Targeting of TAK1 in inflammatory disorders and cancer

被引：415

作者：

Sakurai, Hiroaki ^{[1
]}

机构：

[1] Toyama Univ, Grad Sch Med & Pharmaceut Sci, Dept Canc Cell Biol, Toyama 9300194, Japan

来源：

TRENDS IN PHARMACOLOGICAL SCIENCES | 2012年 / 33卷 / 10期

关键词：

NF-KAPPA-B; ACTIVATED KINASE 1; IKK ACTIVATION; SIGNALING PATHWAYS; UBIQUITIN LIGASE; STRUCTURAL BASIS; PROTEIN-KINASES; GROWTH; TAB2; IL-1;

D O I：

10.1016/j.tips.2012.06.007

中图分类号：

R9 [药学];

学科分类号：

100702 [药剂学];

摘要：

The transcription factors nuclear factor-kappa B (NF-kappa B) and activating protein-1 (AP-1) are critical regulators of stress responses, immunity, inflammation and cancer. A large variety of cellular stimuli utilize these signaling pathways through a common upstream kinase transforming growth factor-beta-activated kinase 1 (TAK1). TAK1 was originally identified as a mitogen-activated kinase kinase kinase (MAP3K) activated by transforming growth factor-beta (TGF-beta); however, it has been characterized as a key regulator in inflammatory and immune signaling pathways. In addition, microbial proteins and components of host cell signaling scramble for the TAK1 complex in innate immunity. This review highlights the recent advances in the activation mechanisms and physiological functions of TAK1. Research targeting TAK1 raises the potential for new therapeutic options for inflammatory disorders, including cancer.

引用

页码：522 / 530

页数：9

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