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Article: The liver-enriched transcription factor CREB-H is a growth suppressor protein underexpressed in hepatocellular carcinoma

TitleThe liver-enriched transcription factor CREB-H is a growth suppressor protein underexpressed in hepatocellular carcinoma
Authors
Issue Date2005
PublisherOxford University Press. The Journal's web site is located at http://nar.oxfordjournals.org/
Citation
Nucleic Acids Research, 2005, v. 33 n. 6, p. 1859-1873 How to Cite?
AbstractWe have previously characterized transcription factor LZIP to be a growth suppressor targeted by hepatitis C virus oncoprotein. In search of proteins closely related to LZIP, we have identified a liver-enriched transcription factor CREB-H. LZIP and CREB-H represent a new subfamily of bZIP factors. CREB-H activates transcription by binding to cAMP responsive element, box B, and ATF6-binding element. Interestingly, CREB-H has a putative transmembrane (TM) domain and it localizes ambiently to the endoplasmic reticulum. Proteolytic cleavage that removes the TM domain leads to nuclear translocation and activation of CREB-H. CREB-H activates the promoter of hepatic gluconeogenic enzyme phosphoenolpyruvate carboxykinase. This activation can be further stimulated by cAMP and protein kinase A. CREB-H transcript is exclusively abundant in adult liver. In contrast, the expression of CREB-H mRNA is aberrantly reduced in hepatoma tissues and cells. The enforced expression of CREB-H suppresses the proliferation of cultured hepatoma cells. Taken together, our findings suggest that the liver-enriched bZIP transcription factor CREB-H is a growth suppressor that plays a role in hepatic physiology and pathology. © The Author 2005. Published by Oxford University Press. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/48991
ISSN
2014 Impact Factor: 9.112
2014 SCImago Journal Rankings: 6.160
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChin, KTen_HK
dc.contributor.authorZhou, HJen_HK
dc.contributor.authorWong, CMen_HK
dc.contributor.authorLee, JMFen_HK
dc.contributor.authorChan, CPen_HK
dc.contributor.authorQiang, BQen_HK
dc.contributor.authorYuan, JGen_HK
dc.contributor.authorNg, IOLen_HK
dc.contributor.authorJin, DYen_HK
dc.date.accessioned2008-06-12T06:31:33Z-
dc.date.available2008-06-12T06:31:33Z-
dc.date.issued2005en_HK
dc.identifier.citationNucleic Acids Research, 2005, v. 33 n. 6, p. 1859-1873en_HK
dc.identifier.issn0305-1048en_HK
dc.identifier.urihttp://hdl.handle.net/10722/48991-
dc.description.abstractWe have previously characterized transcription factor LZIP to be a growth suppressor targeted by hepatitis C virus oncoprotein. In search of proteins closely related to LZIP, we have identified a liver-enriched transcription factor CREB-H. LZIP and CREB-H represent a new subfamily of bZIP factors. CREB-H activates transcription by binding to cAMP responsive element, box B, and ATF6-binding element. Interestingly, CREB-H has a putative transmembrane (TM) domain and it localizes ambiently to the endoplasmic reticulum. Proteolytic cleavage that removes the TM domain leads to nuclear translocation and activation of CREB-H. CREB-H activates the promoter of hepatic gluconeogenic enzyme phosphoenolpyruvate carboxykinase. This activation can be further stimulated by cAMP and protein kinase A. CREB-H transcript is exclusively abundant in adult liver. In contrast, the expression of CREB-H mRNA is aberrantly reduced in hepatoma tissues and cells. The enforced expression of CREB-H suppresses the proliferation of cultured hepatoma cells. Taken together, our findings suggest that the liver-enriched bZIP transcription factor CREB-H is a growth suppressor that plays a role in hepatic physiology and pathology. © The Author 2005. Published by Oxford University Press. All rights reserved.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://nar.oxfordjournals.org/en_HK
dc.relation.ispartofNucleic Acids Researchen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshCarcinoma, Hepatocellular - metabolism - pathologyen_HK
dc.subject.meshLiver - metabolismen_HK
dc.subject.meshLiver Neoplasms - metabolism - pathologyen_HK
dc.subject.meshTumor Suppressor Proteins - metabolism - physiologyen_HK
dc.subject.meshTranscription Factors - analysis - classification - metabolism - physiologyen_HK
dc.titleThe liver-enriched transcription factor CREB-H is a growth suppressor protein underexpressed in hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0305-1048&volume=33&issue=6&spage=1859&epage=1873&date=2005&atitle=The+liver-enriched+transcription+factor+CREB-H+is+a+growth+suppressor+protein+underexpressed+in+hepatocellular+carcinomaen_HK
dc.identifier.emailWong, CM:jackwong@pathology.hku.hken_HK
dc.identifier.emailNg, IOL:iolng@hkucc.hku.hken_HK
dc.identifier.emailJin, DY:dyjin@hkucc.hku.hken_HK
dc.identifier.authorityWong, CM=rp00231en_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.identifier.authorityJin, DY=rp00452en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1093/nar/gki332en_HK
dc.identifier.pmid15800215en_HK
dc.identifier.pmcidPMC1072803en_HK
dc.identifier.scopuseid_2-s2.0-17844395201en_HK
dc.identifier.hkuros98291-
dc.identifier.hkuros159396-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-17844395201&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume33en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1859en_HK
dc.identifier.epage1873en_HK
dc.identifier.isiWOS:000228398400025-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChin, KT=7202995491en_HK
dc.identifier.scopusauthoridZhou, HJ=7404743611en_HK
dc.identifier.scopusauthoridWong, CM=16314668400en_HK
dc.identifier.scopusauthoridLee, JMF=36065603500en_HK
dc.identifier.scopusauthoridChan, CP=7404813842en_HK
dc.identifier.scopusauthoridQiang, BQ=7005510394en_HK
dc.identifier.scopusauthoridYuan, JG=7403401529en_HK
dc.identifier.scopusauthoridNg, IOL=7102753722en_HK
dc.identifier.scopusauthoridJin, DY=7201973614en_HK
dc.identifier.citeulike161551-

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