Inhibitory roles of protein kinase B and peroxisome proliferator-activated receptor gamma coactivator on hepatic HMG-CoA reductase promoter activity
Inhibitory roles of protein kinase B and peroxisome proliferator-activated receptor gamma coactivator on hepatic HMG-CoA reductase promoter activity作者机构：Department of Molecular Medicine Morsani College of Medicine University of South Florida Tampa USA
出 版 物：《Advances in Bioscience and Biotechnology》 (生命科学与技术进展（英文）)
年 卷 期：2013年第4卷第10期
页 面：1-5页
学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
主 题：In Vivo Electroporation HMG-CoA Reductase Insulin Protein Kinase B Peroxisome Proliferator-Activated Receptor γ Coactivator Tristetraprolin
摘 要：Since we had previously demonstrated that siRNAs to tristetraprolin (TTP) markedly inhibited insulin stimulation of hepatic HMG-CoA reductase (HMGR) transcription, we investigated the effects of transfecting rat liver with TTP constructs. We found that transfecting diabetic rats with TTP did not increase HMGR transcription but rather led to modest inhibition. We then investigated whether co-transfection with protein kinase B, hepatic form (AKT2), might lead to phosphorylation and result in activation of HMGR transcription. We found that this treatment resulted in near complete inhibition of transcription. Transfection with peroxisome proliferator-activated receptor g coactivator (PGC-1a) also inhibited HMGR transcription. These results show that although TTP is needed for activation of HMGR transcription, it cannot by itself activate this process. AKT2 and PGC-1a, which mediate the activation of gluconeogenic genes by insulin, exert the opposite effect on HMGR.
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