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Jagn1 Is Induced in Response to ER Stress and Regulates Proinsulin Biosynthesis.

Authors: Nosak, C  Silva, PN  Sollazzo, P  Moon, KM  Odisho, T  Foster, LJ  Rocheleau, JV  Volchuk, A 
Citation: Nosak C, etal., PLoS One. 2016 Feb 16;11(2):e0149177. doi: 10.1371/journal.pone.0149177. eCollection 2016.
Pubmed: (View Article at PubMed) PMID:26882284
DOI: Full-text: DOI:10.1371/journal.pone.0149177

The Jagn1 protein was indentified in a SILAC proteomic screen of proteins that are increased in insulinoma cells expressing a folding-deficient proinsulin. Jagn1 mRNA was detected in primary rodent islets and in insulinoma cell lines and the levels were increased in response to ER stress. The function of Jagn1 was assessed in insulinoma cells by both knock-down and overexpression approaches. Knock-down of Jagn1 caused an increase in glucose-stimulated insulin secretion resulting from an increase in proinsulin biosynthesis. In contrast, overexpression of Jagn1 in insulinoma cells resulted in reduced cellular proinsulin and insulin levels. Our results identify a novel role for Jagn1 in regulating proinsulin biosynthesis in pancreatic beta-cells. Under ER stress conditions Jagn1 is induced which might contribute to reducing proinsulin biosynthesis, in part by helping to relieve the protein folding load in the ER in an effort to restore ER homeostasis.

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CRRD Object Information
CRRD ID: 11520872
Created: 2016-08-03
Species: All species
Last Modified: 2016-08-03
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.