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Article: Hepatitis C virus core protein-induced loss of LZIP function correlates with cellular transformation

TitleHepatitis C virus core protein-induced loss of LZIP function correlates with cellular transformation
Authors
KeywordsbZIP transcription factor
Hepatitis C virus
Hepatitis C virus core protein
Hepatocellular carcinoma
LZIP
Issue Date2000
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/emboj/index.html
Citation
Embo Journal, 2000, v. 19 n. 4, p. 729-740 How to Cite?
AbstractHepatitis C virus (HCV) is the major etiological agent of blood-borne non-A non-B hepatitis and a leading cause of liver cirrhosis and hepatocellular carcinoma worldwide. HCV core protein is a multifunctional protein with regulatory functions in cellular transcription and virus-induced transformation and pathogenesis. Here we report on the identification of a bZIP nuclear transcription protein as an HCV core cofactor for transformation. This bZIP factor, designated LZIP, activates CRE-dependent transcription and regulates cell proliferation. Loss of LZIP function in NIH 3T3 cells triggers morphological transformation and anchorage-independent growth. We show that HCV core protein aberrantly sequesters LZIP in the cytoplasm, inactivates LZIP function and potentiates cellular transformation. Our findings suggest that LZIP might serve a novel cellular tumor suppressor function that is targeted by the HCV core.
Persistent Identifierhttp://hdl.handle.net/10722/49402
ISSN
2015 Impact Factor: 9.643
2015 SCImago Journal Rankings: 7.450
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorJin, DYen_HK
dc.contributor.authorWang, HLen_HK
dc.contributor.authorZhou, Yen_HK
dc.contributor.authorChun, ACSen_HK
dc.contributor.authorKibler, KVen_HK
dc.contributor.authorYunDe, Hen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorJeang, KTen_HK
dc.date.accessioned2008-06-12T06:41:36Z-
dc.date.available2008-06-12T06:41:36Z-
dc.date.issued2000en_HK
dc.identifier.citationEmbo Journal, 2000, v. 19 n. 4, p. 729-740en_HK
dc.identifier.issn0261-4189en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49402-
dc.description.abstractHepatitis C virus (HCV) is the major etiological agent of blood-borne non-A non-B hepatitis and a leading cause of liver cirrhosis and hepatocellular carcinoma worldwide. HCV core protein is a multifunctional protein with regulatory functions in cellular transcription and virus-induced transformation and pathogenesis. Here we report on the identification of a bZIP nuclear transcription protein as an HCV core cofactor for transformation. This bZIP factor, designated LZIP, activates CRE-dependent transcription and regulates cell proliferation. Loss of LZIP function in NIH 3T3 cells triggers morphological transformation and anchorage-independent growth. We show that HCV core protein aberrantly sequesters LZIP in the cytoplasm, inactivates LZIP function and potentiates cellular transformation. Our findings suggest that LZIP might serve a novel cellular tumor suppressor function that is targeted by the HCV core.en_HK
dc.format.extent386 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/emboj/index.htmlen_HK
dc.relation.ispartofEMBO Journalen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectbZIP transcription factoren_HK
dc.subjectHepatitis C virusen_HK
dc.subjectHepatitis C virus core proteinen_HK
dc.subjectHepatocellular carcinomaen_HK
dc.subjectLZIPen_HK
dc.titleHepatitis C virus core protein-induced loss of LZIP function correlates with cellular transformationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0261-4189&volume=19&issue=4&spage=729&epage=740&date=2000&atitle=Hepatitis+C+virus+core+protein-induced+loss+of+LZIP+function+correlates+with+cellular+transformationen_HK
dc.identifier.emailJin, DY:dyjin@hkucc.hku.hken_HK
dc.identifier.authorityJin, DY=rp00452en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1093/emboj/19.4.729en_HK
dc.identifier.pmid10675342-
dc.identifier.pmcidPMC305611en_HK
dc.identifier.scopuseid_2-s2.0-0034651869en_HK
dc.identifier.hkuros51894-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034651869&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume19en_HK
dc.identifier.issue4en_HK
dc.identifier.spage729en_HK
dc.identifier.epage740en_HK
dc.identifier.isiWOS:000085394900026-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridJin, DY=7201973614en_HK
dc.identifier.scopusauthoridWang, HL=8081373900en_HK
dc.identifier.scopusauthoridZhou, Y=7405366890en_HK
dc.identifier.scopusauthoridChun, ACS=7003650706en_HK
dc.identifier.scopusauthoridKibler, KV=6701686388en_HK
dc.identifier.scopusauthoridYunDe, H=8777047100en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridJeang, KT=7004824803en_HK

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