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DOI | 10.1038/s41467-018-03280-2 |
The histone demethylase Phf2 acts as a molecular checkpoint to prevent NAFLD progression during obesity | |
Bricambert, Julien1,2,3; Alves-Guerra, Marie-Clotilde1,2,3; Esteves, Pauline1,2,3; Prip-Buus, Carina1,2,3; Bertrand-Michel, Justine3,4; Guillou, Herve5; Chang, Christopher J.6,7; Vander Wal, Mark N.6; Canonne-Hergaux, Francois8,9,10,16; Mathurin, Philippe11,12,16; Raverdy, Violeta13,14,15; Pattou, Francois13,14,15; Girard, Jean1,2,3; Postic, Catherine1,2,3; Dentin, Renaud1,2,3 | |
2018-05-29 | |
发表期刊 | NATURE COMMUNICATIONS |
ISSN | 2041-1723 |
出版年 | 2018 |
卷号 | 9 |
文章类型 | Article |
语种 | 英语 |
国家 | France; USA |
英文摘要 | Aberrant histone methylation profile is reported to correlate with the development and progression of NAFLD during obesity. However, the identification of specific epigenetic modifiers involved in this process remains poorly understood. Here, we identify the histone demethylase Plant Homeodomain Finger 2 (Phf2) as a new transcriptional co-activator of the transcription factor Carbohydrate Responsive Element Binding Protein (ChREBP). By specifically erasing H3K9me2 methyl-marks on the promoter of ChREBP-regulated genes, Phf2 facilitates incorporation of metabolic precursors into mono-unsaturated fatty acids, leading to hepatosteatosis development in the absence of inflammation and insulin resistance. Moreover, the Phf2-mediated activation of the transcription factor NF-E2-related factor 2 (Nrf2) further reroutes glucose fluxes toward the pentose phosphate pathway and glutathione biosynthesis, protecting the liver from oxidative stress and fibrogenesis in response to dietinduced obesity. Overall, our findings establish a downstream epigenetic checkpoint, whereby Phf2, through facilitating H3K9me2 demethylation at specific gene promoters, protects liver from the pathogenesis progression of NAFLD. |
领域 | 资源环境 |
收录类别 | SCI-E |
WOS记录号 | WOS:000433297900003 |
WOS关键词 | FATTY LIVER-DISEASE ; HEPATIC INSULIN-RESISTANCE ; UNFOLDED PROTEIN RESPONSE ; NONALCOHOLIC STEATOHEPATITIS ; SELECTIVE AUTOPHAGY ; PLANT HOMEODOMAIN ; OXIDATIVE STRESS ; FACTOR NRF2 ; CHREBP ; MICE |
WOS类目 | Multidisciplinary Sciences |
WOS研究方向 | Science & Technology - Other Topics |
URL | 查看原文 |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | http://119.78.100.173/C666/handle/2XK7JSWQ/203681 |
专题 | 资源环境科学 |
作者单位 | 1.INSERM, U1016, Inst Cochin, Paris, France; 2.CNRS, UMR 8104, Paris, France; 3.Univ Paris 05, Sorbonne Paris Cite, Paris, France; 4.INSERM, Plateforme MetaToul, Biomed Federat Res Inst Toulouse, Plateau Lipidom, Toulouse, France; 5.INRA ToxAlim Toxicol Integrat & Metab, Toulouse, France; 6.Univ Calif Berkeley, Dept Chem & Mol & Cell Biol, Berkeley, CA 94720 USA; 7.Univ Calif Berkeley, Howard Hughes Med Inst, Berkeley, CA 94720 USA; 8.INSERM, U1043, CPTP, F-31300 Toulouse, France; 9.CNRS, U5282, F-31300 Toulouse, France; 10.Univ Toulouse, CPTP, UPS, F-31300 Toulouse, France; 11.Lille Univ Hosp, Dept Hepatol, Lille, France; 12.INSERM, U995, Lille, France; 13.INSERM, Biotherapies Diabet U859, Lille, France; 14.Lille Univ, European Genom Inst Diabet, Lille, France; 15.Lille Univ Hosp, Dept Endocrine Surg, Lille, France; 16.Univ Toulouse, INSERM, INRA, IRSD,ENVT,INPT,UMR 1416,UMR 1220,UPS, Toulouse, France |
推荐引用方式 GB/T 7714 | Bricambert, Julien,Alves-Guerra, Marie-Clotilde,Esteves, Pauline,et al. The histone demethylase Phf2 acts as a molecular checkpoint to prevent NAFLD progression during obesity[J]. NATURE COMMUNICATIONS,2018,9. |
APA | Bricambert, Julien.,Alves-Guerra, Marie-Clotilde.,Esteves, Pauline.,Prip-Buus, Carina.,Bertrand-Michel, Justine.,...&Dentin, Renaud.(2018).The histone demethylase Phf2 acts as a molecular checkpoint to prevent NAFLD progression during obesity.NATURE COMMUNICATIONS,9. |
MLA | Bricambert, Julien,et al."The histone demethylase Phf2 acts as a molecular checkpoint to prevent NAFLD progression during obesity".NATURE COMMUNICATIONS 9(2018). |
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