Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 318, Issue 4, Pages 814-818Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2004.04.105
Keywords
transcription; HMG-CoA reductase promoter; cyclic AMP response element; H4IIE cells; insulin responsive regions; sterol response element
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An insulin-responsive line of rat hepatoma cells, H4IIE, was used to investigate the basis for insulin's transcriptional regulation of HMG-CoA reductase. Insulin addition to the media of these cells resulted in at least a 10-fold increase in levels of HMG-CoA reductase protein. Adding insulin to H4IIE cells transfected with pHMGR1 (containing the proximal reductase promoter from -270 to +20 ligated to luciferase) caused greater than 10-fold increases in luciferase activity. Transfections carried out with a series of deletion constructs identified insulin responsive regions between -203 and -130 (contains the SRE sequence) and between -85 and -105 (contains a CRE sequence). Mutation of the SRE in the -203 to -130 sequence did not decrease activation by insulin. In contrast, mutation of the C at -90 of the CRE completely eliminated the insulin response. The data suggest that insulin's activation of HMG-CoA reductase involves the CRE in the -85 to -105 region and the -203 to -130 region of the promoter exclusive of the SRE. (C) 2004 Elsevier Inc. All rights reserved.
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