Abstract
The contraction of striated muscle is known to be caused by an active relative sliding of the thick and thin myofilaments.1,2 In addition, there is an increasing amount of evidence suggesting that active sliding between protein filaments occurs not only between the thin actin-containing filaments and the thick myosin-containing filaments, involved in the motility of a wide variety of cells,3 but also in the cilia motion involving dynein and tubulin rather than myosin and actin.4 The most widely held view for the molecular mechanism of the sliding process in striated muscle is that the cross-bridges which are projected outward from the thick myofilament moves cyclically upon activation. The cross-bridge motions in turn pull the thin myofilament. So far, this scheme has been supported only by indirect evidence.5,6
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