Rendon A, Waksman A
Biochim Biophys Acta. 1980 Dec 2;603(1):178-84. doi: 10.1016/0005-2736(80)90400-9.
Mitoplasts isolated from rat liver mitochondria were treated with dimethyladipimidate, a bifunctional alkylating agent. This agent causes, concurrently with modification of amino groups, loss of osmotic response. It was found that after cross-linking, the movement effector, succinate, was unable to induce the aspartate aminotransferase release from mitoplasts. In contrast, dimethyladipimidate-treated mitoplasts were still able to internalize 125I-labeled aspartate aminotransferase upon removal of exogenous succinate. The possible involvement of membrane asymmetry in the mechanism of translocation of porteins through the inner mitochondrial membrane is discussed.
从大鼠肝脏线粒体中分离出的线粒体被双功能烷基化剂己二酸二甲酯处理。该试剂在修饰氨基的同时会导致渗透反应丧失。研究发现，交联后，运动效应物琥珀酸无法诱导天冬氨酸氨基转移酶从线粒体中释放。相反，去除外源琥珀酸后，经己二酸二甲酯处理的线粒体仍能够内化125I标记的天冬氨酸氨基转移酶。本文讨论了膜不对称性在蛋白质通过线粒体内膜转运机制中的可能作用。
