The Kruppel-like protein Gli-similar 3 (Glis3) functions as a key regulator of insulin transcription.

ABSTRACT: Transcriptional regulation of insulin in pancreatic β-cells is mediated primarily through enhancer elements located within the 5' upstream regulatory region of the preproinsulin gene. Recently, the Krüppel-like transcription factor, Gli-similar 3 (Glis3), was shown to bind the insulin (INS) promoter and positively influence insulin transcription. In this report, we examined in detail the synergistic activation of insulin transcription by Glis3 with coregulators, CREB-binding protein (CBP)/p300, pancreatic and duodenal homeobox 1 (Pdx1), neuronal differentiation 1 (NeuroD1), and v-maf musculoaponeurotic fibrosarcoma oncogene homolog A (MafA). Our data show that Glis3 expression, the binding of Glis3 to GlisBS, and its recruitment of CBP are required for optimal activation of the insulin pro

SUBMITTER: ZeRuth GT 

PROVIDER: S-EPMC3787130 | biostudies-literature | 2013 Oct

REPOSITORIES: biostudies-literature