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Making sense of IL-6 signalling cues in pathophysiology
FEBS Letters ( IF 3.0 ) Pub Date : 2021-10-07 , DOI: 10.1002/1873-3468.14201
David Millrine 1, 2 , Robert H Jenkins 1, 2 , Stuart T O Hughes 1, 2 , Simon A Jones 1, 2
Affiliation  

Unravelling the molecular mechanisms that account for functional pleiotropy is a major challenge for researchers in cytokine biology. Cytokine–receptor cross-reactivity and shared signalling pathways are considered primary drivers of cytokine pleiotropy. However, reports epitomized by studies of Jak-STAT cytokine signalling identify interesting biochemical and epigenetic determinants of transcription factor regulation that affect the delivery of signal-dependent cytokine responses. Here, a regulatory interplay between STAT transcription factors and their convergence to specific genomic enhancers support the fine-tuning of cytokine responses controlling host immunity, functional identity, and tissue homeostasis and repair. In this review, we provide an overview of the signalling networks that shape the way cells sense and interpret cytokine cues. With an emphasis on the biology of interleukin-6, we highlight the importance of these mechanisms to both physiological processes and pathophysiological outcomes.

中文翻译:


理解病理生理学中的 IL-6 信号传导线索



阐明功能多效性的分子机制是细胞因子生物学研究人员面临的主要挑战。细胞因子-受体交叉反应性和共享信号通路被认为是细胞因子多效性的主要驱动因素。然而,以 Jak-STAT 细胞因子信号传导研究为代表的报告发现了转录因子调节的有趣的生化和表观遗传决定因素,这些决定因素影响信号依赖性细胞因子反应的传递。在这里,STAT转录因子及其与特定基因组增强子的融合之间的调节相互作用支持细胞因子反应的微调,控制宿主免疫、功能特性以及组织稳态和修复。在这篇综述中,我们概述了塑造细胞感知和解释细胞因子线索方式的信号网络。我们重点关注 IL-6 的生物学,强调这些机制对生理过程和病理生理结果的重要性。
更新日期:2021-10-07
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