HOME Class Schedule	Bioen 599 F, Autumn 2000 Bioengineering Principles of Physiology
	Lecture Material and Notes Week 2, Lecture 6: Ca2+ regulation of actomyosin interactions Michael Regnier Lecture theme and outline: Cross-bridge cycling can continue indefinitely as long ATP supply is sufficient when actomyosin is activated. During rest (quiescent) periods, actomyosin interaction is inhibited. While myosin ATPase activity is accelerated by one protein of the thin filament (actin), it is modulated by other proteins of the thin filament (the regulatory proteins troponin (Tn) and tropomyosin (Tm)). In the presence of Ca2+, allosteric interactions between myosin, actin, Tn and Tm control the availability of myosin binding sites on actin to regulate cross-bridge formation. Some form of these interactions also control the relaxation properties of muscle. Review the structure of the thin filament. Proposed sequence of events leading to thin filament activation. Regulation of steady-state force in skeletal and cardiac muscle. Methods to study - biochemistry and mechanics of isolated myosin and thin filaments, single de-membranated fiber studies, site-directed mutagenesis. Kinetic aspects of thin filament regulation of contraction. Simulations of Ca2+ regulation of thin filament activation and force development. Suggested reading: see Lecture 4.
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