泛素
生物
转录因子
细胞生物学
调节器
NF-κB
泛素蛋白连接酶类
神经退行性变
泛素连接酶
磷酸化
信号转导
遗传学
基因
疾病
医学
病理
作者
Dhanendra Tomar,Rajesh Singh
标识
DOI:10.1111/boc.201400046
摘要
The nuclear factor κB (NF-κB) transcription factor family plays a key role in regulation of the inflammatory pathway in response to different physiological stimuli starting from development to ageing. The dysregulation of NF-κB has been associated with many pathological conditions like inflammatory diseases, neurodegeneration, metabolic diseases and various kinds of malignancies. The NF-κB pathway is regulated by number of post-translational modifications, including phosphorylation and ubiquitination. Ubiquitin (Ub) E3 ligases are key regulators of the process of ubiquitination and provide specificity to the pathway as they recognise the substrate and determine the topology of ubiquitination. TRIMs, members of RING family of Ub E3 ligases, are characterised by the presence of three conserved domains, RING, B-Box and coiled-coil (RBCC). Emerging evidence suggests that TRIMs regulate innate immune signalling during infection and different pathological conditions. The studies have demonstrated the role of TRIMs in regulation of inflammatory pathways including NF-κB. Recent reports suggest that TRIMs play a critical role in regulation of the NF-κB pathway by ubiquitinating proteins at different steps. In the current review, we discuss the role of TRIMs as novel NF-κB regulators and their role in different pathophysiological conditions.
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