WIP regulates N-WASP-mediated actin polymerization and filopodium formation
作者： Narcisa Martinez-Quiles , Rajat Rohatgi , Inés M Antón , Miguel Medina , Stephen P Saville
DOI: 10.1038/35074551
关键词:
摘要: Induction of filopodia is dependent on activation the small GTPase Cdc42 and neural Wiskott-Aldrich-syndrome protein (N-WASP). Here we show that WASP-interacting (WIP) interacts directly with N-WASP actin. WIP retards N-WASP/Cdc42-activated actin polymerization mediated by Arp2/3 complex, stabilizes filaments. Microinjection into NIH 3T3 fibroblasts induces filopodia; this inhibited microinjection anti-N-WASP antibody. anti-WIP antibody inhibits induction bradykinin, an active mutant (Cdc42(V12)) N-WASP. Our results indicate may act as a functional unit in filopodium formation, which consistent their role actin-tail formation cells infected vaccinia virus or Shigella.
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