Abstract

α-Tropomyosin (αTm) is a 66kDa alpha-helical coiled-coil protein in thin filaments of cardiac muscle. Together with the Troponin complex (Tn), it is responsible for Ca2+ regulation of striated muscle contraction. When Ca2+ is released from sarcoplasmic reticulum and bound to Tn, the complex undergoes a conformational change that moves Tm away from myosin binding sites on actin, sites that are blocked in the absence of Ca2+. This allows actomyosin cross-bridge cycling, resulting in force generation and/or sarcomere shortening.

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