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Chromatin Remodeling and Transcriptional Control in Innate Immunity: Emergence of Akirin2 as a Novel Player

机译:固有免疫中的染色质重塑和转录控制:Akirin2作为一种新型播放器的出现。

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摘要

Transcriptional regulation of inflammatory gene expression has been at the forefront of studies of innate immunity and is coordinately regulated by transcription factors, including NF-κB, and chromatin modifiers. The growing evidence for involvement of chromatin in the regulation of gene expression in innate immune cells, has uncovered an evolutionarily conserved role of microbial sensing and chromatin remodeling. Toll-like receptors and RIG-I-like receptors trigger these signaling pathways leading to transcriptional expression of a set of genes involved in inflammation. Tightly regulated control of this gene expression is a paramount, and often foremost, goal of most biological endeavors. In this review, we will discuss the recent progress about the molecular mechanisms governing control of pro-inflammatory gene expression by an evolutionarily conserved novel nuclear protein Akirin2 in macrophages and its emergence as an essential link between NF-κB and chromatin remodelers for transcriptional regulation.
机译:炎性基因表达的转录调控一直是先天免疫研究的前沿,并受包括NF-κB和染色质修饰剂在内的转录因子的调控。染色质参与先天免疫细胞基因表达调控的证据越来越多,已经揭示了微生物传感和染色质重塑的进化保守作用。 Toll样受体和RIG-1样受体触发这些信号传导途径,导致涉及炎症的一组基因的转录表达。严格调节对该基因表达的控制是大多数生物学努力的首要目标,并且通常是首要目标。在这篇综述中,我们将讨论有关在巨噬细胞中由进化保守的新型核蛋白Akirin2调控促炎基因表达的分子机制的最新进展,以及其作为NF-κB与染色质重塑剂之间转录调控的重要联系的出现。

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