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Non-conducting function of the Kv2.1 channel enables it to recruit vesicles for release in neuroendocrine and nerve cells.

Authors: Feinshreiber, L  Singer-Lahat, D  Friedrich, R  Matti, U  Sheinin, A  Yizhar, O  Nachman, R  Chikvashvili, D  Rettig, J  Ashery, U  Lotan, I 
Citation: Feinshreiber L, etal., J Cell Sci. 2010 Jun 1;123(Pt 11):1940-7. doi: 10.1242/jcs.063719.
Pubmed: (View Article at PubMed) PMID:20484665
DOI: Full-text: DOI:10.1242/jcs.063719

Regulation of exocytosis by voltage-gated K(+) channels has classically been viewed as inhibition mediated by K(+) fluxes. We recently identified a new role for Kv2.1 in facilitating vesicle release from neuroendocrine cells, which is independent of K(+) flux. Here, we show that Kv2.1-induced facilitation of release is not restricted to neuroendocrine cells, but also occurs in the somatic-vesicle release from dorsal-root-ganglion neurons and is mediated by direct association of Kv2.1 with syntaxin. We further show in adrenal chromaffin cells that facilitation induced by both wild-type and non-conducting mutant Kv2.1 channels in response to long stimulation persists during successive stimulation, and can be attributed to an increased number of exocytotic events and not to changes in single-spike kinetics. Moreover, rigorous analysis of the pools of released vesicles reveals that Kv2.1 enhances the rate of vesicle recruitment during stimulation with high Ca(2+), without affecting the size of the readily releasable vesicle pool. These findings place a voltage-gated K(+) channel among the syntaxin-binding proteins that directly regulate pre-fusion steps in exocytosis.

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CRRD Object Information
CRRD ID: 10047179
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.