首页> 外文期刊>The biochemical journal >Tumour necrosis factor-α regulates expression of the CCAAT-enhancer-binding proteins (C/EBPs) α and β and determines the occupation of the C/EBP site in the promoter of the insulin-responsive glucose-transporter gene in 3T3-L1 adipocytes
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Tumour necrosis factor-α regulates expression of the CCAAT-enhancer-binding proteins (C/EBPs) α and β and determines the occupation of the C/EBP site in the promoter of the insulin-responsive glucose-transporter gene in 3T3-L1 adipocytes

机译:肿瘤坏死因子-α调节CCAAT-增强子结合蛋白(C / EBPs)α和β的表达,并确定3T3-L1脂肪细胞中胰岛素反应性葡萄糖转运蛋白基因启动子中C / EBP位点的占据

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pWe have demonstrated previously that treatment of 3T3-L1 adipocytes with tumour necrosis factor-α (TNF) results in a rapid (4 h) and significant (75–80%) reduction in the rate of transcription of the iGLUT4/i gene. Control of iGLUT4/i gene transcription has been suggested at least in part to reside with the CCAAT-enhancer-binding protein (C/EBP) family (α, β and δ isoforms) of transcription factors. Using electrophoretic mobility shift assays, we have examined the ability of TNF to alter the occupation of the C/EBP site in the GLUT4 promoter. The data suggest that in fully differentiated adipocytes the C/EBP site is a ligand for predominantly α/α homodimers; however, after exposure to TNF, a shift in occupancy of the site occurs and the ligands become α/β heterodimers and β/β homodimers. Partner selection in dimer formation appears to be controlled by selective translocation of the β-isoform from the cytosol to the nucleus after exposure of the cells to TNF./p
机译:>我们以前已经证明,用肿瘤坏死因子-α(TNF)处理3T3-L1脂肪细胞会导致(i)的转录速率快速降低(4&h)和显着(75-80%)降低> GLUT4 基因。有人建议至少控制 GLUT4 基因转录,使其与转录因子的CCAAT-增强子结合蛋白(C / EBP)家族(α,β和δ亚型)共存。使用电泳迁移率变动分析,我们已经检查了TNF改变GLUT4启动子中C / EBP位点占据的能力。数据表明,在完全分化的脂肪细胞中,C / EBP位点是主要是α/α同二聚体的配体。然而,在暴露于TNF后,该位点的占据发生了变化,并且配体变成了α/β异二聚体和β/β同二聚体。细胞暴露于TNF后,β-亚型从胞质溶胶到核的选择性移位似乎可以控制二聚体形成中的伙伴选择。

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