Show simple item record

dc.contributor.authorMarei, Hadir
dc.contributor.authorMalliri, Angeliki
dc.date.accessioned2016-07-15T15:14:44Z
dc.date.available2016-07-15T15:14:44Z
dc.date.issued2016
dc.identifier.citationGEFs: Dual regulation of Rac1 signaling. 2016:0 Small GTPasesen
dc.identifier.issn2154-1256
dc.identifier.pmid27314616
dc.identifier.doi10.1080/21541248.2016.1202635
dc.identifier.urihttp://hdl.handle.net/10541/617030
dc.description.abstractGEFs play a critical role in regulating Rac1 signaling. They serve as signaling nodes converting upstream signals into downstream Rac1-driven cellular responses. Through associating with membrane-bound Rac1, GEFs facilitate the exchange of GDP for GTP, thereby activating Rac1. As a result, Rac1 undergoes conformational changes that mediate its interaction with downstream effectors, linking Rac1 to a multitude of physiological and pathological processes. Interestingly, at least 20 GEFs have been shown to activate Rac1, suggesting a more complex role of GEFs in regulating Rac1 signaling apart from promoting the exchange of GDP for GTP. Indeed, accumulating evidence implicates GEFs in directing the specificity of Rac1-driven signaling cascades, although the underlying mechanisms were poorly defined. Recently, through conducting a comparative study, we highlighted the role of two Rac-specific GEFs, Tiam1 and P-Rex1, in dictating the biological outcome downstream of Rac1. Importantly, further proteomic analysis uncovered a GEF activity-independent role of both GEFs in modulating the Rac1 interactome, which results in the stimulation of GEF-specific signaling cascades. Here, we provide an overview of our recent findings and discuss the role of GEFs as master regulators of Rac1 signaling with a particular focus on GEF-mediated modulation of cell migration following Rac1 activation.
dc.languageENG
dc.language.isoenen
dc.rightsArchived with thanks to Small GTPasesen
dc.titleGEFs: Dual regulation of Rac1 signaling.en
dc.typeMeetings and Proceedingsen
dc.contributor.departmentCell Signaling Group, Cancer Research UK Manchester Institute, The University of Manchester , Manchester M20 4BXen
dc.identifier.journalSmall GTPasesen
refterms.dateFOA2018-12-17T14:36:26Z
html.description.abstractGEFs play a critical role in regulating Rac1 signaling. They serve as signaling nodes converting upstream signals into downstream Rac1-driven cellular responses. Through associating with membrane-bound Rac1, GEFs facilitate the exchange of GDP for GTP, thereby activating Rac1. As a result, Rac1 undergoes conformational changes that mediate its interaction with downstream effectors, linking Rac1 to a multitude of physiological and pathological processes. Interestingly, at least 20 GEFs have been shown to activate Rac1, suggesting a more complex role of GEFs in regulating Rac1 signaling apart from promoting the exchange of GDP for GTP. Indeed, accumulating evidence implicates GEFs in directing the specificity of Rac1-driven signaling cascades, although the underlying mechanisms were poorly defined. Recently, through conducting a comparative study, we highlighted the role of two Rac-specific GEFs, Tiam1 and P-Rex1, in dictating the biological outcome downstream of Rac1. Importantly, further proteomic analysis uncovered a GEF activity-independent role of both GEFs in modulating the Rac1 interactome, which results in the stimulation of GEF-specific signaling cascades. Here, we provide an overview of our recent findings and discuss the role of GEFs as master regulators of Rac1 signaling with a particular focus on GEF-mediated modulation of cell migration following Rac1 activation.


Files in this item

Thumbnail
Name:
GEFs Dual regulation of Rac1 ...
Size:
1.007Mb
Format:
PDF
Description:
Open access full text article

This item appears in the following Collection(s)

Show simple item record