Phenotypes associated with this allele

• Allele Symbol: Abi3bp^tm1Tac
• Allele Name: targeted mutation 1, Taconic
• Allele ID: MGI:6356821
• Summary: 1 genotype

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Abi3bp^tm1Tac/Abi3bp^tm1Tac	involves: 129S5/SvEvBrd	MGI:6763158

Genotype
MGI:6763158

hm1

• Allelic Composition: Abi3bp^tm1Tac/Abi3bp^tm1Tac
• Genetic Background: involves: 129S5/SvEvBrd

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

cardiovascular system

decreased cardiac muscle contractility ( J:251000 )

• at 1 month after myocardial infarction, mice exhibit a lower ejection fraction and fractional shortening of the left ventricle than wild-type controls

increased susceptibility to myocardial ischemic injury ( J:251000 )

• at 1 month, but not at 1 week, after myocardial infarction, mice exhibit higher cardiac fibrosis levels than wild-type controls and cardiac tissue is more fragile with ~90% of the heart sections exhibiting breakage in the injured area relative to ~10% in sections from wild-type hearts

cellular

abnormal cell differentiation ( J:251000 )

• when cultured in vitro under differentiating conditions, c-Kit+ cardiac progenitor cells (CPCs) isolated from homozygous mutant mice show reduced expression of both early and late cardiomyocyte markers

• at 1 week after myocardial infarction, mice fail to show an increase in the percentage of double-positive (c-Kit+/Gata4+) cells suggesting that CPC differentiation/commitment is inhibited, unlike in wild-type controls

• however, cardiomyocyte proliferation in the border zone is normal at 1 week after myocardial injury

increased cell proliferation ( J:251000 )

• in vitro, c-Kit+ CPCs isolated from homozygous mutant mice exhibit a higher proliferative capacity than wild-type cells

• in vivo, c-Kit+ CPC number and proliferative capacity are increased

homeostasis/metabolism

increased susceptibility to myocardial ischemic injury ( J:251000 )

• at 1 month, but not at 1 week, after myocardial infarction, mice exhibit higher cardiac fibrosis levels than wild-type controls and cardiac tissue is more fragile with ~90% of the heart sections exhibiting breakage in the injured area relative to ~10% in sections from wild-type hearts

muscle

decreased cardiac muscle contractility ( J:251000 )

• at 1 month after myocardial infarction, mice exhibit a lower ejection fraction and fractional shortening of the left ventricle than wild-type controls