Analysis Tools|
Allele Symbol Allele Name Allele ID |
Kdr+ wild type MGI:1857565 |
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| Summary |
14 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Defect in angioblast differentiation in Ptentm1Hwu/Ptentm1Hwu Kdrtm1Jrt/Kdr+ Twist2tm1.1(cre)Dor/Twist2+ mice
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• vasculogenesis defect
• impaired differentiation of angioblasts into mature endothelial cells and blood vessels
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• increase in angioblasts in E18.5 lungs
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in the brain and liver of tamoxifen treated mice compared with control mice but not as severe as in mice also lacking the Kdr null allele
• some small focal areas in the retina in tamoxifen-treated mice relative to mice lacking the Kdr null allele
• however, angiogenesis in the heart is normal
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• unlike single Wnk1 homozygotes, heart morphology is grossly normal
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• the incidence of abnormal embryos is increased compared to controls indicating only a partial rescue
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• die between E9.5 and E10.5
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• all exhibit angiogenesis defects as only the primary vascular plexus is observed in E9.5 and E10.5 yolk sacs
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• the number of hematopoietic colonies in a hematopoietic progenitor assay at E8.5 is decreased by about 50%
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• all exhibit angiogenesis defects as only the primary vascular plexus is observed in E9.5 and E10.5 yolk sacs
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• trabeculae in the ventricles is much thinner at E9.5
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• the atrioventricular canal endocardial cushion is absent
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• the number of hematopoietic colonies in a hematopoietic progenitor assay at E8.5 is decreased by about 50%
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• trabeculae in the ventricles is much thinner at E9.5
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• die between E10.5 and E11.5
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• E10.5 yolk sacs show only the primary vascular plexus of poorly developed vascular channels instead of large vessels with extensive branching and well-developed capillary network
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• fail to develop beyond E11.5 as indicated by the small size and failure to form digits at E12.5
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• 21 of 69 exhibit pale yolk sacs at E10.5 and by E11.5, all mutants have pale yolk sacs
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• exhibit defective vessel development
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• often show abnormal branching in the trunk
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• E10.5 yolk sacs show only the primary vascular plexus of poorly developed vascular channels instead of large vessels with extensive branching and well-developed capillary network
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• exhibit fewer smooth muscle cell numbers around the dorsal aortas and those that are present do not make close contacts with adjacent endothelial cells
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• often show dilated vessels in the brain
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• at E10.5, the atrioventricular canal endocardial cushion is absent, however the development of the outflow tract cushion appears normal
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• cavity between the pericardial sac and the heart is distended
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• all mutants exhibit hemorrhage throughout the trunk region of the embryo at E11.5
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• embryos surviving to E11.5 are morphologically normal at E10.5 but subsequently succumb to death displaying abdominal hemorrhage
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• exhibit fewer smooth muscle cell numbers around the dorsal aortas and those that are present do not make close contacts with adjacent endothelial cells
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| N |
• exhibit normal embryonic and definitive hematopoiesis
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• cavity between the pericardial sac and the heart is distended
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• at E12.5, embryos are totally pale, although some of them still have red fluid within the amnion
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• all embryos die by E12.5 due to severe hemorrhaging within the central nervous system
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• in E12.5 embryos, endothelial cells and pericytes are entirely absent from the neuroepithelium
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• hemorrhaging is detected throughout the developing brain of E12.5 embryos
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• hemorrhaging is detected throughout the developing spine of E12.5 embryos
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• hemorrhaging and downregulation of the endothelial marker GLUT-1 suggest a defect in the blood brain barrier of developing embryos
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• hemorrhaging is detected throughout the developing brain of E12.5 embryos
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• hemorrhaging is detected throughout the developing spine of E12.5 embryos
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• hemorrhaging and downregulation of the endothelial marker GLUT-1 suggest a defect in the blood brain barrier of developing embryos
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• fetal capillaries fail to extend into the labyrinth tissue and instead are largely restricted to the base of the labyrinth
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• fetal capillaries fail to extend into the labyrinth tissue and instead are largely restricted to the base of the labyrinth
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• no obvious alteration in capillary density or patterning
• normal lymphatic vessel patterning and sprouting
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• abnormal smooth muscle cell coating
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• enlarged lymphatic vessels are even more dilated than in Tmem204tm1.1Ali single knock-outs
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• abnormal smooth muscle cell coating
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at E9.5, mice fail to exhibit remodeling of the initial plexus in embryonic tissue unlike wild-type mice
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• at E9.5, mice fail to exhibit remodeling of the initial plexus in the yolk sac unlike wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Loss of trabeculations in the heart of E9.5 and E10.5 Angpt1tm1.2Seq/Angpt1tm1.2Seq Kdrtm2.1Jrt/Kdr+ embryos
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• mice die between E9.5 and E12.5
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• at E10.5, mice exhibit an increase in vasculature in the hindbrain compared with wild-type mice
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• at E10.5, mice exhibit vascular defects with fusion of large diameter vessels and absence of patterning compared with wild-type mice
• however, pericyte coverage is normal
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• at E 9.5, mice exhibit heart defects and loss of heart trabeculation unlike wild-type mice
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• at E10.5
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• at E10.5, mice exhibit an increase in vasculature in the hindbrain compared with wild-type mice
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• at E10.5
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at E12.5, liver vasculature is less organized and vessels are dilated
• at E13.5, microvascular network is more disorganized with fewer branches than in control livers; newborns have very little microvascular network is observed
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• about 90% of mutants die as embryos
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• differentiation of vascular endothelial cells is disturbed
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• Kdr+ cells (lacZ expressing) abnormally accumulate in the middle to posterior portion of the embryo
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• differentiation of vascular endothelial cells is disturbed
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• Kdr+ cells (lacZ expressing) abnormally accumulate in the middle to posterior portion of the embryo
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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 10/06/2026 MGI 6.29 |
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