Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 3.4.22.B70 extracted from

  • Dai, X.Q.; Plummer, G.; Casimir, M.; Kang, Y.; Hajmrle, C.; Gaisano, H.Y.; Manning Fox, J.E.; MacDonald, P.E.
    SUMOylation regulates insulin exocytosis downstream of secretory granule docking in rodents and humans (2011), Diabetes, 60, 838-847.
    View publication on PubMedView publication on EuropePMC

Organism

Organism UniProt Comment Textmining
Mus musculus P59110
-
-

General Information

General Information Comment Organism
malfunction SENP1 knockdown impairs exocytosis at stimulatory glucose levels and blunts glucose-dependent insulin secretion from mouse and human islets. SENP1 overexpression also disrupts the association of SUMO1 with synaptotagmin VII and mimics the effect of glucose to enhance exocytosis Mus musculus
physiological function SENP1, is required for glucose-dependent insulin secretion. SUMOylation acutely regulates insulin secretion by the direct and reversible inhibition of beta-cell exocytosis in response to intracellular Ca(2+) elevation Mus musculus