Hantaan virus nucleocapsid protein stimulates MDM2-dependent p53 degradation

Sun Whan Park, Myung Guk Han, Chan Park, Young Ran Ju, Byung Yoon Ahn, Jungsang Ryou

Research output: Contribution to journalArticlepeer-review

17 Citations (Scopus)


Apoptosis has been shown to be induced and downregulated by the Hantaan virus (HTNV) nucleocapsid (N) protein. To address these conflicting data, expression of the p53 protein, one of the key molecules involved in apoptosis, was assessed in the presence of the N protein in A549 and HeLa cells. The amount of p53, increased by drug treatment, was reduced when cells were infected with HTNV or transfected with an expression vector of the HTNV N protein. When cells were treated with a proteasome inhibitor (MG132) or an MDM2 antagonist (Nutlin-3), p53 expression was not reduced in N protein-overexpressed cells. We concluded that the HTNV N protein ubiquitinates and degrades p53 MDM2-dependently. Here we report downregulation of p53 expression through a post-translational mechanism: MDM2-dependent ubiquitination and degradation by the HTNV N protein. These results indicate that N protein-dependent p53 degradation through the ubiquitin proteasome system is one of the anti-apoptotic mechanisms employed by HTNV.

Original languageEnglish
Pages (from-to)2424-2428
Number of pages5
JournalJournal of General Virology
Issue numberPART 11
Publication statusPublished - 2013 Nov

ASJC Scopus subject areas

  • Virology


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