HNF-1α-SNARE connection

• Published in: Diabetes, obesity & metabolism Vol. 9; no. s2; pp. 40 - 45
• Main Authors: Yamagata, K, Nammo, T, Sato, Y, Saisho, K, Shoda, H, Fukui, K
• Format: Journal Article
• Language: English
• Published: Oxford, UK Oxford, UK : Blackwell Publishing Ltd 01.11.2007; Blackwell Publishing Ltd
• Subjects: collectrin; exocytosis; HNF-1α; maturity-onset diabetes of the young; noninsulin-dependent diabetes mellitus; snapin
• ISSN: 1462-8902; 1463-1326
• DOI: 10.1111/j.1463-1326.2007.00773.x

Maturity-onset diabetes of the young (MODY) is a monogenic form of type 2 diabetes mellitus that is characterized by impairment of glucose-stimulated insulin secretion from pancreatic β-cells. We previously reported that heterozygous mutations of the hepatocyte nuclear factor (HNF)-1α gene cause a form of MODY (MODY3). We have subsequently found that collectrin, a recently cloned kidney-specific gene of unknown function, is a novel target of HNF-1α in pancreatic β-cells. In addition, we have demonstrated that collectrin forms a complex with the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex by direct interaction with snapin, a protein that is thought to be involved in neurotransmission by binding to synaptosomal-associated protein, 25 KD (SNAP25). Collectrin favours the formation of SNARE complexes and controls insulin exocytosis.