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Phenotypes Associated with This Genotype
Genotype
MGI:3527229
Allelic
Composition
Mybpc3tm1Rmos/Mybpc3tm1Rmos
Genetic
Background
either: (involves: 129) or (involves: 129 * C57BL/6)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mybpc3tm1Rmos mutation (0 available); any Mybpc3 mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• myocyte disarray and loss of the close lateral alignment of myofibrils are seen (J:95725)
• myocyte disarray and loss of the close lateral alignment of myofibrils are seen (J:95725)
• heart to body weight ratios are increased as is the thickness of the anterior and posterior walls (J:95725)
• hypertrophy is seen in 3 week old homozygotes (J:95725)
• heart to body weight ratios are increased as is the thickness of the anterior and posterior walls (J:95725)
• hypertrophy is seen in 3 week old homozygotes (J:95725)
• foci of interstitial fibrosis were seen in 3 out of 5 homozygotes (J:95725)
• foci of interstitial fibrosis were seen in 3 out of 5 homozygotes (J:95725)
• Ca2+ sensitivity of tension is reduced in myocytes from mutant hearts (J:95725)
• Ca2+ sensitivity of tension is reduced in myocytes from mutant hearts (J:95725)
• left ventricular fractional shortening is significantly reduced (J:95725)
• left ventricular fractional shortening is significantly reduced (J:95725)
• skinned cardiomyocytes from homozygotes exhibit faster loaded shortening velocities, greater power output, and increased force redevelopment rates, due to increased crossbridge interaction kinetics resulting from absence of myosin head constraints (J:109391)
• peak normalized power output is increased by 26% in mutant cardiomyocytes during maximal Ca2+ activations (J:109391)
• peak power output is increased to an even greater extent (46%) during half-maximal Ca2+ activations (J:109391)
• the rate constant of force redevelopment (ktr) is unaltered during maximal Ca2+ activations; however, ktr at half-maximal Ca2+ activation is significantly greater in mutant cardiomyocytes relative to wild-type (J:109391)
• skinned cardiomyocytes from homozygotes exhibit faster loaded shortening velocities, greater power output, and increased force redevelopment rates, due to increased crossbridge interaction kinetics resulting from absence of myosin head constraints (J:109391)
• peak normalized power output is increased by 26% in mutant cardiomyocytes during maximal Ca2+ activations (J:109391)
• peak power output is increased to an even greater extent (46%) during half-maximal Ca2+ activations (J:109391)
• the rate constant of force redevelopment (ktr) is unaltered during maximal Ca2+ activations; however, ktr at half-maximal Ca2+ activation is significantly greater in mutant cardiomyocytes relative to wild-type (J:109391)
• hypertrophic cardiomyopathy is seen (J:95725)
• hypertrophic cardiomyopathy is seen (J:95725)

muscle
• Ca2+ sensitivity of tension is reduced in myocytes from mutant hearts (J:95725)
• Ca2+ sensitivity of tension is reduced in myocytes from mutant hearts (J:95725)
• left ventricular fractional shortening is significantly reduced (J:95725)
• left ventricular fractional shortening is significantly reduced (J:95725)
• hypertrophic cardiomyopathy is seen (J:95725)
• hypertrophic cardiomyopathy is seen (J:95725)

Mouse Models of Human Disease
OMIM ID Ref(s)
Cardiomyopathy, Familial Hypertrophic, 4; CMH4 115197 J:95725


Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Tumor Biology (MTB), Gene Ontology (GO), MouseCyc
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last database update
02/02/2016
MGI 6.02
The Jackson Laboratory