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Phenotypes Associated with This Genotype
Genotype
MGI:5661916
Allelic
Composition
Krit1tm1Kwhi/Krit1tm1.1Kwhi
Tg(Pdgfb-icre/ERT2,-EGFP)1Frut/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * C57BL/6NCrl * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krit1tm1.1Kwhi mutation (0 available); any Krit1 mutation (34 available)
Krit1tm1Kwhi mutation (0 available); any Krit1 mutation (34 available)
Tg(Pdgfb-icre/ERT2,-EGFP)1Frut mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• all mice treated with tamoxifen at birth form cerebral cavernous malformations in the brain by 2 months which progress in severity over time
• the lesions in mice treated with tamoxifen at birth show dilated, thin-walled caverns surrounded by hemosiderin deposits, inflammation, and fibrosis
• mice treated with tamoxifen at birth first show vessel dilation and failure of plexus coalescence in the vascular network at P7, and over time the vascular dilations resolve into caverns and appear as mature retinal cerebral cavernous malformation by P21
• cerebral cavernous malformation lesions in tamoxifen treated mice arise from the superficial vascular plexus and remain superficial until later in disease progression
• mice treated with tamoxifen at P7 develop lesions in the periphery of the retina by P21; these lesions show a similar morphology as those from mice treated with tamoxifen at birth, however severity and size are smaller
• mice treated with tamoxifen at P21 do not develop retinal lesions
• mice treated with tamoxifen at birth exhibit vascular leak in the brain
• mice treated with tamoxifen at P1 exhibit retinal endothelial hypersprouting
• mice treated with tamoxifen at birth develop simple, dilated telangiectasias that progress to large multi-chambered caverns over time

mortality/aging
• presence of lesions in mice treated with tamoxifen at birth decrease the survival rate

muscle
• mice treated with tamoxifen at birth develop simple, dilated telangiectasias that progress to large multi-chambered caverns over time

nervous system
• all mice treated with tamoxifen at birth form cerebral cavernous malformations in the brain by 2 months which progress in severity over time
• the lesions in mice treated with tamoxifen at birth show dilated, thin-walled caverns surrounded by hemosiderin deposits, inflammation, and fibrosis

neoplasm
• mice treated with tamoxifen at birth develop mature cerebral cavernous malformation in the retina that recapitulate retinal angiomas by P21

vision/eye
• mice treated with tamoxifen at birth first show vessel dilation and failure of plexus coalescence in the vascular network at P7, and over time the vascular dilations resolve into caverns and appear as mature retinal cerebral cavernous malformation by P21
• cerebral cavernous malformation lesions in tamoxifen treated mice arise from the superficial vascular plexus and remain superficial until later in disease progression
• mice treated with tamoxifen at P7 develop lesions in the periphery of the retina by P21; these lesions show a similar morphology as those from mice treated with tamoxifen at birth, however severity and size are smaller
• mice treated with tamoxifen at P21 do not develop retinal lesions
• mice treated with tamoxifen at birth develop mature cerebral cavernous malformation in the retina that recapitulate retinal angiomas by P21
• cavernous malformation lesions form in the retinas of mice treated with tamoxifen at birth
• retinal lesions in mice treated with tamoxifen at birth arise in the veins located both most superior and inferior within the retina


Contributing Projects:
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
04/16/2024
MGI 6.23
The Jackson Laboratory