TAK1: a potent tumour necrosis factor inhibitor for the treatment of inflammatory diseases

被引：40

作者：

Totzke, Juliane ^{[1
]}

Scarneo, Scott A. ^{[1
]}

Yang, Kelly W. ^{[1
]}

Haystead, Timothy A. J. ^{[1
]}

机构：

[1] Duke Univ, Sch Med, Dept Pharmacol & Canc Biol, Durham, NC 27710 USA

来源：

OPEN BIOLOGY | 2020年 / 10卷 / 09期

关键词：

TAK1; TNF; inflammation; kinase; rheumatoid arthritis; ACTIVATED KINASE 1; COLLAGEN-INDUCED ARTHRITIS; ANTI-TNF THERAPY; TGF-BETA; RHEUMATOID-ARTHRITIS; STRUCTURAL BASIS; FACTOR-ALPHA; IN-VITRO; PROTEIN; CELLS;

D O I：

10.1098/rsob.200099

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Aberrant tumour necrosis factor (TNF) signalling is a hallmark of many inflammatory diseases including rheumatoid arthritis (RA), irritable bowel disease and lupus. Maladaptive TNF signalling can lead to hyper active downstream nuclear factor (NF)-kappa beta signalling in turn amplifying a cell's inflammatory response and exacerbating disease. Within the TNF intracellular inflammatory signalling cascade, transforming growth factor-beta -activated kinase 1 (TAK1) has been shown to play a critical role in mediating signal transduction and downstream NF-kappa beta activation. Owing to its role in TNF inflammatory signalling, TAK1 has become a potential therapeutic target for the treatment of inflammatory diseases such as RA. This review highlights the current development of targeting the TNF-TAK1 signalling axis as a novel therapeutic strategy for the treatment of inflammatory diseases.

引用

页数：9

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