Tinkering with a viral ribonucleotide reductase

被引：67

作者：

Lembo, David ^{[1
]}

Brune, Wolfram ^{[2
]}

机构：

[1] Univ Turin, S Luigi Gonzaga Hosp, Dept Clin & Biol Sci, I-10043 Turin, Italy

[2] Robert Koch Inst, Div Viral Infect, D-13353 Berlin, Germany

来源：

TRENDS IN BIOCHEMICAL SCIENCES | 2009年 / 34卷 / 01期

关键词：

HERPES-SIMPLEX-VIRUS; KAPPA-B ACTIVATION; HOMOTYPIC INTERACTION MOTIF; LARGE DNA VIRUSES; HUMAN CYTOMEGALOVIRUS; R1; SUBUNIT; MURINE CYTOMEGALOVIRUS; CELL-CYCLE; PROTEIN-KINASE; APOPTOSIS;

D O I：

10.1016/j.tibs.2008.09.008

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：

Ribonucleotide reductase (RNR), a crucial enzyme for nucleotide anabolism, is encoded by all living organisms and by large DNA viruses such as the herpesviruses. Surprisingly, the P-herpesvirus subfamily RNR R1 subunit homologues are catalytically inactive and their function remained enigmatic for many years. Recent work sheds light on the function of M45, the murine cytomegalovirus R1 homologue; during viral evolution, M45 apparently lost its original RNR activity but gained the ability, via inhibiting RIP1, a cellular adaptor protein, to block cellular signaling pathways involved in innate immunity and inflammation. The discovery of this novel mechanism of viral immune subversion provides further support to the concept of evolutionary tinkering.

引用

页码：25 / 32

页数：8

共 54 条

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