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学科主题: 临床医学
题名:
TAK1 ubiquitination regulates doxorubicin-induced NF-kappa B activation
作者: 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
发表日期: 2013
DOI: 10.1016/j.cellsig.2012.09.003
卷: 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
所属项目编号: 1R01NS072420-01 ; 201002009
项目资助者: NIH/NINDS ; state Ministry of Health of China ; China Scholarship Council
WOS记录号: WOS:000312616900028
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/67674
Appears in Collections:北京大学第三临床医学院_期刊论文

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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

Recommended Citation:
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.
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