A family affair: A Ral-exocyst-centered network links Ras, Rac, Rho signaling to control cell migration.
Rac
Ral
Ras
Rho
Wave
exocyst
migration
Journal
Small GTPases
ISSN: 2154-1256
Titre abrégé: Small GTPases
Pays: United States
ID NLM: 101530974
Informations de publication
Date de publication:
09 2019
09 2019
Historique:
pubmed:
13
5
2017
medline:
10
4
2020
entrez:
13
5
2017
Statut:
ppublish
Résumé
Cell migration is central to many developmental, physiologic and pathological processes, including cancer progression. The Ral GTPases (RalA and RalB) which act down-stream the Ras oncogenes, are key players in the coordination between membrane trafficking and actin polymerization. A major direct effector of Ral, the exocyst complex, works in polarized exocytosis and is at the center of multiple protein-protein interactions that support cell migration by promoting protrusion formation, front-rear polarization, and extra-cellular matrix degradation. In this review we describe the recent advancements in deciphering the molecular mechanisms underlying this role of Ral via exocyst on cell migration. Among others, we will discuss the recently identified cross-talk between Ral and Rac1 pathways: exocyst binds to a negative regulator (the RacGAP SH3BP1) and to the major effector (the Wave Regulatory Complex, WRC) of Rac1, the master regulator of protrusions. Next challenge will be to better characterize the dynamics in space and in time of these molecular interplays, to better understand the pleiotropic functions of Ral in both normal and cancer cells.
Identifiants
pubmed: 28498728
doi: 10.1080/21541248.2017.1310649
pmc: PMC6748358
doi:
Substances chimiques
GTPase-Activating Proteins
0
Neoplasm Proteins
0
RAC1 protein, human
0
Ralb protein, human
0
SH3BP1 protein, human
0
RALA protein, human
EC 3.6.1.-
rac1 GTP-Binding Protein
EC 3.6.5.2
ral GTP-Binding Proteins
EC 3.6.5.2
ras Proteins
EC 3.6.5.2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Video-Audio Media
Langues
eng
Sous-ensembles de citation
IM
Pagination
323-330Références
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