期刊
PLOS ONE
卷 7, 期 6, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0038517
关键词
-
资金
- Cancer Research UK
- EC Marie Curie Fellowship
- Career Re-entry Fellowship from the Wellcome Trust
The role of G alpha i proteins coupled to chemokine receptors in directed migration of immune cells is well understood. In this study we show that the separate class of G alpha q/11 proteins is required for the underlying ability of T cells to migrate both randomly and in a directed chemokine-dependent manner. Interfering with G alpha q or G alpha 11 using dominant negative cDNA constructs or siRNA for G alpha q causes accumulation of LFA-1 adhesions and stalled migration. G alpha q/11 has an impact on LFA-1 expression at plasma membrane level and also on its internalization. Additionally G alpha q co-localizes with LFA-1- and EEA1-expressing intracellular vesicles and partially with Rap1- but not Rab11-expressing vesicles. However the influence of G alpha q is not confined to the vesicles that express it, as its reduction alters intracellular trafficking of other vesicles involved in recycling. In summary vesicle-associated G alpha q/11 is required for the turnover of LFA-1 adhesion that is necessary for migration. These G proteins participate directly in the initial phase of recycling and this has an impact on later stages of the endo-exocytic pathway.
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