期刊
MOLECULAR AND CELLULAR NEUROSCIENCE
卷 33, 期 1, 页码 36-46出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.mcn.2006.06.002
关键词
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资金
- NICHD NIH HHS [HD23315] Funding Source: Medline
- NINDS NIH HHS [NS21072] Funding Source: Medline
Signaling through Trk receptor tyrosine kinases can occur in the absence of neurotrophins through certain G-protein-coupled receptors (GPCRs). It has previously been suggested that GPCR-mediated Trk activation occurs on intracellular membranes and involves several second messengers, including Src family kinases and intracellular calcium. Here, we describe a novel role for the Src family kinase, Fyn, in regulating signaling events between GPCRs and Trk. We find that Fyn expression is sufficient to allow transactivation of Trk by adenosine and that Fyn and Trk are colocalized in a juxtanuclear membrane compartment. Adenosine activation of Fyn results in direct phosphorylation of Trk in vitro and follows a delayed time course that coincides with Trk activation. These results indicate that Fyn is activated by GPCR stimulation and is responsible for transactivation of Trk receptors on intracellular membranes. (c) 2006 Elsevier Inc. All rights reserved.
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