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Hantaan virus nucleocapsid protein stimulates MDM2-dependent p53 degradation
- Date2018-02-05 15:40
- Update2018-02-05 15:40
- CountersignatureDivision of Research Planning
- Tel043-719-8033
Journal of General Virology, 2013, 01, 2424─2428
Hantaan virus nucleocapsid protein stimulates MDM2-dependent p53 degradation
SunWhan Park, MyungGuk Han, Chan Park, Young Ran Ju, ByungYoon Ahn, Jungsang Ryou
Abstract
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.
- ISBN or ISSN: 0022-1317
- 본 연구는 질병관리본부 연구개발과제(과제번호 2011-N53001-00) 연구비를 지원받아 수행되었습니다.
- This research was supported by a fund(code 2011-N53001-00) by Research of Korea Centers for Disease Control and Prevention.
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