normal phenotype
• mice do not exhibit any developmental abnormalities
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Allele Symbol Allele Name Allele ID |
Tg(Tek-cre)1Arnd transgene insertion 1, Bernd Arnold MGI:2651392 |
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Summary |
3 genotypes
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• mice do not exhibit any developmental abnormalities
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
N |
• heat insensitivity is not observed in mutants
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• animals show significantly lengthened grooming times compared to wild-type controls with deletion of Hoxb8 in hematopoietic system; behavior is comparable to complete Hoxb8 null animals
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N |
• morphology of dorsal spinal cord laminae I and II appears normal, based on labeling for interneurons
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• hairless patches develop in most animals due to excessive grooming
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• mice develop splenomegaly by 16 weeks of age
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• mice develop splenomegaly by 16 weeks of age
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• increase in total colony formation, particularly in the number of granulocyte/macrophage (CFU-GM) progenitor cells
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• decrease in bone marrow erythropoiesis and an increase in splenic erythropoiesis
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• CD41/CD61-positive megakaryocytes are increased in the bone marrow and spleen
• greatly increased magakaryopoiesis at 16 weeks of age
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• increase in total colony formation, particularly in the number of megakaryocyte (CFU-MK) progenitor cells
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• mice show increased red-cell distribution width without differences in mean cell volume at 22 weeks of age, indicating premyelofibrosis
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• neutrophilia is seen at 8 weeks of age which gets worse by 16 weeks of age
• however no differences in red blood cell or total lymphocyte count is seen
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• thrombocytosis is seen at 8 weeks of age which gets worse by 16 weeks of age
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• reduction in the number of CD3-positive T cells in the bone marrow and spleen
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• blood fails to agglutinate in the presence of ristocetin compared to wild-type
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• plasma levels of von Willebrand Factor (VWF) are normal, however distribution of VWF multimers is different, with mice showing a reduction in ultralarge multimers and a compensatory increase in the levels of smaller VWF multimers
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• blood aggregates quicker and to a greater extent in response to a combination of epinephrine and ADP or collagen than whole blood from wild-type mice, however this is due to increased platelet numbers and not due to increased aggregation and platelets appear to have normal function
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• blood fails to agglutinate in the presence of ristocetin compared to wild-type
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• mice fail to occlude in response to FeCl3 injury over a 30 minute period indicating severely attenuated thrombosis following injury; while platelets adhere to injury site, the platelet plug appears to fail to propagate into an occlusive thrombus
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• increase in bleeding time following injury to the tail compared to wild-type mice
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• mice develop splenomegaly by 16 weeks of age
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• neutrophilia is seen at 8 weeks of age which gets worse by 16 weeks of age
• however no differences in red blood cell or total lymphocyte count is seen
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• reduction in the number of CD3-positive T cells in the bone marrow and spleen
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• predominant cell type in the bone marrow is GR1/Mac-1-positive myeloid cells
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• mice develop extensive bone marrow osteopetrosis by 32 weeks of age
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
blood coagulation disease | DOID:1247 | J:206659 |
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 11/12/2024 MGI 6.24 |
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