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. Although high concentrations of ROS are catatonic, they are now known to function as signal transducing molecules at lower concentrations, modulating indirectly the activity of many enzymes and transcription factors. Classical regulation of the activity of
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Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Institute, Kobe, Japan
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Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Institute, Kobe, Japan
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Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Institute, Kobe, Japan
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Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Institute, Kobe, Japan
Division of Molecular and Metabolic Medicine, Department of Physiology and Cell Biology, Kobe University Graduate School of Medicine, Kobe, Japan
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glucose levels were similar to those of WT mice (113.16 ± 14.03 (WT) vs 125.33 ± 13.19 ( Chrebp −/− ) , respectively). mRNA expression of Srebf2, a key transcription factor controlling synthesis and uptake of cholesterol and their target genes, was
Department of Physiology, University of Medicine 2, Yangon, Myanmar
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renal cortical tissue in HF rats was attenuated by dapagliflozin and metformin administration ( P < 0.05) ( Fig. 1I and J ). The effect of dapagliflozin on renal gluconeogenic enzyme expression might be mediated through transcription factors p
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transcription factors to regulate gene expression and composite binding in which GC/GR requires both GRE elements and physical interaction with other transcription factors to exert its transcriptional activity. BTM: basal transcription machinery. Once
Metabolic Research Laboratory, Oxford Centre for Diabetes, Endocrinology and Metabolism, Nuffield Department of Clinical Medicine, University of Oxford Churchill Hospital, Oxford, UK
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Metabolic Research Laboratory, Oxford Centre for Diabetes, Endocrinology and Metabolism, Nuffield Department of Clinical Medicine, University of Oxford Churchill Hospital, Oxford, UK
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Metabolic Research Laboratory, Oxford Centre for Diabetes, Endocrinology and Metabolism, Nuffield Department of Clinical Medicine, University of Oxford Churchill Hospital, Oxford, UK
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Metabolic Research Laboratory, Oxford Centre for Diabetes, Endocrinology and Metabolism, Nuffield Department of Clinical Medicine, University of Oxford Churchill Hospital, Oxford, UK
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activation of peroxisome proliferator-activated receptor (PPAR) γ ( Guan et al. 2002 , Picard & Auwerx 2002 , Tordjman et al. 2003 , Li et al. 2005 ), a lipogenic transcription factor. Contrasting with the role of PPARγ, PPARα acts as a
Department of Physiology, The University of Melbourne, Parkville, Victoria, Australia
Tufts Medical Center, Boston, Massachusetts, USA
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Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, UK
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Introduction The mineralocorticoid receptor (MR) is a ligand-activated transcription factor best known for regulating sodium/potassium and water in the kidney in response to aldosterone ( Fuller & Young 2005 ). The MR has equivalent high
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) transcription factor, a family member of the SREBPs that promote lipid and cholesterol synthesis ( Yecies et al . 2011 ). Moreover, mTORC2 and PDK1 suppress the Foxo1 forkhead transcription factor that promotes gluconeogenesis, mediating the effect of insulin
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blocking gene transcription. In addition, DNA methylation may block the expression of specific genes by silencing essential transcription factors ( Fluck & Miller 2004 ). DNA methylation has been shown to regulate steroidogenesis. Changes in methylation
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in genes whose protein products control p53 activity (MDM2 or CDKN2A). Following genotoxic or oncogenic stress, p53 exerts its tumor-suppressive activities mainly by acting as a transcription factor to transactivate gene expression. Under mild stress
Université Catholique de Louvain, Institut de Recherche Expérimentale et Clinique, Pôle d’Endocrinologie, Diabète et Nutrition, Brussels, Belgium
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St Vincent’s Clinical School, UNSW Sydney, Sydney, New South Wales, Australia
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controlled activation/repression of specific transcription factors and downstream gene clusters in a time-dependent manner. These complex signalling events drive the transition from definitive endoderm cells to mature insulin-secreting β-cells with the