Phenotypes Associated with This Genotype

Genotype
MGI:5470080

• Allelic Composition: Pak1^tm1.1Xwg/Pak1^tm1.1Xwg; Myl2^tm1(cre)Krc/Myl2⁺
• Genetic Background: involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6

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

cardiovascular system

increased myocardial fiber size ( J:193804 )

• increased following transverse aortic constriction and prolonged load stress

• in response to Ang II infusion

increased heart weight ( J:193804 )

• following transverse aortic constriction and prolonged load stress

• in response to Ang II infusion

cardiac hypertrophy ( J:193804 )

• following transverse aortic constriction

• in response to Ang II infusion

• treatment with FTY720 does not blocked cardiac hypertrophy induced by transverse aortic constriction

cardiac fibrosis ( J:193804 )

• increased collagen-deposition following prolonged load stress

• in response to Ang II infusion

decreased cardiac muscle contractility ( J:193804 )

• following prolonged load stress

• in response to Ang II infusion

increased response of heart to induced stress ( J:193804 )

• following transverse aortic constriction, cardiomyocytes exhibit exacerbated pressure overload-induced hypertrophy and increased cardiomyocytes size and apoptosis compared with control mice

• prolonged load stress sensitizes mice to heart failure, pulmonary edema, reduced fractional shortening, increased heart weight, increased myocyte cross-sectional area and collagen deposition

• however, contractile performance is normal following limited transverse aortic contriction

congestive heart failure ( J:193804 )

• following prolonged load stress

respiratory system

pulmonary edema ( J:193804 )

• following prolonged load stress

cellular

increased cardiomyocyte apoptosis ( J:193804 )

• 5-fold increase following transverse aortic constriction

homeostasis/metabolism

increased response of heart to induced stress ( J:193804 )

• following transverse aortic constriction, cardiomyocytes exhibit exacerbated pressure overload-induced hypertrophy and increased cardiomyocytes size and apoptosis compared with control mice

• prolonged load stress sensitizes mice to heart failure, pulmonary edema, reduced fractional shortening, increased heart weight, increased myocyte cross-sectional area and collagen deposition

• however, contractile performance is normal following limited transverse aortic contriction

pulmonary edema ( J:193804 )

• following prolonged load stress

muscle

increased myocardial fiber size ( J:193804 )

• increased following transverse aortic constriction and prolonged load stress

• in response to Ang II infusion

decreased cardiac muscle contractility ( J:193804 )

• following prolonged load stress

• in response to Ang II infusion

increased cardiomyocyte apoptosis ( J:193804 )

• 5-fold increase following transverse aortic constriction

growth/size/body

increased heart weight ( J:193804 )

• following transverse aortic constriction and prolonged load stress

• in response to Ang II infusion

cardiac hypertrophy ( J:193804 )

• following transverse aortic constriction

• in response to Ang II infusion

• treatment with FTY720 does not blocked cardiac hypertrophy induced by transverse aortic constriction