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.
| Original language | English |
|---|---|
| Pages (from-to) | 2424-2428 |
| Number of pages | 5 |
| Journal | Journal of General Virology |
| Volume | 94 |
| Issue number | PART 11 |
| DOIs | |
| Publication status | Published - 2013 Nov 1 |
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ASJC Scopus subject areas
- Virology
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Hantaan virus nucleocapsid protein stimulates MDM2-dependent p53 degradation. / Park, Sun Whan; Han, Myung Guk; Park, Chan; Ju, Young Ran; Ahn, Byung-Yoon; Ryou, Jungsang.
In: Journal of General Virology, Vol. 94, No. PART 11, 01.11.2013, p. 2424-2428.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Hantaan virus nucleocapsid protein stimulates MDM2-dependent p53 degradation
AU - Park, Sun Whan
AU - Han, Myung Guk
AU - Park, Chan
AU - Ju, Young Ran
AU - Ahn, Byung-Yoon
AU - Ryou, Jungsang
PY - 2013/11/1
Y1 - 2013/11/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84885657871&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84885657871&partnerID=8YFLogxK
U2 - 10.1099/vir.0.054312-0
DO - 10.1099/vir.0.054312-0
M3 - Article
C2 - 23994832
AN - SCOPUS:84885657871
VL - 94
SP - 2424
EP - 2428
JO - Journal of General Virology
JF - Journal of General Virology
SN - 0022-1317
IS - PART 11
ER -