IR@PKUHSC  > 北京大学第三临床医学院
学科主题临床医学
TAK1 ubiquitination regulates doxorubicin-induced NF-kappa B activation
Liang, Li2,3; Fan, Yihui1; Cheng, Jin1,4; Cheng, Da1; Zhao, Yanling1; Cao, Baoshan2; Ma, Liwen2; An, Lei3; Jia, Wei3,5; Su, Xu6; Yang, Jianhua1; Zhang, Hong3
关键词TAK1 Ubiquitination Doxorubicin USP4 ITCH
刊名CELLULAR SIGNALLING
2013
DOI10.1016/j.cellsig.2012.09.003
25期:1页:247-254
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Cell Biology
研究领域[WOS]Cell Biology
关键词[WOS]DNA-DAMAGE ; PROTEIN STABILITY ; LIGASE ITCH ; GENOTOXIC STRESS ; CANCER ; CHEMOTHERAPY ; RADIOTHERAPY ; DEGRADATION ; P73 ; POLY(ADP-RIBOSYL)ATION
英文摘要

Chemotherapeutic agents- and radiation therapy-induced NF-kappa B activation in cancer cells contributes to aggressive tumor growth and resistance to chemotherapy and ionizing radiation during cancer treatment. TAXI has been shown to be required for genotoxic stress-induced NF-kappa B activation. However, whether TAK1 ubiquitination is involved in genotoxic stress-induced NF-kappa B activation remains unknown. Herein, we demonstrate that TAXI ubiquitination plays an important role in the positive and negative regulation of doxorubicin (Dox)-induced NF-kappa B activation. We found that TAXI was required for Dox-induced NF-kappa B activation. At the early stage of Dox treatment, Dox induced Lys63-linked TAK1 polyubiquitination at lysine 158 residue. USP4 inhibited Dox-induced TAXI Lys63-linked polyubiquitination and knockdown of USP4 enhanced Dox-induced NF-kappa B activation. At the late stage of Dox treatment, Dox induced Lys48-linked TAK1 polyubiquitination to promote TAXI degradation. ITCH inhibited Dox-induced NF-kappa B activation by promoting Lys48-linked TAXI polyubiquitination and its subsequent degradation. Our study indicates that TAXI ubiquitination plays critical roles in the regulation of Dox-induced NF-kappa B activation. Thus, intervention of TAXI kinase activity or TAK1 Lys63-linked polyubiquitination pathways might greatly enhance the therapeutic efficacy of Dox. (C) 2012 Elsevier Inc. All rights reserved.

语种英语
WOS记录号WOS:000312616900028
项目编号1R01NS072420-01 ; 201002009
资助机构NIH/NINDS ; state Ministry of Health of China ; China Scholarship Council
引用统计
被引频次:16[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/67674
专题北京大学第三临床医学院
北京大学第三临床医学院_肿瘤治疗中心
作者单位1.Baylor Coll Med, Dept Pediat, Dan L Duncan Canc Ctr, Texas Childrens Canc Ctr, Houston, TX 77030 USA
2.Peking Univ, Hosp 3, Dept Tumor Chemotherapy & Radiat Sickness, Beijing 100191, Peoples R China
3.Univ Texas MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA
4.Peking Univ, Hlth Sci Ctr, Dept Microbiol, Beijing 100191, Peoples R China
5.Shihezi Univ, Dept Pathol, Sch Med, Shihezi 832002, Peoples R China
6.Chinese Ctr Dis Control & Prevention, Natl Inst Radiol Protect, Beijing 100088, Peoples R China
推荐引用方式
GB/T 7714
Liang, Li,Fan, Yihui,Cheng, Jin,et al. TAK1 ubiquitination regulates doxorubicin-induced NF-kappa B activation[J]. CELLULAR SIGNALLING,2013,25(1):247-254.
APA Liang, Li.,Fan, Yihui.,Cheng, Jin.,Cheng, Da.,Zhao, Yanling.,...&Zhang, Hong.(2013).TAK1 ubiquitination regulates doxorubicin-induced NF-kappa B activation.CELLULAR SIGNALLING,25(1),247-254.
MLA Liang, Li,et al."TAK1 ubiquitination regulates doxorubicin-induced NF-kappa B activation".CELLULAR SIGNALLING 25.1(2013):247-254.
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