IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v418y2002i6899d10.1038_nature00859.html
   My bibliography  Save this article

Mechanism of regulation of WAVE1-induced actin nucleation by Rac1 and Nck

Author

Listed:
  • Sharon Eden

    (Harvard Medical School)

  • Rajat Rohatgi

    (Harvard Medical School)

  • Alexandre V. Podtelejnikov

    (University of Southern Denmark-Odense Campusvej 55
    MDS Proteomics)

  • Matthias Mann

    (University of Southern Denmark-Odense Campusvej 55)

  • Marc W. Kirschner

    (Harvard Medical School)

Abstract

Rac signalling to actin—a pathway that is thought to be mediated by the protein Scar/WAVE (WASP (Wiskott–Aldrich syndrome protein)-family verprolin homologous protein)—has a principal role in cell motility. In an analogous pathway, direct interaction of Cdc42 with the related protein N-WASP stimulates actin polymerization1. For the Rac–WAVE pathway, no such direct interaction has been identified. Here we report a mechanism by which Rac and the adapter protein Nck activate actin nucleation through WAVE1. WAVE1 exists in a heterotetrameric complex that includes orthologues of human PIR121 (p53-inducible messenger RNA with a relative molecular mass (Mr) of 140,000), Nap125 (NCK-associated protein with an Mr of 125,000) and HSPC300. Whereas recombinant WAVE1 is constitutively active, the WAVE1 complex is inactive. We therefore propose that Rac1 and Nck cause dissociation of the WAVE1 complex, which releases active WAVE1–HSPC300 and leads to actin nucleation.

Suggested Citation

  • Sharon Eden & Rajat Rohatgi & Alexandre V. Podtelejnikov & Matthias Mann & Marc W. Kirschner, 2002. "Mechanism of regulation of WAVE1-induced actin nucleation by Rac1 and Nck," Nature, Nature, vol. 418(6899), pages 790-793, August.
    • Handle: RePEc:nat:nature:v:418:y:2002:i:6899:d:10.1038_nature00859
    DOI: 10.1038/nature00859
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/nature00859
    File Function: Abstract
    Download Restriction: Access to the full text of the articles in this series is restricted.
    File URL: https://libkey.io/10.1038/nature00859?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    As the access to this document is restricted, you may want to search for a different version of it.

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:nature:v:418:y:2002:i:6899:d:10.1038_nature00859. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.