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Adenovirus-mediated silencing of synaptotagmin 9 inhibits Ca2+-dependent insulin secretion in islets.

Authors: Iezzi, M  Eliasson, L  Fukuda, M  Wollheim, CB 
Citation: Iezzi M, etal., FEBS Lett. 2005 Sep 26;579(23):5241-6.
Pubmed: (View Article at PubMed) PMID:16165130
DOI: Full-text: DOI:10.1016/j.febslet.2005.08.047

Synaptotagmins (Syts) are involved in Ca(2+)-dependent insulin release. However, which Syt isoform is functional in primary beta-cells remains unknown. We demonstrate by electron microscopy of pancreatic islets, the association of Syt 9 with insulin granules. Silencing of Syt 9 by RNA interference adenovirus in islet cells had no effect on the expression of Syt 5, Syt 7 and Syt 3 isoforms. The latter was localized at the plasma membrane of pancreatic polypeptide cells. Insulin release in response to glucose or tolbutamide was strongly inhibited in Syt 9 deficient islets, whereas exocytosis potentiated by raising cAMP levels, was unaltered. Thus, Syt 9 may act as Ca(2+) sensor for beta-cell secretion.


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CRRD Object Information
CRRD ID: 2311147
Created: 2009-06-26
Species: All species
Last Modified: 2009-06-26
Status: ACTIVE


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