麻疹病毒V蛋白抑制p53家族成员p73。
Measles virus V protein inhibits p53 family member p73.
作者信息
Cruz Cristian D, Palosaari Heidi, Parisien Jean-Patrick, Devaux Patricia, Cattaneo Roberto, Ouchi Toru, Horvath Curt M
机构信息
Pancoe-ENH Research Pavilion, Northwestern University, 2200 Campus Drive, Evanston, IL 60208, USA.
出版信息
J Virol. 2006 Jun;80(11):5644-50. doi: 10.1128/JVI.02400-05.
Abstract
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.
摘要
副粘病毒V蛋白作为宿主干扰因子发挥作用，可使包括干扰素在内的抗病毒反应失活。对与异位表达的麻疹病毒V蛋白共纯化的细胞蛋白进行表征，揭示了其与p53家族蛋白p53和p73的DNA结合域之间的相互作用。特异性转录分析表明，麻疹病毒V cDNA的表达抑制p73，但不抑制p53。麻疹病毒V cDNA的表达可延迟基因毒性应激诱导的细胞死亡，还可降低促凋亡因子PUMA（一种p73靶标）的丰度。具有工程化V蛋白缺陷的重组麻疹病毒比野生型能够诱导更严重的细胞病变效应，这表明麻疹病毒V蛋白是细胞死亡的抑制剂。这些发现还表明，p73-PUMA信号传导可能是细胞先天性抗病毒免疫中一个以前未被认识的分支。
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