Measles virus V protein inhibits p53 family member p73
Measles virus V protein inhibits p53 family member p73
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DOI：
10.1128/jvi.02400-05
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发表时间：
2006-06-01
影响因子：
5.4
通讯作者：
Horvath, Curt A.
中科院分区：
文献类型：
--
作者：
Cruz, Cristian D.;Palosaari, Heidi;Horvath, Curt A.
副粘病毒V蛋白作为宿主干扰因子发挥功能，干扰抗病毒反应，包括干扰素。与异位表达的麻疹病毒V蛋白共同纯化的细胞蛋白的表征揭示了与p53家族蛋白p53和p73的DNA结合结构域的相互作用。特异性转录检测显示麻疹病毒V cDNA的表达抑制p73，但不抑制p53。麻疹病毒V cDNA的表达可以延迟由遗传毒性应激诱导的细胞死亡，并且还可以减少p73靶点的促凋亡因子α A的丰度。具有V蛋白工程缺陷的重组麻疹病毒能够诱导比野生型更严重的细胞病变效应，暗示麻疹病毒V蛋白是细胞死亡的抑制剂。这些发现还表明，p73-p53信号转导可能是一个以前未被认识到的细胞先天性抗病毒免疫的手臂。
Paramyxovirus V proteins function as host interference factors that inactivate antiviral responses, including interferon. Characterization of cellular proteins that copurify with ectopically expressed measles virus V protein has revealed interactions with DNA binding domains of p53 family proteins, p53 and p73. Specific transcriptional assays reveal that expression of measles virus V cDNA inhibits p73, but not p53. Expression of measles virus V cDNA can delay cell death induced by genotoxic stress and also can decrease the abundance of the proapoptotic factor PUMA, a p73 target. Recombinant measles virus with an engineered deficiency in V protein is capable of inducing more severe cytopathic effects than the wild type, implicating measles virus V protein as an inhibitor of cell death. These findings also suggest that p73-PUMA signaling may be a previously unrecognized arm of cellular innate antiviral immunity.