作者: E. Morkin , J. G. Edwards , R. W. Tsika , J. J. Bahl , I. L. Flink
DOI: 10.1007/978-1-4684-6015-5_12
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摘要: Rat cardiac myosin heavy chain (MHC) genes are regulated in ventricular myocardium by 3,5,3′-triiodo-L-thyronine (T3), which stimulates expression of the α-MHC gene and decreases β-MHC mRNA production (1,2). The protein products MHC combine to produce three isoforms, V1(α,α), V2(α,β), V3(β,β), order decreasing electrophoretic mobility Ca2+-ATPase activity (3). relative proportions these isoforms may be functionally important because speed contraction both skeletal muscles has been shown related ATPase (4). Recently, some forms familial hypertrophic cardiomyopathy have reported linked directly either a partial duplication or missense mutation (5,6)