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Article: Id1 interacts and stabilizes the Epstein-Barr virus latent membrane protein 1 (LMP1) in nasopharyngeal epithelial cells

TitleId1 interacts and stabilizes the Epstein-Barr virus latent membrane protein 1 (LMP1) in nasopharyngeal epithelial cells
Authors
Issue Date2011
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
Plos One, 2011, v. 6 n. 6 How to Cite?
AbstractThe EBV-encoded latent membrane protein 1 (LMP1) functions as a constitutive active form of tumor necrosis factor receptor (TNFR) and activates multiple downstream signaling pathways similar to CD40 signaling in a ligand-independent manner. LMP1 expression in EBV-infected cells has been postulated to play an important role in pathogenesis of nasopharyngeal carcinoma. However, variable levels of LMP1 expression were detected in nasopharyngeal carcinoma. At present, the regulation of LMP1 levels in nasopharyngeal carcinoma is poorly understood. Here we show that LMP1 mRNAs are transcribed in an EBV-positive nasopharyngeal carcinoma (NPC) cell line (C666-1) and other EBV-negative nasopharyngeal carcinoma cells stably re-infected with EBV. The protein levels of LMP1 could readily be detected after incubation with proteasome inhibitor, MG132 suggesting that LMP1 protein is rapidly degraded via proteasome-mediated proteolysis. Interestingly, we observed that Id1 overexpression could stabilize LMP1 protein in EBV-infected cells. In contrary, Id1 knockdown significantly reduced LMP1 levels in cells. Co-immunoprecipitation studies revealed that Id1 interacts with LMP1 by binding to the CTAR1 domain of LMP1. N-terminal region of Id1 is required for the interaction with LMP1. Furthermore, binding of Id1 to LMP1 suppressed polyubiquitination of LMP1 and may be involved in stabilization of LMP1 in EBV-infected nasopharyngeal epithelial cells. © 2011 Hau et al.
Persistent Identifierhttp://hdl.handle.net/10722/135015
ISSN
2015 Impact Factor: 3.057
2015 SCImago Journal Rankings: 1.395
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong General Research FundHKU 7770/07M
AoE NPCAoE/M-06/08
University of Hong Kong
CRCG200807176131
Funding Information:

This work was supported by the Hong Kong General Research Fund, grant number HKU 7770/07M; the AoE NPC, grant number AoE/M-06/08; The University of Hong Kong CRCG Grant; and the CRCG Grant, grant number: 200807176131. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorHau, PMen_HK
dc.contributor.authorTsang, CMen_HK
dc.contributor.authorYip, YLen_HK
dc.contributor.authorHuen, MSYen_HK
dc.contributor.authorTsao, SWen_HK
dc.date.accessioned2011-07-27T01:25:51Z-
dc.date.available2011-07-27T01:25:51Z-
dc.date.issued2011en_HK
dc.identifier.citationPlos One, 2011, v. 6 n. 6en_HK
dc.identifier.issn1932-6203en_HK
dc.identifier.urihttp://hdl.handle.net/10722/135015-
dc.description.abstractThe EBV-encoded latent membrane protein 1 (LMP1) functions as a constitutive active form of tumor necrosis factor receptor (TNFR) and activates multiple downstream signaling pathways similar to CD40 signaling in a ligand-independent manner. LMP1 expression in EBV-infected cells has been postulated to play an important role in pathogenesis of nasopharyngeal carcinoma. However, variable levels of LMP1 expression were detected in nasopharyngeal carcinoma. At present, the regulation of LMP1 levels in nasopharyngeal carcinoma is poorly understood. Here we show that LMP1 mRNAs are transcribed in an EBV-positive nasopharyngeal carcinoma (NPC) cell line (C666-1) and other EBV-negative nasopharyngeal carcinoma cells stably re-infected with EBV. The protein levels of LMP1 could readily be detected after incubation with proteasome inhibitor, MG132 suggesting that LMP1 protein is rapidly degraded via proteasome-mediated proteolysis. Interestingly, we observed that Id1 overexpression could stabilize LMP1 protein in EBV-infected cells. In contrary, Id1 knockdown significantly reduced LMP1 levels in cells. Co-immunoprecipitation studies revealed that Id1 interacts with LMP1 by binding to the CTAR1 domain of LMP1. N-terminal region of Id1 is required for the interaction with LMP1. Furthermore, binding of Id1 to LMP1 suppressed polyubiquitination of LMP1 and may be involved in stabilization of LMP1 in EBV-infected nasopharyngeal epithelial cells. © 2011 Hau et al.en_HK
dc.languageengen_US
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_HK
dc.relation.ispartofPLoS ONEen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshCell Line, Tumor-
dc.subject.meshEpstein-Barr Virus Infections - genetics - metabolism-
dc.subject.meshInhibitor of Differentiation Protein 1 - genetics - metabolism-
dc.subject.meshNasopharyngeal Neoplasms - genetics - metabolism - virology-
dc.subject.meshViral Matrix Proteins - genetics - metabolism - physiology-
dc.titleId1 interacts and stabilizes the Epstein-Barr virus latent membrane protein 1 (LMP1) in nasopharyngeal epithelial cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailHuen, MSY:huen.michael@hku.hken_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.authorityHuen, MSY=rp01336en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0021176en_HK
dc.identifier.pmid21701587-
dc.identifier.pmcidPMC3118807-
dc.identifier.scopuseid_2-s2.0-79959295164en_HK
dc.identifier.hkuros186959en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79959295164&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume6en_HK
dc.identifier.issue6en_HK
dc.identifier.spagee21176-
dc.identifier.epagee21176-
dc.identifier.eissn1932-6203-
dc.identifier.isiWOS:000291983800028-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectCentre for Nasopharyngeal Carcinoma Research-
dc.identifier.scopusauthoridHau, PM=14060079200en_HK
dc.identifier.scopusauthoridTsang, CM=24831236400en_HK
dc.identifier.scopusauthoridYip, YL=7005596403en_HK
dc.identifier.scopusauthoridHuen, MSY=23004751500en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.citeulike9471016-

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