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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Pdgfb-icre/ERT2)1Frut
transgene insertion 1, Marcus Fruttiger
MGI:3793852
Summary 7 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Ctnnb1tm2Kem/Ctnnb1tm2Kem
Tg(Pdgfb-icre/ERT2)1Frut/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * C57BL/6J * CBA MGI:3833562
cn2
Jag1tm1Jlew/Jag1tm1Grid
Tg(Pdgfb-icre/ERT2)1Frut/0
involves: 129S1/Sv * C57BL/6 * CBA MGI:4437857
cn3
Krit1tm1Kwhi/Krit1tm1.1Kwhi
Tg(Pdgfb-icre/ERT2)1Frut/0
involves: 129S6/SvEvTac * C57BL/6 * C57BL/6NCrl * CBA MGI:5661916
cn4
Adgra2tm1Cjku/Adgra2tm2Cjku
Tg(Pdgfb-icre/ERT2)1Frut/0
involves: 129/Sv * C57BL/6 * CBA MGI:4840269
cn5
Ccm2tm1Kwhi/Ccm2tm1.1Kwhi
Tg(Pdgfb-icre/ERT2)1Frut/?
involves: C57BL/6 * CBA MGI:5052330
cn6
Pdcd10tm1Kwhi/Pdcd10tm1.1Kwhi
Tg(Pdgfb-icre/ERT2)1Frut/?
involves: C57BL/6 * CBA MGI:5052328
cn7
Jag1tm1Jlew/Jag1tm1Jlew
Tg(Pdgfb-icre/ERT2)1Frut/0
involves: C57BL/6 * CBA MGI:4437856


Genotype
MGI:3833562
cn1
Allelic
Composition
Ctnnb1tm2Kem/Ctnnb1tm2Kem
Tg(Pdgfb-icre/ERT2)1Frut/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * C57BL/6J * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm2Kem mutation (1 available); any Ctnnb1 mutation (18 available)
Tg(Pdgfb-icre/ERT2)1Frut mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• following treatment with tamoxifen, retinal vascular density is reduced compared to in wild-type retina (J:144980)
• however, endothelial junctional assemblies are normal (J:144980)
• following treatment with tamoxifen, retinal vascular density is reduced compared to in wild-type retina (J:144980)
• however, endothelial junctional assemblies are normal (J:144980)
• excessive in the retina following tamoxifen treatment (J:144980)
• excessive in the retina following tamoxifen treatment (J:144980)

vision/eye
• following treatment with tamoxifen, retinal vascular density is reduced compared to in wild-type retina (J:144980)
• however, endothelial junctional assemblies are normal (J:144980)
• following treatment with tamoxifen, retinal vascular density is reduced compared to in wild-type retina (J:144980)
• however, endothelial junctional assemblies are normal (J:144980)

cellular
• excessive in the retina following tamoxifen treatment (J:144980)
• excessive in the retina following tamoxifen treatment (J:144980)




Genotype
MGI:4437857
cn2
Allelic
Composition
Jag1tm1Jlew/Jag1tm1Grid
Tg(Pdgfb-icre/ERT2)1Frut/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Jag1tm1Grid mutation (1 available); any Jag1 mutation (8 available)
Jag1tm1Jlew mutation (0 available); any Jag1 mutation (8 available)
Tg(Pdgfb-icre/ERT2)1Frut mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• with postnatal tamoxifen treatment from P1-P3, pups are generally smaller than tamoxifen-treated control littermates (J:157345)
• with postnatal tamoxifen treatment from P1-P3, pups are generally smaller than tamoxifen-treated control littermates (J:157345)

vision/eye
• perpendicular sprouting and neovascularization of the deeper retina are strongly compromised with tamoxifen treatment between P5 and P9 (J:157345)
• perpendicular sprouting and neovascularization of the deeper retina are strongly compromised with tamoxifen treatment between P5 and P9 (J:157345)

cardiovascular system
N
• stability of blood vessels is not affected in mutants with tamoxifen treatment at P1; stability of established vessels in the superficial capillary plexus is not affected with tamoxifen administration between P5 and P9 (J:157345)
• stability of blood vessels is not affected in mutants with tamoxifen treatment at P1; stability of established vessels in the superficial capillary plexus is not affected with tamoxifen administration between P5 and P9 (J:157345)
• postnatal tamoxifen treatment from P1-P3 results in decreased coverage of retinal arteries by vascular smooth muscle cells; however pericyte coverage of capillary beds shows no change (J:157345)
• postnatal tamoxifen treatment from P1-P3 results in decreased coverage of retinal arteries by vascular smooth muscle cells; however pericyte coverage of capillary beds shows no change (J:157345)
• perpendicular sprouting and neovascularization of the deeper retina are strongly compromised with tamoxifen treatment between P5 and P9 (J:157345)
• perpendicular sprouting and neovascularization of the deeper retina are strongly compromised with tamoxifen treatment between P5 and P9 (J:157345)
• postnatal tamoxifen treatment from P1-P3 to delete Jag1 in endothelial cells results in significant decreases in numbers of filopodia and filopodia-extending endothelial tip cells (J:157345)
• postnatal tamoxifen treatment from P1-P3 to delete Jag1 in endothelial cells results in significant decreases in numbers of filopodia and filopodia-extending endothelial tip cells (J:157345)
• postnatal tamoxifen treatment from P1-P3 results in strong inhibition of angiogenesis in the retina resulting in reduced branching and delayed extension toward the periphery (J:157345)
• postnatal tamoxifen treatment from P1-P3 results in strong inhibition of angiogenesis in the retina resulting in reduced branching and delayed extension toward the periphery (J:157345)




Genotype
MGI:5661916
cn3
Allelic
Composition
Krit1tm1Kwhi/Krit1tm1.1Kwhi
Tg(Pdgfb-icre/ERT2)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 (3 available)
Krit1tm1Kwhi mutation (0 available); any Krit1 mutation (3 available)
Tg(Pdgfb-icre/ERT2)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 (J:215458)
• the lesions in mice treated with tamoxifen at birth show dilated, thin-walled caverns surrounded by hemosiderin deposits, inflammation, and fibrosis (J:215458)
• all mice treated with tamoxifen at birth form cerebral cavernous malformations in the brain by 2 months which progress in severity over time (J:215458)
• the lesions in mice treated with tamoxifen at birth show dilated, thin-walled caverns surrounded by hemosiderin deposits, inflammation, and fibrosis (J:215458)
• 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 (J:215458)
• cerebral cavernous malformation lesions in tamoxifen treated mice arise from the superficial vascular plexus and remain superficial until later in disease progression (J:215458)
• 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 (J:215458)
• mice treated with tamoxifen at P21 do not develop retinal lesions (J:215458)
• 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 (J:215458)
• cerebral cavernous malformation lesions in tamoxifen treated mice arise from the superficial vascular plexus and remain superficial until later in disease progression (J:215458)
• 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 (J:215458)
• mice treated with tamoxifen at P21 do not develop retinal lesions (J:215458)
• mice treated with tamoxifen at birth exhibit vascular leak in the brain (J:215458)
• mice treated with tamoxifen at birth exhibit vascular leak in the brain (J:215458)
• mice treated with tamoxifen at P1 exhibit retinal endothelial hypersprouting (J:215458)
• mice treated with tamoxifen at P1 exhibit retinal endothelial hypersprouting (J:215458)
• mice treated with tamoxifen at birth develop simple, dilated telangiectasias that progress to large multi-chambered caverns over time (J:215458)
• mice treated with tamoxifen at birth develop simple, dilated telangiectasias that progress to large multi-chambered caverns over time (J:215458)

mortality/aging
• presence of lesions in mice treated with tamoxifen at birth decrease the survival rate (J:215458)
• presence of lesions in mice treated with tamoxifen at birth decrease the survival rate (J:215458)

muscle
• mice treated with tamoxifen at birth develop simple, dilated telangiectasias that progress to large multi-chambered caverns over time (J:215458)
• mice treated with tamoxifen at birth develop simple, dilated telangiectasias that progress to large multi-chambered caverns over time (J:215458)

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 (J:215458)
• the lesions in mice treated with tamoxifen at birth show dilated, thin-walled caverns surrounded by hemosiderin deposits, inflammation, and fibrosis (J:215458)
• all mice treated with tamoxifen at birth form cerebral cavernous malformations in the brain by 2 months which progress in severity over time (J:215458)
• the lesions in mice treated with tamoxifen at birth show dilated, thin-walled caverns surrounded by hemosiderin deposits, inflammation, and fibrosis (J:215458)

tumorigenesis
• mice treated with tamoxifen at birth develop mature cerebral cavernous malformation in the retina that recapitulate retinal angiomas by P21 (J:215458)
• mice treated with tamoxifen at birth develop mature cerebral cavernous malformation in the retina that recapitulate retinal angiomas by P21 (J:215458)

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 (J:215458)
• cerebral cavernous malformation lesions in tamoxifen treated mice arise from the superficial vascular plexus and remain superficial until later in disease progression (J:215458)
• 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 (J:215458)
• mice treated with tamoxifen at P21 do not develop retinal lesions (J:215458)
• 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 (J:215458)
• cerebral cavernous malformation lesions in tamoxifen treated mice arise from the superficial vascular plexus and remain superficial until later in disease progression (J:215458)
• 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 (J:215458)
• mice treated with tamoxifen at P21 do not develop retinal lesions (J:215458)
• cavernous malformation lesions form in the retinas of mice treated with tamoxifen at birth (J:215458)
• retinal lesions in mice treated with tamoxifen at birth arise in the veins located both most superior and inferior within the retina (J:215458)
• cavernous malformation lesions form in the retinas of mice treated with tamoxifen at birth (J:215458)
• retinal lesions in mice treated with tamoxifen at birth arise in the veins located both most superior and inferior within the retina (J:215458)

Mouse Models of Human Disease
OMIM ID Ref(s)
Cerebral Cavernous Malformations; CCM 116860 J:215458




Genotype
MGI:4840269
cn4
Allelic
Composition
Adgra2tm1Cjku/Adgra2tm2Cjku
Tg(Pdgfb-icre/ERT2)1Frut/0
Genetic
Background
involves: 129/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adgra2tm1Cjku mutation (0 available); any Adgra2 mutation (5 available)
Adgra2tm2Cjku mutation (0 available); any Adgra2 mutation (5 available)
Tg(Pdgfb-icre/ERT2)1Frut mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• basally localized glomeruloid malformations in hemorrhagic areas of the CNS (J:166127)
• basally localized glomeruloid malformations in hemorrhagic areas of the CNS (J:166127)
• central nervous system (CNS) angiogenic arrest (J:166127)
• central nervous system (CNS) angiogenic arrest (J:166127)
• stated to fully recapitulate the phenotype seen in mice homozygous for Gpr124tm1Cjku (J:166127)
• forebrain hemorrhage (J:166127)
• stated to fully recapitulate the phenotype seen in mice homozygous for Gpr124tm1Cjku (J:166127)
• forebrain hemorrhage (J:166127)




Genotype
MGI:5052330
cn5
Allelic
Composition
Ccm2tm1Kwhi/Ccm2tm1.1Kwhi
Tg(Pdgfb-icre/ERT2)1Frut/?
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ccm2tm1.1Kwhi mutation (0 available); any Ccm2 mutation (31 available)
Ccm2tm1Kwhi mutation (0 available); any Ccm2 mutation (31 available)
Tg(Pdgfb-icre/ERT2)1Frut mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• increased early mortality (J:173947)
• increased early mortality (J:173947)

cardiovascular system
• cerebral cavernous malformations develop as early as two months after tamoxifen treatment at 1 day of age (J:173947)
• most mice have lesions at 4 months and all mice at 6 months (J:173947)
• additional abnormalities include capillary telangiectasias, isolated caverns and multiple back to back caverns, thrombosis, hemorrhage, formation of secondary channels (J:173947)
• attenuation of endothelial cells in larger secondary channels but no gaps (J:173947)
• cerebral cavernous malformations develop as early as two months after tamoxifen treatment at 1 day of age (J:173947)
• most mice have lesions at 4 months and all mice at 6 months (J:173947)
• additional abnormalities include capillary telangiectasias, isolated caverns and multiple back to back caverns, thrombosis, hemorrhage, formation of secondary channels (J:173947)
• attenuation of endothelial cells in larger secondary channels but no gaps (J:173947)
• foot processes are missing (J:173947)
• foot processes are missing (J:173947)

nervous system
• cerebral cavernous malformations develop as early as two months after tamoxifen treatment at 1 day of age (J:173947)
• most mice have lesions at 4 months and all mice at 6 months (J:173947)
• additional abnormalities include capillary telangiectasias, isolated caverns and multiple back to back caverns, thrombosis, hemorrhage, formation of secondary channels (J:173947)
• attenuation of endothelial cells in larger secondary channels but no gaps (J:173947)
• cerebral cavernous malformations develop as early as two months after tamoxifen treatment at 1 day of age (J:173947)
• most mice have lesions at 4 months and all mice at 6 months (J:173947)
• additional abnormalities include capillary telangiectasias, isolated caverns and multiple back to back caverns, thrombosis, hemorrhage, formation of secondary channels (J:173947)
• attenuation of endothelial cells in larger secondary channels but no gaps (J:173947)
• foci of mononuclear inflammatory cells also seen (J:173947)
• foci of mononuclear inflammatory cells also seen (J:173947)
• foot processes are missing (J:173947)
• foot processes are missing (J:173947)

immune system
• foci of mononuclear inflammatory cells also seen (J:173947)
• foci of mononuclear inflammatory cells also seen (J:173947)




Genotype
MGI:5052328
cn6
Allelic
Composition
Pdcd10tm1Kwhi/Pdcd10tm1.1Kwhi
Tg(Pdgfb-icre/ERT2)1Frut/?
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pdcd10tm1.1Kwhi mutation (0 available); any Pdcd10 mutation (7 available)
Pdcd10tm1Kwhi mutation (0 available); any Pdcd10 mutation (7 available)
Tg(Pdgfb-icre/ERT2)1Frut mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• increased early mortality (J:173947)
• increased early mortality (J:173947)

cardiovascular system
• cerebral cavernous malformations develop by one month after tamoxifen treatment at 1 day of age (J:173947)
• additional abnormalities include capillary telangiectasias, isolated caverns and multiple back to back caverns, thrombosis, hemorrhage, formation of secondary channels (J:173947)
• attenuation of endothelial cells in larger secondary channels but no gaps (J:173947)
• cerebral cavernous malformations develop by one month after tamoxifen treatment at 1 day of age (J:173947)
• additional abnormalities include capillary telangiectasias, isolated caverns and multiple back to back caverns, thrombosis, hemorrhage, formation of secondary channels (J:173947)
• attenuation of endothelial cells in larger secondary channels but no gaps (J:173947)
• foot processes are missing (J:173947)
• foot processes are missing (J:173947)

nervous system
• cerebral cavernous malformations develop by one month after tamoxifen treatment at 1 day of age (J:173947)
• additional abnormalities include capillary telangiectasias, isolated caverns and multiple back to back caverns, thrombosis, hemorrhage, formation of secondary channels (J:173947)
• attenuation of endothelial cells in larger secondary channels but no gaps (J:173947)
• cerebral cavernous malformations develop by one month after tamoxifen treatment at 1 day of age (J:173947)
• additional abnormalities include capillary telangiectasias, isolated caverns and multiple back to back caverns, thrombosis, hemorrhage, formation of secondary channels (J:173947)
• attenuation of endothelial cells in larger secondary channels but no gaps (J:173947)
• foci of mononuclear inflammatory cells also seen (J:173947)
• foci of mononuclear inflammatory cells also seen (J:173947)
• foot processes are missing (J:173947)
• foot processes are missing (J:173947)

immune system
• foci of mononuclear inflammatory cells also seen (J:173947)
• foci of mononuclear inflammatory cells also seen (J:173947)




Genotype
MGI:4437856
cn7
Allelic
Composition
Jag1tm1Jlew/Jag1tm1Jlew
Tg(Pdgfb-icre/ERT2)1Frut/0
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Jag1tm1Jlew mutation (0 available); any Jag1 mutation (8 available)
Tg(Pdgfb-icre/ERT2)1Frut mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• postnatal tamoxifen treatment from P1-P3 results in decreased angiogenesis in the retina assessed at P6; significantly decreased vascular branching and endothelial cell coverage at P6 (J:157345)
• postnatal tamoxifen treatment from P1-P3 results in decreased angiogenesis in the retina assessed at P6; significantly decreased vascular branching and endothelial cell coverage at P6 (J:157345)





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last database update
02/02/2016
MGI 6.02
The Jackson Laboratory