4.6 Article

WIP/ITSN1 complex is involved in cellular vesicle trafficking and formation of filopodia-like protrusions

期刊

GENE
卷 674, 期 -, 页码 49-56

出版社

ELSEVIER
DOI: 10.1016/j.gene.2018.06.078

关键词

Filopodia-like protrusions; ITSN1; N-WASP; Vesicular trafficking; WIP

资金

  1. NAS of Ukraine [0115U002947]
  2. National Center for Scientific Research of France (CNRS) Human pathology, from the molecular to the cellular level [0115U002947, 0113U002831]

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WIP (WASP interacting protein) together with N-WASP (neural Wiskott-Aldrich syndrome protein) regulates actin polymerization that is crucial for invadopodia and filopodia formation. Recently, we reported the WIP interaction with ITSN1 which is highly implicated in endo-/exocytosis, apoptosis, mitogenic signaling and cytoskeleton rearrangements. Here we demonstrate that the WIP/ITSN1 complex is involved in the transferrin receptor recycling and partially co-localizes with a marker of the fast recycling endosomes, RAB4. Moreover, ITSN1 recruits WIP to RAB4-positive vesicles upon overexpression. Our data indicate that WIP enhances the interaction of N-WASP with ITSN1 and promotes ITSN1/beta-actin association. Moreover, the WIP/ITSN1-L complex facilitates formation of filopodia-like protrusions in MCF-7 cells. Thus, WIP/ITSN1 complex is involved in the cellular vesicle trafficking and actin-dependent membrane processes.

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