Phenotypes associated with this allele

• Allele Symbol: Pak1^tm1.1Xwg
• Allele Name: targeted mutation 1.1, Xin Wang
• Allele ID: MGI:5470058
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Pak1^tm1.1Xwg/Pak1^tm1.1Xwg	B6.129-Pak1^tm1.1Xwg	MGI:5470078
cn2	Pak1^tm1.1Xwg/Pak1^tm1.1Xwg Myl2^tm1(cre)Krc/Myl2^+	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6	MGI:5470080

Genotype
MGI:5470078

hm1

• Allelic Composition: Pak1^tm1.1Xwg/Pak1^tm1.1Xwg
• Genetic Background: B6.129-Pak1^tm1.1Xwg

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

normal phenotype

no abnormal phenotype detected ( J:193804 )

• mice are healthy and fertile

Genotype
MGI:5470080

cn2

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

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