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Functional Analysis of Promoters of Genes in Lipid Metabolism and Their Transcriptional Response to STAT3 under Leptin Signals

机译:瘦素信号下脂质代谢基因启动子的功能分析及其对STAT3的转录反应

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摘要

We characterized the promoters of target genes of the signal transducer and activator of transcription 3, STAT3 (carnitine palmitoyltransferase I, CPT Iα1b, acetyl-CoA carboxylase alpha, ACCα; fatty acid synthase, FAS; and peroxisome proliferator-activated receptor gamma, PPARγ) in a teleost Pelteobagrus fulvidraco. Binding sites of STAT3 were predicted on these promoters, indicating that STAT3 probably mediated their transcriptional activities. Leptin had no effect on the activity of ACCα and PPARγ promoters, but increased CPT Iα1b promoter activity and decreased FAS promoter activity. The −979/−997 STAT3 binding site of CPT Iα1b and the −794/−812 STAT3 binding site of FAS were functional binding loci responsible for leptin-induced transcriptional activation. The study provided direct evidence that STAT3 regulated the expression of CPT Iα1b and FAS at the transcription level, and determined the STAT3 response element on promoters of CPT Iα1b and FAS under leptin signal.
机译:我们表征了信号转导和转录激活因子STAT3(肉碱棕榈酰转移酶I,CPTIα1b,乙酰辅酶A羧化酶α,ACCα,脂肪酸合酶,FAS;和过氧化物酶体增殖物激活受体γ,PPARγ)的靶基因的启动子。在硬骨的Pelteobagrus fulvidraco中。在这些启动子上预测了STAT3的结合位点,表明STAT3可能介导了它们的转录活性。瘦素对ACCα和PPARγ启动子的活性没有影响,但是增加了CPTIα1b启动子的活性而降低了FAS启动子的活性。 CPTIα1b的-979 / -997 STAT3结合位点和FAS的-794 / -812 STAT3结合位点是负责瘦蛋白诱导的转录激活的功能性结合位点。该研究提供了直接的证据,表明STAT3在转录水平上调节CPTIα1b和FAS的表达,并在瘦蛋白信号下确定CPTIα1b和FAS启动子上的STAT3反应元件。

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