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Article: CREB - A real culprit in oncogenesis

TitleCREB - A real culprit in oncogenesis
Authors
KeywordsCREB
Fusion oncoprotein
Human T-cell leukemia virus type I oncoprotein Tax
Oncogenesis
Proto-oncogene
TORC coactivators
Issue Date2007
PublisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.febsjournal.org/
Citation
Febs Journal, 2007, v. 274 n. 13, p. 3224-3232 How to Cite?
AbstractThe cAMP response element-binding protein (CREB) is a stimulus-induced transcription factor that responds rapidly to phosphorylation and/or coactivator activation. Regulated activation of CREB has a significant impact on cellular growth, proliferation and survival. To overturn the cellular control of these processes, tumor cells have developed various mechanisms to achieve constitutive activation of CREB, including gene amplification, chromosome translocation, interaction with viral oncoproteins, and inactivation of tumor suppressor genes. These mechanisms converge on the phosphorylation of CREB and/or the activation of transducer of regulated CREB activity (TORC) coactivators to effect uncontrolled proliferation of cells. This minireview summarizes the different lines of existing evidence that support a direct role of CREB in oncogenesis. © 2007 The Authors.
Persistent Identifierhttp://hdl.handle.net/10722/68080
ISSN
2023 Impact Factor: 5.5
2023 SCImago Journal Rankings: 2.003
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSiu, YTen_HK
dc.contributor.authorJin, DYen_HK
dc.date.accessioned2010-09-06T06:01:09Z-
dc.date.available2010-09-06T06:01:09Z-
dc.date.issued2007en_HK
dc.identifier.citationFebs Journal, 2007, v. 274 n. 13, p. 3224-3232en_HK
dc.identifier.issn1742-464Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/68080-
dc.description.abstractThe cAMP response element-binding protein (CREB) is a stimulus-induced transcription factor that responds rapidly to phosphorylation and/or coactivator activation. Regulated activation of CREB has a significant impact on cellular growth, proliferation and survival. To overturn the cellular control of these processes, tumor cells have developed various mechanisms to achieve constitutive activation of CREB, including gene amplification, chromosome translocation, interaction with viral oncoproteins, and inactivation of tumor suppressor genes. These mechanisms converge on the phosphorylation of CREB and/or the activation of transducer of regulated CREB activity (TORC) coactivators to effect uncontrolled proliferation of cells. This minireview summarizes the different lines of existing evidence that support a direct role of CREB in oncogenesis. © 2007 The Authors.en_HK
dc.languageengen_HK
dc.publisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.febsjournal.org/en_HK
dc.relation.ispartofFEBS Journalen_HK
dc.rightsThe F E B S Journal. Copyright © Blackwell Publishing Ltd.en_HK
dc.subjectCREB-
dc.subjectFusion oncoprotein-
dc.subjectHuman T-cell leukemia virus type I oncoprotein Tax-
dc.subjectOncogenesis-
dc.subjectProto-oncogene-
dc.subjectTORC coactivators-
dc.subject.meshAnimalsen_HK
dc.subject.meshCell Proliferationen_HK
dc.subject.meshCell Survivalen_HK
dc.subject.meshCell Transformation, Neoplasticen_HK
dc.subject.meshCyclic AMP Response Element-Binding Protein - metabolism - physiologyen_HK
dc.subject.meshDimerizationen_HK
dc.subject.meshGene Expression Regulation, Leukemicen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLeukemia, Myeloid, Acute - metabolismen_HK
dc.subject.meshModels, Biologicalen_HK
dc.subject.meshNeoplasms - etiology - metabolismen_HK
dc.subject.meshPhosphorylationen_HK
dc.subject.meshProtein Structure, Tertiaryen_HK
dc.subject.meshProtein-Serine-Threonine Kinases - metabolismen_HK
dc.titleCREB - A real culprit in oncogenesisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1742-464X&volume=274&spage=3224&epage=3232&date=2007&atitle=CREB+-+a+real+culprit+in+oncogenesisen_HK
dc.identifier.emailJin, DY:dyjin@hkucc.hku.hken_HK
dc.identifier.authorityJin, DY=rp00452en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1742-4658.2007.05884.xen_HK
dc.identifier.pmid17565603-
dc.identifier.scopuseid_2-s2.0-34347391261en_HK
dc.identifier.hkuros128036en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34347391261&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume274en_HK
dc.identifier.issue13en_HK
dc.identifier.spage3224en_HK
dc.identifier.epage3232en_HK
dc.identifier.isiWOS:000247661800005-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridSiu, YT=8953557400en_HK
dc.identifier.scopusauthoridJin, DY=7201973614en_HK
dc.identifier.citeulike1430111-
dc.identifier.issnl1742-464X-

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