Phenotypes associated with this allele

• Allele Symbol: Tg(Myh6-Nox4)#Jusa
• Allele Name: transgene insertion, Junichi Sadoshima
• Allele ID: MGI:4834504
• Summary: 1 genotype

Jump to	Allelic Composition	Genetic Background	Genotype ID
tg1	Tg(Myh6-Nox4)#Jusa/0	FVB-Tg(Myh6-Nox4)#Jusa	MGI:4834505

Genotype
MGI:4834505

tg1

• Allelic Composition: Tg(Myh6-Nox4)#Jusa/0
• Genetic Background: FVB-Tg(Myh6-Nox4)#Jusa

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

cardiovascular system

abnormal ventricle myocardium morphology ( J:163751 , J:164275 )

• LV cardiac myocyte cross-sectional area is significantly greater (J:163751)

• increased LV myocyte cross-sectional area after transverse aortic constriction induced pressure overload (J:164275)

cardiac fibrosis ( J:163751 )

cardiac interstitial fibrosis ( J:164275 )

• increased fibrosis in response to transverse aortic constriction induced pressure overload

decreased ventricle muscle contractility ( J:163751 , J:164275 )

• mice at the age of 13 to 14 months show modestly but significantly increased LV end diastolic dimension and reduced LV ejection fraction (LVEF) (J:163751)

• transverse aortic constriction induced pressure overload induces LV dilation and reduces LV systolic function (J:164275)

increased cardiomyocyte apoptosis ( J:163751 , J:164275 )

• increase in the number of TUNEL positive cells (J:163751)

• increased apoptosis in response to transverse aortic constriction induced pressure overload (J:164275)

muscle

abnormal ventricle myocardium morphology ( J:163751 , J:164275 )

• LV cardiac myocyte cross-sectional area is significantly greater (J:163751)

• increased LV myocyte cross-sectional area after transverse aortic constriction induced pressure overload (J:164275)

decreased ventricle muscle contractility ( J:163751 , J:164275 )

• mice at the age of 13 to 14 months show modestly but significantly increased LV end diastolic dimension and reduced LV ejection fraction (LVEF) (J:163751)

• transverse aortic constriction induced pressure overload induces LV dilation and reduces LV systolic function (J:164275)

increased cardiomyocyte apoptosis ( J:163751 , J:164275 )

• increase in the number of TUNEL positive cells (J:163751)

• increased apoptosis in response to transverse aortic constriction induced pressure overload (J:164275)

cellular

cardiac interstitial fibrosis ( J:164275 )

• increased fibrosis in response to transverse aortic constriction induced pressure overload

increased cardiomyocyte apoptosis ( J:163751 , J:164275 )

• increase in the number of TUNEL positive cells (J:163751)

• increased apoptosis in response to transverse aortic constriction induced pressure overload (J:164275)

abnormal mitochondrial physiology ( J:163751 )

• in mitochondrial fractions from 12-month-old NADH-dependent superoxide production is significantly greater

• cysteine residues of many mitochondrial proteins are oxidized

• gene expression analysis show that mitochondrial biogenesis is attenuated

oxidative stress ( J:163751 )

• The level of oxidative stress, including oxidative DNA damage and superoxide production by immunostaining of 8-hydroxyl-deoxyguanosine and dihydroethidium respectively, are greater

• cysteine residues of many mitochondrial proteins are oxidized