RalA-Exocyst Interaction Mediates GTP-dependent Exocytosis
نویسندگان
چکیده
منابع مشابه
RalA and RalB function as the critical GTP sensors for GTP-dependent exocytosis.
Although it has been established that the activation of GTPases by non-hydrolyzable GTP stimulates neurotransmitter release from many different secretory cell types, the underlying mechanisms remain unclear. In the present study we aimed to elucidate the functional role(s) for endogenous Ras-like protein A (RalA) and RalB GTPases in GTP-dependent exocytosis. For this purpose stable neuroendocri...
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Anchorage dependence of cell growth is a key metastasis-suppression mechanism that is mediated by effects of integrins on growth signaling pathways. The small GTPase RalA is activated in metastatic cancers through multiple mechanisms and specifically induces anchorage independence. Loss of integrin-mediated adhesion triggers caveolin-dependent internalization of cholesterol- and sphingolipid-ri...
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Cell polarization is essential for neuronal development in both the embryonic and postnatal brain. Here, using primary cultures, in vivo postnatal electroporation and conditional genetic ablation, we show that the Ras-like small GTPase RalA and its effector, the exocyst, regulate the morphology and polarized migration of neural progenitors derived from the subventricular zone, a major neurogeni...
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In eukaryotic cells, recycling endosome-mediated trafficking contributes to the completion of cytokinesis, in a manner under the control of the centrosome. We report that the exocyst complex and its interacting GTPase RalA play a critical role in this polarized trafficking process. RalA resides in the recycling endosome and relocates from the pericentrosomal region to key cytokinetic structures...
متن کاملExocytosis: The Many Masters of the Exocyst
The exocyst is a conserved eight-subunit complex involved in the docking of exocytic vesicles. The exocyst has now been identified as an effector for five small GTPases, including Sec4, Rho1, Rho3, Cdc42 and, most recently, RalA.
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ژورنال
عنوان ژورنال: Journal of Biological Chemistry
سال: 2004
ISSN: 0021-9258
DOI: 10.1074/jbc.m400522200