CAV3:TRIM72:DYSF binds ANXAs

Mechanical stress and repetitive muscle contraction often causes membrane disruption to the sarcolemma. Healthy muscle is able to repair these disruptions by a Ca2+-dependent pathway. The combination of dysferlin (DYSF), caveolin 3 (CAV3) and tripartite motif-containing protein 72 (TRIM72 aka MG53) appears to be essential for the repair of muscle membrane damage (Cai et al. 2009). DYSF subsequently binds annexin A6 (ANXA6), a member of a family of phospholipid-binding proteins in a Ca2+-dependent manner. This interaction has been demonstrated in imaging experiments in zebrafish (Roostalu U & Strahle 2012). This interaction creates a platform for interacting proteins at the sarcolemma membrane surface and sequential recruitment of annexin A1 and A2 (ANXA1 and 2) to the repair site. The human event is deduced on the basis of experiments performed in mice (Lennon et al. 2003).

机械应力和反复的肌肉收缩常导致肌纤维膜损伤。健康的肌肉通过依赖于Ca2+的途径来修复这些损伤。DYSF（肌萎缩蛋白）、caveolin 3（Cav3）以及包含三联体基序的蛋白72（TRIM72，又称MG53）的结合似乎对于肌膜损伤的修复至关重要（Cai等人，2009年）。DYSF随后以Ca2+依赖的方式与annexin A6（ANXA6）结合，annexin A6是磷脂结合蛋白家族的一员。这一相互作用已在斑马鱼的成像实验中得到证实（Roostalu U与Strahle，2012年）。这种相互作用在肌纤维膜表面形成了一个蛋白质相互作用的平台，并依次招募annexin A1和A2（ANXA1和2）至修复位点。人类事件是基于在老鼠身上进行的实验推断得出的（Lennon等人，2003年）。