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    Differential Rac1 signalling by guanine nucleotide exchange factors implicates FLII in regulating Rac1-driven cell migration.

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    Authors
    Marei, Hadir
    Carpy, A
    Woroniuk, Anna
    Vennin, C
    White, Gavin R M
    Timpson, P
    Macek, B
    Malliri, Angeliki
    Affiliation
    Cell Signalling Group, Cancer Research UK Manchester Institute, The University of Manchester, Manchester M204BX, UK
    Issue Date
    2016
    
    Metadata
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    Abstract
    The small GTPase Rac1 has been implicated in the formation and dissemination of tumours. Upon activation by guanine nucleotide exchange factors (GEFs), Rac1 associates with a variety of proteins in the cell thereby regulating various functions, including cell migration. However, activation of Rac1 can lead to opposing migratory phenotypes raising the possibility of exacerbating tumour progression when targeting Rac1 in a clinical setting. This calls for the identification of factors that influence Rac1-driven cell motility. Here we show that Tiam1 and P-Rex1, two Rac GEFs, promote Rac1 anti- and pro-migratory signalling cascades, respectively, through regulating the Rac1 interactome. In particular, we demonstrate that P-Rex1 stimulates migration through enhancing the interaction between Rac1 and the actin-remodelling protein flightless-1 homologue, to modulate cell contraction in a RhoA-ROCK-independent manner.
    Citation
    Differential Rac1 signalling by guanine nucleotide exchange factors implicates FLII in regulating Rac1-driven cell migration. 2016, 7:10664 Nat Commun
    Journal
    Nature Communications
    URI
    http://hdl.handle.net/10541/604203
    DOI
    10.1038/ncomms10664
    PubMed ID
    26887924
    Type
    Article
    Language
    en
    ISSN
    2041-1723
    ae974a485f413a2113503eed53cd6c53
    10.1038/ncomms10664
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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