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Direct interaction of endogenous Kv channels with syntaxin enhances exocytosis by neuroendocrine cells.

Authors: Singer-Lahat, D  Chikvashvili, D  Lotan, I 
Citation: Singer-Lahat D, etal., PLoS One. 2008 Jan 2;3(1):e1381. doi: 10.1371/journal.pone.0001381.
Pubmed: (View Article at PubMed) PMID:18167541
DOI: Full-text: DOI:10.1371/journal.pone.0001381

K(+) efflux through voltage-gated K(+) (Kv) channels can attenuate the release of neurotransmitters, neuropeptides and hormones by hyperpolarizing the membrane potential and attenuating Ca(2+) influx. Notably, direct interaction between Kv2.1 channels overexpressed in PC12 cells and syntaxin has recently been shown to facilitate dense core vesicle (DCV)-mediated release. Here, we focus on endogenous Kv2.1 channels and show that disruption of their interaction with native syntaxin after ATP-dependent priming of the vesicles by Kv2.1 syntaxin-binding peptides inhibits Ca(2+) -triggered exocytosis of DCVs from cracked PC12 cells in a specific and dose-dependent manner. The inhibition cannot simply be explained by the impairment of the interaction of syntaxin with its SNARE cognates. Thus, direct association between endogenous Kv2.1 and syntaxin enhances exocytosis and in combination with the Kv2.1 inhibitory effect to hyperpolarize the membrane potential, could contribute to the known activity dependence of DCV release in neuroendocrine cells and in dendrites where Kv2.1 commonly expresses and influences release.

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CRRD Object Information
CRRD ID: 10047360
Created: 2015-07-11
Species: All species
Last Modified: 2015-07-11
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.