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首页> 外文期刊>Biochimica et Biophysica Acta. Gene Regulatory Mechanisms >A TEAD1/p65 complex regulates the eutherian-conserved MnSOD intronic enhancer, eRNA transcription and the innate immune response
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A TEAD1/p65 complex regulates the eutherian-conserved MnSOD intronic enhancer, eRNA transcription and the innate immune response

机译：TEAD1 / p65复合物可调节保守的MnSOD内含子增强子，eRNA转录和先天免疫应答

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摘要

Manganese superoxide dismutase (MnSOD), a critical anti-oxidant enzyme, detoxifies the mitochondrial-derived reactive oxygen species, superoxide, elicited through normal respiration or the inflammatory response. Proinflammatory stimuli induce MnSOD gene expression through a eutherian-conserved, intronic enhancer element. We identified two prototypic enhancer binding proteins, TEAD1 and p65, that when co-expressed induce MnSOD expression comparable to pro-inflammatory stimuli. TEAD1 causes the nuclear sequestration of p65 leading to a novel TEAD1/p65 complex that associates with the intronic enhancer and is necessary for cytokine induction of MnSOD. Unlike typical NF-κB-responsive genes, the induction of MnSOD does not involve p50. Beyond MnSOD, the TEAD1/p65 complex regulates a subset of genes controlling the innate immune response that were previously viewed as solely NF-κB-dependent. We also identified an enhancer-derived RNA (eRNA) that is induced by either proinflammatory stimuli or the TEAD1/p65 complex, potentially linking the intronic enhancer to intra- and interchromosomal gene regulation through the inducible eRNA.
机译：锰超氧化物歧化酶（MnSOD）是一种重要的抗氧化酶，可将线粒体来源的活性氧超氧化物解毒，这种氧是通过正常呼吸或炎症反应引起的。促炎性刺激通过保存在欧洲人体内的内含子增强子元件诱导MnSOD基因表达。我们鉴定了两个原型增强子结合蛋白，TEAD1和p65，当它们共同表达时，其诱导的MnSOD表达与促炎性刺激相当。 TEAD1导致p65的核螯合，导致形成一种新型TEAD1 / p65复合物，该复合物与内含子增强子缔合，是细胞因子诱导MnSOD所必需的。与典型的NF-κB反应基因不同，MnSOD的诱导不涉及p50。除MnSOD以外，TEAD1 / p65复合物还调节控制固有免疫应答的基因的子集，这些基因先前仅被认为是NF-κB依赖性的。我们还确定了由促炎性刺激或TEAD1 / p65复合物诱导的增强子衍生的RNA（eRNA），可能通过诱导型eRNA将内含子增强子与染色体内和染色体间基因调控联系起来。

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