The BM2 protein of influenza B virus interacts with p53 and inhibits its transcriptional and apoptotic activities

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• 作者：H. Zhang (1)
  H. Yu (1)
  J. Wang (1)
  M. Zhang (1)
  X. Wang (1)
  W. Ahmad (1)
  M. Duan (1)
  Z. Guan (1)
  
  1. Key Lab of Zoonosis Research ; Ministry of Education ; Institute of Zoonosis ; Jilin University ; Changchun ; 130062 ; People鈥檚 Republic of China
  
• 关键词：BM2 ; p53 ; Protein鈥損rotein interaction ; Apoptosis
• 刊名：Molecular and Cellular Biochemistry
• 出版年：2015
• 出版时间：May 2015
• 年：2015
• 卷：403
• 期：1-2
• 页码：187-197
• 全文大小：1,529 KB
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• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Life Sciences
  Biochemistry
  Medical Biochemistry
  Oncology
  Cardiology
  
• 出版者：Springer Netherlands
• ISSN：1573-4919

文摘

The influenza virus integral membrane proteins BM2 (M2 of influenza B virus) and A/M2 (M2 of influenza A virus) functions as an ion channel, important for virus uncoating in endosomes of virus-infected cells and essential for viral replication. M2 ion channel activity is also required to stimulate NLRP3 inflammasome activation by perturbing ionic concentrations in the Golgi. In the present study, we have investigated further the interaction between BM2 and p53 to confirm our previous studies using yeast two-hybrid assays. The interaction between BM2 and p53 was confirmed by GST pull-down, co-immunoprecipitation assays, and confocal microscopy. Expression of BM2 results in down-regulation of p53 mRNA and protein expression in a dose-dependent manner. In addition, we demonstrated that exogenous expression of BM2 functionally blocked p53-mediated transcriptional activity and apoptosis by luciferase reporter assay and TUNEL assay, respectively. Together, the present results indicate that BM2 is able to functionally interact with p53, and provide valuable insights into the modulation of p53 functions by influenza virus.