Calsequestrin, triadin and more: the molecules that modulate calcium release in cardiac and skeletal muscle.

摘要

Calcium signals play a role in every cell where functional switching takes place. These signals were demonstrated first in striated muscles, where they control the force-generating interaction among contractile filaments, the function named excitation-contraction (EC) coupling. The three main molecular players that cooperate to produce these signals are the Ca~2+ release channel of the sarcoplasmic reticulum (or RyR), the voltage sensor (or DHPR) - a molecule resident in the plasma membrane and its invaginations, which transduces the membrane potential changes to a control signal for the RyR - and the ATP-powered pump that brings Ca~2+ back into the storage organelle. Melzer et al. (1995), Bers (2002) and Guatimosim et al. (2002) provide useful background information on skeletal and cardiac muscle EC coupling.