Show simple item record

dc.contributor.authorCastro Castro, Antonio
dc.contributor.authorMuriel, Olivia
dc.contributor.authorPozo, Miguel Ángel del
dc.contributor.authorBustelo, Xose R.
dc.identifier.citationCastro Castro, A., Muriel, O., del Pozo, M.Á., Bustelo, X.R. (2016). Characterization of novel molecular mechanisms favoring Rac1 membrane translocation. PLOS ONE, 11es_ES
dc.description.abstract[EN] The Rac1 GTPase plays key roles in cytoskeletal organization, cell motility and a variety of physiological and disease-linked responses. Wild type Rac1 signaling entails dissociation of the GTPase from cytosolic Rac1-Rho GDP dissociation inhibitor (GDI) complexes, translocation to membranes, activation by exchange factors, effector binding, and activation of downstream signaling cascades. Out of those steps, membrane translocation is the less understood. Using transfections of a expression cDNA library in cells expressing a Rac1 bioreporter, we previously identified a cytoskeletal feedback loop nucleated by the F-actin binding protein coronin 1A (Coro1A) that promotes Rac1 translocation to the plasma membrane by facilitating the Pak-dependent dissociation of Rac1-Rho GDI complexes. This screening identified other potential regulators of this process, including WDR26, basigin, and TMEM8A. Here, we show that WDR26 promotes Rac1 translocation following a Coro1A-like and Coro1A-dependent mechanism. By contrast, basigin and TMEM8A stabilize Rac1 at the plasma membrane by inhibiting the internalization of caveolin-rich membrane subdomains. This latter pathway is F-actin-dependent but Coro1A-, Pak- and Rho GDI-independent.es_ES
dc.format.extent23 p.
dc.publisherPLOS ONEes_ES
dc.rightsAttribution-NonCommercial-NoDerivs 4.0 International
dc.subjectCell and molecular biologyes_ES
dc.subjectMembrana celulares_ES
dc.titleCharacterization of novel molecular mechanisms favoring Rac1 membrane translocationes_ES

Files in this item


This item appears in the following Collection(s)

Show simple item record

Attribution-NonCommercial-NoDerivs 4.0 International
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 4.0 International