Phenotypes associated with this allele

• Allele Symbol: Nox4^tm1.1Jusa
• Allele Name: targeted mutation 1.1, Junichi Sadoshima
• Allele ID: MGI:4830885
• Summary: 1 genotype

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Nox4^tm1.1Jusa/Nox4^tm1.1Jusa Tg(Myh6-cre)2182Mds/0	involves: C57BL/6 * FVB	MGI:4830886

Genotype
MGI:4830886

cn1

• Allelic Composition: Nox4^tm1.1Jusa/Nox4^tm1.1Jusa; Tg(Myh6-cre)2182Mds/0
• Genetic Background: involves: C57BL/6 * FVB

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

mortality/aging

decreased susceptibility to induced morbidity/mortality ( J:163751 )

• reduced mortality in response to applied transverse aortic constriction induced pressure overload

cellular

cardiac interstitial fibrosis ( J:163751 )

• in response to pressure overload exhibit significantly attenuated interstitial fibrosis

decreased cardiomyocyte apoptosis ( J:163751 )

• in response to pressure overload exhibit significantly decreased TUNEL positive cells compared to wild-type

abnormal mitochondrial physiology ( J:163751 )

• superoxide production, in the mitochondria in response to transverse aortic constriction induced pressure overload is abolished compared to wild-type

• mitochondrial swelling, cytochrome c release, and a decrease in both mitochondrial DNA and aconitase activity in response to pressure overload are attenuated compared to wild-type

oxidative stress ( J:163751 )

• decreased production of superoxide in left ventricular myocardial sections

cardiovascular system

heart left ventricle hypertrophy ( J:163751 )

• in response to pressure overload exhibit significantly attenuated cardiac hypertrophy

cardiac interstitial fibrosis ( J:163751 )

• in response to pressure overload exhibit significantly attenuated interstitial fibrosis

decreased heart ventricle muscle contractility ( J:163751 )

• decrease in echocardiographically evaluated LV ejection fraction (EF) and fractional shortening in response to transverse aortic constriction induced pressure overload

decreased heart left ventricle muscle contractility ( J:163751 )

• decrease in echocardiographically evaluated LV ejection fraction (EF) and fractional shortening in response to transverse aortic constriction induced pressure overload

decreased response of heart to induced stress ( J:163751 )

• better cardiac function compared to wild-type in response to transverse aortic constriction induced pressure overload

muscle

heart left ventricle hypertrophy ( J:163751 )

• in response to pressure overload exhibit significantly attenuated cardiac hypertrophy

decreased heart ventricle muscle contractility ( J:163751 )

• decrease in echocardiographically evaluated LV ejection fraction (EF) and fractional shortening in response to transverse aortic constriction induced pressure overload

decreased heart left ventricle muscle contractility ( J:163751 )

• decrease in echocardiographically evaluated LV ejection fraction (EF) and fractional shortening in response to transverse aortic constriction induced pressure overload

decreased cardiomyocyte apoptosis ( J:163751 )

• in response to pressure overload exhibit significantly decreased TUNEL positive cells compared to wild-type

homeostasis/metabolism

decreased response of heart to induced stress ( J:163751 )

• better cardiac function compared to wild-type in response to transverse aortic constriction induced pressure overload

growth/size/body

heart left ventricle hypertrophy ( J:163751 )

• in response to pressure overload exhibit significantly attenuated cardiac hypertrophy