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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Syntaxin 4 and Synip ( syntaxin 4 interacting protein) regulate insulin secretion in the pancreatic beta HC-9 cell.

Although syntaxin 1 is generally thought to function as the primary target-N-ethylmaleimide-sensitive factor attachment protein receptor required for pancreatic beta cell insulin secretion, we have observed that overexpression of a dominant-interfering syntaxin 4 mutant (syntaxin 4/DeltaTM) attenuated glucose-stimulated insulin secretion in betaHC-9 cells. Furthermore, these cells express the selective syntaxin 4- binding protein Synip ( syntaxin 4 interacting protein), and Synip was specifically co-immunoprecipitated with syntaxin 4 but not syntaxin 1. Overexpression of the full-length Synip protein ( Synip/wild type) inhibited VAMP2 association with syntaxin 4 and decreased glucose-stimulated insulin secretion. This did not occur with a Synip mutant ( Synip/ DeltaEF) that was incapable of binding syntaxin 4. Consistent with a functional role of syntaxin 4 in this process, expression of syntaxin 4/DeltaTM also inhibited glucose-stimulated insulin secretion. Furthermore, analysis of first and second phase insulin secretion demonstrated that syntaxin 4/DeltaTM mainly suppressed the second phase of insulin secretion. In contrast, overexpression of Synip resulted in an inhibition of both the first and second phase of glucose-stimulated insulin secretion. These data demonstrate that syntaxin 4 plays a functional role on insulin release and granule fusion in beta cells and that this process is regulated by the syntaxin 4-specific binding protein Synip.[1]


  1. Syntaxin 4 and Synip (syntaxin 4 interacting protein) regulate insulin secretion in the pancreatic beta HC-9 cell. Saito, T., Okada, S., Yamada, E., Ohshima, K., Shimizu, H., Shimomura, K., Sato, M., Pessin, J.E., Mori, M. J. Biol. Chem. (2003) [Pubmed]
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