Fallotoksiny kak instrument dlia issledovaniia vnutrimiofibrilliarnoi reguliatsii myshechnogo sokrashcheniia.

The contraction of myofibrils is regulated by the coordinated action of Ca2+ and myosin cross-bridges. Phallotoxins induce a variety of specific changes in myofibrillar functioning and are therefore a potentially valuable tool for muscle research. There are two greatly differing classes of drugs among phallotoxins: (1) recently discovered secophalloidin and its derivatives. The unique property of secophalloidin is muscle activation without Ca2+, possibly by direct influence on actomyosin interaction. These drugs seem to be especially useful for studying the role of cross-bridges in muscle regulation; (2) the phalloidin group, which includes the majority of phallotoxins. When binding to the phalloidin site on F-actin, they cause muscle-specific changes. In cardiac muscle they work as Ca2+ sensitizers, increasing both the maximal force and Ca2+ sensitivity. An advantage of these drugs is that the target site is known, which allows one to unravel the sequence of molecular events leading to increased contractile function. Presumably, the complex effect of phalloidin in skeletal muscle is related to the disturbance of the actin-nebulin interaction, which may help to clarify the role of nebulin in the regulation contraction.