Altered regulation of cardiac muscle contraction by Troponin T mutations that cause familial hypertrophic cardiomyopathy

Trends in Cardiovascular Medicine

Volumn 11, Issue 5, 2001, Pages 206-212

  Knollmann, Björn C ^a   Potter, James D ^a  

^a UNIVERSITY OF MIAMI MILLER SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CALCIUM ION; TROPONIN T;

BINDING AFFINITY; BLOOD PRESSURE REGULATION; CALCIUM CELL LEVEL; CALCIUM TRANSPORT; CORRELATION FUNCTION; DIASTOLIC BLOOD PRESSURE; FAMILIAL DISEASE; HEART CONTRACTION; HEART FUNCTION; HEART MUSCLE CONTRACTILE FORCE; HEART MUSCLE RELAXATION; HEART STIMULATION; HEART VENTRICLE COMPLIANCE; HUMAN; HYPERTROPHIC CARDIOMYOPATHY; IN VITRO STUDY; INOTROPISM; MUTATION; MYOFILAMENT; NONHUMAN; PATHOPHYSIOLOGY; PH; PHENOTYPE; PRIORITY JOURNAL; REVIEW; SYSTOLIC BLOOD PRESSURE; TRANSGENIC ANIMAL;

ANIMALS; ANIMALS, GENETICALLY MODIFIED; CALCIUM; CARDIOMYOPATHY, HYPERTROPHIC; HUMANS; MODELS, ANIMAL; MUTATION; MYOCARDIAL CONTRACTION; PHENOTYPE; TROPONIN T;

EID: 0034796231     PISSN: 10501738     EISSN: None     Source Type: Journal    
DOI: 10.1016/S1050-1738(01)00115-3     Document Type: Review

References (42)

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14. Hypertrophic cardiomyopathy caused by a novel alpha-tropomyosin mutation (V95A) is associated with mild cardiac phenotype, abnormal calcium binding to troponin, abnormal myosin cycling, and poor prognosis
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