Article
Munc18c heterozygous knockout mice display increased susceptibility for severe glucose intolerance.
Diabetes - 1 Mar 2005
Oh Eunjin, Spurlin Beth A, Pessin Jeffrey E, Thurmond Debbie C
Abstract excerpt
The disruption of Munc18c binding to syntaxin 4 impairs insulin-stimulated GLUT4 vesicle translocation in 3T3L1 adipocytes. To investigate the physiological function and requirement for Munc18c in the regulation of GLUT4 translocation and glucose homeostasis in vivo, we used homologous recombination to generate Munc18c-knockout (KO) mice. Homozygotic disruption of the Munc18c gene resulted in early embryonic...
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