How viruses hijack cell regulation

被引:291
作者
Davey, Norman E. [1 ]
Trave, Gilles [2 ]
Gibson, Toby J. [1 ]
机构
[1] European Mol Biol Lab, Struct & Computat Biol Unit, D-69117 Heidelberg, Germany
[2] CNRS, FRE 3211, ESBS, Equipe Oncoprot, F-67412 Illkirch Graffenstaden, France
关键词
EPSTEIN-BARR-VIRUS; NF-KAPPA-B; MEMBRANE-PROTEIN; C-TERMINAL DOMAIN; HIV-1; NEF; UBIQUITIN LIGASE; ADENOVIRUS E1A; DOWN-REGULATION; LINEAR MOTIFS; SH3; DOMAIN;
D O I
10.1016/j.tibs.2010.10.002
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
Viruses, as obligate intracellular parasites, are the pathogens that have the most intimate relationship with their host, and as such, their genomes have been shaped directly by interactions with the host proteome. Every step of the viral life cycle, from entry to budding, is orchestrated through interactions with cellular proteins. Accordingly, viruses will hijack and manipulate these proteins utilising any achievable mechanism. Yet, the extensive interactions of viral proteomes has yielded a conundrum: how do viruses commandeer so many diverse pathways and processes, given the obvious spatial constraints imposed by their compact genomes? One important approach is slowly being revealed, the extensive mimicry of host protein short linear motifs (SLiMs).
引用
收藏
页码:159 / 169
页数:11
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