color dilution. This pigment dilution results from defective trafficking of melanosomes that are normally found throughout the dendrites of melanocytes. Similar to that seen in leaden mutants, ashen melanosomes are clumped around the nucleus and sparse in the dendrites where normally they are released. Melanosome trafficking from the melanocyte cell body to the ends of the dendrites results from a microtubule-based bidirectional transport. MYO5A is essential for retaining the melanosomes in the ends of the dendrites and preventing their retrograde transport back t
..... For more information please see the full descriiption on the strain data sheet | ||
| 000110 | C57BL/6J-Rabggtagm/J | Repository-Cryopreserved |
| Mice homozygous for the Rabggtagm allele are grayish-black on a non-agouti background due to pigment dilution. Eye color is not affected. Homozygotes have reduced viability and do not breed well. These mutants have a prolonged bleeding time. Although gunmetal mice have an increased number of megakariocytes, they have about half the number platelets found in wildtype siblings. This decrease in platelet number results from a slower rate of platelet synthesis. These platelets are heterogeneous in size and are larger than normal, but have fewer dense granules per platelet and approximately half of the normal level of serotonin. The prolonged bleeding time and decreased platelet count and volume can be transferred to wildtype mice through bone marrow transplantion. Likewise bone marrow transplants from wildtype mice reversed the platelet deficiency in gunmetal recipients. Western blots of platelet extracts showed a decrease in fibrinogen, von Willebrand factor, and platel
..... For more information please see the full descriiption on the strain data sheet | ||
| 002329 | FVB.129S2-Plautm1Mlg/J | Repository-Cryopreserved |
| Homozygotes develop normally, are fertile and have a normal life span. Rectal prolapse of a non-infectious origin develops in 9% of homozygotes and/or extensive non-healing ulcerations occur at the eyelids and around the face. Small, focal fibrin deposits are occasionally seen in the intestines and in the sinusoids of the liver, and excessive fibrin deposits are seen in ulcerated skin or prolapsed rectum. Pulmonary clot lysis is comparable to that seen in normal wildtype siblings. Endotoxin induced venous thrombosis is increased over normal wildtype siblings. Fibrin dissolution by PLAU-deficient macrophages is greatly reduced but macrophage invasion into the peritoneal cavity after thioglycollate injection is unaffected. Homozygous knockout mice have increased levels of Abeta42 and Abeta40 in plasma. Brain Abeta levels are not significantly different than controls. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a
..... For more information please see the full descriiption on the strain data sheet | ||
| 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
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| 002326 | STOCK Plattm1Mlg/J | Repository-Cryopreserved |
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