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Paper Details

Hypertrophic cardiomyopathy β-cardiac myosin mutation (P710R) leads to hypercontractility by disrupting super relaxed state.
Proc Natl Acad Sci U S A
49
2021
-cardiac myosin, ATPase, Akt, Cellular hypertrophy, ERK, HCM, Hypertrophic cardiomyopathy, MYH7, MYH7 mutations, P710R, P710R cells, actin, actin-activated ATPase, cardiac myosin, cardiomyocyte, cardiomyocyte hypertrophy, cells, human, human induced pluripotent derived stem cell (hiPSC)-cardiomyocytes, hypercontractility, inherited form of heart disease, isogenic control cells, myosin, myosin constructs, myosin molecules, myosin motor
Author NameAffiliation
Beth L PruittStanford University
Beth L PruittSchool of Engineering and School of Medicine, Stanford University
Beth L PruittStanford Cardiovascular Institute, Stanford University School of Medicine
Beth L PruittUniversity of California santa barbara
Daniel BernsteinStanford University School of Medicine
Daniel BernsteinStanford Cardiovascular Institute, Stanford University School of Medicine
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