The TWEAK - Fn14 cytokine-receptor axis: discovery, biology and therapeutic targeting

被引：475
作者：
Winkles, Jeffrey A. [1 ,2 ,3 ]
机构：
[1] Univ Maryland, Sch Med, Ctr Vasc & Inflammatory Dis, Dept Surg, Baltimore, MD 21201 USA
[2] Univ Maryland, Sch Med, Ctr Vasc & Inflammatory Dis, Dept Physiol, Baltimore, MD 21201 USA
[3] Univ Maryland, Sch Med, Marlene Stewart Greenebaum Canc Ctr, Baltimore, MD 21201 USA
来源：
NATURE REVIEWS DRUG DISCOVERY | 2008年 / 7卷 / 05期
关键词：
D O I：
10.1038/nrd2488
中图分类号：
Q81 [生物工程学（生物技术）]; Q93 [微生物学];
学科分类号：
071005 ; 0836 ; 090102 ; 100705 ;
摘要：
TWEAK is a multifunctional cytokine that controls many cellular activities including proliferation, migration, differentiation, apoptosis, angiogenesis and inflammation. TWEAK acts by binding to Fn14, a highly inducible cell-surface receptor that is linked to several intracellular signalling pathways, including the nuclear factor-kappa B (NF-kappa B) pathway. The TWEAK-Fn14 axis normally regulates various physiological processes, in particular it seems to play an important, beneficial role in tissue repair following acute injury. Furthermore, recent studies have indicated that TWEAK-Fn14 axis signalling may contribute to cancer, chronic autoimmune diseases and acute ischaemic stroke. This Review provides an overview of TWEAK-Fn14 axis biology and summarizes the available data supporting the proposal that both TWEAK and Fn14 should be considered as potential targets for the development of novel therapeutics.
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收藏
页码：411 / 425
页数：15
相关论文
共 134 条
[41]   TWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regeneration [J].
Girgenrath, Mahasweta ;
Weng, Shawn ;
Kostek, Christine A. ;
Browning, Beth ;
Wang, Monica ;
Brown, Sharron A. N. ;
Winkles, Jeffrey A. ;
Michaelson, Jennifer S. ;
Allaire, Norm ;
Schneider, Pascal ;
Scott, Martin L. ;
Hsu, Yen-ming ;
Yagita, Hideo ;
Flavell, Richard A. ;
Miller, Jeffrey Boone ;
Burkly, Linda C. ;
Zheng, Timothy S. .
EMBO JOURNAL, 2006, 25 (24) :5826-5839
[42]   Profiling microdissected epithelium and stroma to model genomic signatures for cervical carcinogenesis accommodating for covariates [J].
Gius, David ;
Funk, Margo C. ;
Chuang, Eric Y. ;
Feng, Sheng ;
Huettner, Phyllis C. ;
Nguyen, Loan ;
Bradbury, C. Matthew ;
Mishra, Mark ;
Gao, Shuping ;
Buttin, Barbara M. ;
Cohn, David E. ;
Powell, Matthew A. ;
Horowitz, Neil S. ;
Whitcomb, Bradford P. ;
Rader, Janet S. .
CANCER RESEARCH, 2007, 67 (15) :7113-7123
[43]   Early diversification of the TNF superfamily in teleosts: Genomic characterization and expression analysis [J].
Glenney, Gavin W. ;
Wiens, Gregory D. .
JOURNAL OF IMMUNOLOGY, 2007, 178 (12) :7955-7973
[44]   Cancer metastasis:: Building a framework [J].
Gupta, Gaorav P. ;
Massague, Joan .
CELL, 2006, 127 (04) :679-695
[45]   Multiple sclerosis [J].
Hafler, DA ;
Slavik, JM ;
Anderson, DE ;
O'Connor, KC ;
De Jager, P ;
Baecher-Allan, C .
IMMUNOLOGICAL REVIEWS, 2005, 204 :208-231
[46]   Age-dependent effects of TWEAK/Fn14 receptor activation on neural progenitor cells [J].
Hamill, C. A. ;
Michaelson, J. S. ;
Hahm, Kyungmin ;
Burkly, Linda C. ;
Kessler, J. A. .
JOURNAL OF NEUROSCIENCE RESEARCH, 2007, 85 (16) :3535-3544
[47]   TNF-related weak inducer of apoptosis receptor, a TNF receptor superfamily member, activates NF-κB through TNF receptor-associated factors [J].
Han, SY ;
Yoon, K ;
Lee, K ;
Kim, K ;
Jang, H ;
Lee, NK ;
Hwang, K ;
Lee, SY .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2003, 305 (04) :789-796
[48]   The hallmarks of cancer [J].
Hanahan, D ;
Weinberg, RA .
CELL, 2000, 100 (01) :57-70
[49]   Inflammation and atherosclerosis [J].
Hansson, Goran K. ;
Robertson, Anna-Karin L. ;
Soderberg-Naucler, Cecilia .
ANNUAL REVIEW OF PATHOLOGY-MECHANISMS OF DISEASE, 2006, 1 (01) :297-329
[50]   Pro-inflammatory effect of TWEAK/Fn14 interaction on human umbilical vein endothelial cells [J].
Harada, N ;
Nakayama, M ;
Nakano, H ;
Fukuchi, Y ;
Yagita, H ;
Okumura, K .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2002, 299 (03) :488-493
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