Abstract:
:Neurite outgrowth is key to the formation of functional circuits during neuronal development. Neurotrophins, including nerve growth factor (NGF), increase neurite outgrowth in part by altering the function and expression of Ca(2+)-permeable cation channels. Here we report that transient receptor potential vanilloid 2 (TRPV2) is an intracellular Ca(2+)-permeable TRPV channel upregulated by NGF via the mitogen-activated protein kinase (MAPK) signaling pathway to augment neurite outgrowth. TRPV2 colocalized with Rab7, a late endosome protein, in addition to TrkA and activated extracellular signal-regulated kinase (ERK) in neurites, indicating that the channel is closely associated with signaling endosomes. In line with these results, we showed that TRPV2 acts as an ERK substrate and identified the motifs necessary for phosphorylation of TRPV2 by ERK. Furthermore, neurite length, TRPV2 expression, and TRPV2-mediated Ca(2+) signals were reduced by mutagenesis of these key ERK phosphorylation sites. Based on these findings, we identified a previously uncharacterized mechanism by which ERK controls TRPV2-mediated Ca(2+) signals in developing neurons and further establish TRPV2 as a critical intracellular ion channel in neuronal function.
journal_name
Mol Cell Bioljournal_title
Molecular and cellular biologyauthors
Cohen MR,Johnson WM,Pilat JM,Kiselar J,DeFrancesco-Lisowitz A,Zigmond RE,Moiseenkova-Bell VYdoi
10.1128/MCB.00549-15subject
Has Abstractpub_date
2015-12-01 00:00:00pages
4238-52issue
24eissn
0270-7306issn
1098-5549pii
MCB.00549-15journal_volume
35pub_type
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