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Article: Latent membrane protein 1 of Epstein-Barr virus regulates p53 phosphorylation through MAP kinases
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TitleLatent membrane protein 1 of Epstein-Barr virus regulates p53 phosphorylation through MAP kinases
 
AuthorsLi, L2
Guo, L2
Tao, Y2
Zhou, S2
Wang, Z2
Luo, W2
Hu, D2
Li, Z2
Xiao, L2
Tang, M2
Yi, W2
Tsao, SW1
Cao, Y2
 
Issue Date2007
 
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
 
CitationCancer Letters, 2007, v. 255 n. 2, p. 219-231 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.canlet.2007.04.014
 
AbstractThe Epstein-Barr virus (EBV) encoded latent membrane protein 1 (LMP1), an oncogenic protein, plays an important role in the carcinogenesis of nasopharyngeal carcinoma (NPC). Phosphorylation of p53 protein is likely to play the key role in regulating its activity. p53 protein accumulates but mutation of p53 gene is not common in NPC. The molecular mechanisms of p53 augmentation have not been completely elucidated. Here, the role of MAP kinases in the phosphorylation of p53 modulated by LMP1 was determined. p53 could be activated and phosphorylated clearly at Ser15, Ser20, Ser392, and Thr81 modulated by LMP1. Furthermore, LMP1-induced phosphorylation of p53 at Ser15 was directly by ERKs; at Ser20 and Thr81 by JNK, at Ser 15 and Ser392 by p38 kinase. The phosphorylation of p53 was associated with its transcriptional activity and stability modulated by LMP1. These results strongly suggest that MAP kinases have a direct role in LMP1-induced phosphorylation of p53 at multiple sites, which provide a novel view for us to understand the mechanism of the activation of p53 in the carcinogenesis of nasopharyngeal carcinoma. © 2007 Elsevier Ireland Ltd. All rights reserved.
 
ISSN0304-3835
2013 Impact Factor: 5.016
 
DOIhttp://dx.doi.org/10.1016/j.canlet.2007.04.014
 
ISI Accession Number IDWOS:000249676700006
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLi, L
 
dc.contributor.authorGuo, L
 
dc.contributor.authorTao, Y
 
dc.contributor.authorZhou, S
 
dc.contributor.authorWang, Z
 
dc.contributor.authorLuo, W
 
dc.contributor.authorHu, D
 
dc.contributor.authorLi, Z
 
dc.contributor.authorXiao, L
 
dc.contributor.authorTang, M
 
dc.contributor.authorYi, W
 
dc.contributor.authorTsao, SW
 
dc.contributor.authorCao, Y
 
dc.date.accessioned2012-06-26T05:56:54Z
 
dc.date.available2012-06-26T05:56:54Z
 
dc.date.issued2007
 
dc.description.abstractThe Epstein-Barr virus (EBV) encoded latent membrane protein 1 (LMP1), an oncogenic protein, plays an important role in the carcinogenesis of nasopharyngeal carcinoma (NPC). Phosphorylation of p53 protein is likely to play the key role in regulating its activity. p53 protein accumulates but mutation of p53 gene is not common in NPC. The molecular mechanisms of p53 augmentation have not been completely elucidated. Here, the role of MAP kinases in the phosphorylation of p53 modulated by LMP1 was determined. p53 could be activated and phosphorylated clearly at Ser15, Ser20, Ser392, and Thr81 modulated by LMP1. Furthermore, LMP1-induced phosphorylation of p53 at Ser15 was directly by ERKs; at Ser20 and Thr81 by JNK, at Ser 15 and Ser392 by p38 kinase. The phosphorylation of p53 was associated with its transcriptional activity and stability modulated by LMP1. These results strongly suggest that MAP kinases have a direct role in LMP1-induced phosphorylation of p53 at multiple sites, which provide a novel view for us to understand the mechanism of the activation of p53 in the carcinogenesis of nasopharyngeal carcinoma. © 2007 Elsevier Ireland Ltd. All rights reserved.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationCancer Letters, 2007, v. 255 n. 2, p. 219-231 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.canlet.2007.04.014
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.canlet.2007.04.014
 
dc.identifier.epage231
 
dc.identifier.isiWOS:000249676700006
 
dc.identifier.issn0304-3835
2013 Impact Factor: 5.016
 
dc.identifier.issue2
 
dc.identifier.pmid17582679
 
dc.identifier.scopuseid_2-s2.0-34547965826
 
dc.identifier.spage219
 
dc.identifier.urihttp://hdl.handle.net/10722/149674
 
dc.identifier.volume255
 
dc.languageeng
 
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
 
dc.publisher.placeIreland
 
dc.relation.ispartofCancer Letters
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshCell Line, Tumor
 
dc.subject.meshEpstein-Barr Virus Infections - Metabolism
 
dc.subject.meshHerpesvirus 4, Human - Metabolism
 
dc.subject.meshHumans
 
dc.subject.meshMitogen-Activated Protein Kinases - Physiology
 
dc.subject.meshNasopharyngeal Neoplasms - Virology
 
dc.subject.meshPhosphorylation
 
dc.subject.meshSerine - Metabolism
 
dc.subject.meshThreonine - Metabolism
 
dc.subject.meshTumor Suppressor Protein P53 - Metabolism
 
dc.subject.meshViral Matrix Proteins - Metabolism
 
dc.titleLatent membrane protein 1 of Epstein-Barr virus regulates p53 phosphorylation through MAP kinases
 
dc.typeArticle
 
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<contributor.author>Wang, Z</contributor.author>
<contributor.author>Luo, W</contributor.author>
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<contributor.author>Li, Z</contributor.author>
<contributor.author>Xiao, L</contributor.author>
<contributor.author>Tang, M</contributor.author>
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<contributor.author>Tsao, SW</contributor.author>
<contributor.author>Cao, Y</contributor.author>
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<description.abstract>The Epstein-Barr virus (EBV) encoded latent membrane protein 1 (LMP1), an oncogenic protein, plays an important role in the carcinogenesis of nasopharyngeal carcinoma (NPC). Phosphorylation of p53 protein is likely to play the key role in regulating its activity. p53 protein accumulates but mutation of p53 gene is not common in NPC. The molecular mechanisms of p53 augmentation have not been completely elucidated. Here, the role of MAP kinases in the phosphorylation of p53 modulated by LMP1 was determined. p53 could be activated and phosphorylated clearly at Ser15, Ser20, Ser392, and Thr81 modulated by LMP1. Furthermore, LMP1-induced phosphorylation of p53 at Ser15 was directly by ERKs; at Ser20 and Thr81 by JNK, at Ser 15 and Ser392 by p38 kinase. The phosphorylation of p53 was associated with its transcriptional activity and stability modulated by LMP1. These results strongly suggest that MAP kinases have a direct role in LMP1-induced phosphorylation of p53 at multiple sites, which provide a novel view for us to understand the mechanism of the activation of p53 in the carcinogenesis of nasopharyngeal carcinoma. &#169; 2007 Elsevier Ireland Ltd. All rights reserved.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong
  2. Central South University China