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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Akap13Gt(CSJ306)Byg
gene trap CSJ306, BayGenomics
MGI:3880669
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Akap13Gt(CSJ306)Byg/Akap13Gt(CSJ306)Byg involves: 129P2/OlaHsd * C57BL/6 MGI:5775134


Genotype
MGI:5775134
hm1
Allelic
Composition
Akap13Gt(CSJ306)Byg/Akap13Gt(CSJ306)Byg
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Akap13Gt(CSJ306)Byg mutation (1 available); any Akap13 mutation (178 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Increased fibrosis in Akap13Gt(CSJ306)Byg/Akap13Gt(CSJ306)Byg hearts in response to isoproterenol treatment

mortality/aging
N
• unexpectedly, homozygotes are born at normal Mendelian ratios and exhibit normal development and viability

cardiovascular system
• in response to chronic beta-adrenergic stimulation, isoproterenol-treated mice appear to develop more cardiac fibrosis than isoproterenol-treated wild-type controls
• one of the isoproterenol-treated hearts showed a large area of fibrosis at the top of the right and left ventricular walls (>25% of myocardial area)
• following isoproterenol treatment, mice fail to exhibit increased left ventricle fractional shortening (FS) and ejection fraction (EF), unlike isoproterenol-treated wild-type controls
• despite similar cardiac hypertrophic remodeling, isoproterenol-treated mice tend to exhibit lower left ventricle FS and EF than wild-type controls on day 13 of isoproterenol treatment
• in response to chronic beta-adrenergic stimulation, isoproterenol-treated mice exhibit hypertrophic cardiac structural changes to a similar extent as in isoproterenol-treated wild-type controls but display a tend towards lower levels cardiac contractility (as measured by fractional shortening and ejection fraction) and increased cardiac fibrosis (as assessed by Massons trichrome staining)
• however, under normal physiological conditions, adult heart size and morphology is normal, with no significant alterations in cardiomyocyte organization and structure, levels of fibrosis or cardiac electrical activity

homeostasis/metabolism
• in response to chronic beta-adrenergic stimulation, isoproterenol-treated mice exhibit hypertrophic cardiac structural changes to a similar extent as in isoproterenol-treated wild-type controls but display a tend towards lower levels cardiac contractility (as measured by fractional shortening and ejection fraction) and increased cardiac fibrosis (as assessed by Massons trichrome staining)
• however, under normal physiological conditions, adult heart size and morphology is normal, with no significant alterations in cardiomyocyte organization and structure, levels of fibrosis or cardiac electrical activity

muscle
• following isoproterenol treatment, mice fail to exhibit increased left ventricle fractional shortening (FS) and ejection fraction (EF), unlike isoproterenol-treated wild-type controls
• despite similar cardiac hypertrophic remodeling, isoproterenol-treated mice tend to exhibit lower left ventricle FS and EF than wild-type controls on day 13 of isoproterenol treatment

cellular
• in response to chronic beta-adrenergic stimulation, isoproterenol-treated mice appear to develop more cardiac fibrosis than isoproterenol-treated wild-type controls
• one of the isoproterenol-treated hearts showed a large area of fibrosis at the top of the right and left ventricular walls (>25% of myocardial area)





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last database update
11/12/2024
MGI 6.24
The Jackson Laboratory