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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
2019 Impact Factor: 11.501
2015 SCImago Journal Rankings: 7.458
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.rights© The Author 2005. Published by Oxford University Press. All rights reserved. The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oupjournals.org-
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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