对aPKC-Par6及其多位极性基质Lgl的捕获,相互抑制和释放机制

Christopher P Earl1, Mathias Cobbaut2,3, André Barros-Carvalho4,5

  • 1Signalling and Structural Biology Laboratory, Francis Crick Institute, London, UK.

概括

一个新的结构揭示了非典型的蛋白激酶C (aPKC) 和分区缺陷蛋白6 (Par6) 如何与致命的 (2) 巨型幼虫 (Lgl) 蛋白相互作用. 这种相互作用通过形成抑制酸化的稳定复合体来调节细胞极性.

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