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Article: Study of the hypoxia-dependent regulation of human CYGB gene

TitleStudy of the hypoxia-dependent regulation of human CYGB gene
Authors
Issue Date2007
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description
Citation
Biochemical And Biophysical Research Communications, 2007, v. 364 n. 1, p. 145-150 How to Cite?
AbstractCytoglobin (CYGB) is ubiquitously expressed in all tissues and has been characterized as a respiratory protein in connective tissues. CYGB is up-regulated during hypoxia, implicating its function in maintaining the homeostasis redox of the cell. Here, we study the underlying molecular mechanisms by which hypoxia regulates human CYGB gene expression. When cells were subjected to hypoxia, the expression of endogenous CYGB was up-regulated ∼1.7-fold in BEAS-2B cells (p ≤ 0.05) and ∼1.6-fold in HeLa cells (p ≤ 0.05). Dual-luciferase assays and site directed mutagenesis showed the presence of hypoxia responsive elements (HREs) at positions -141, -144 and -448 that were essential for activation of CYGB expression under hypoxic conditions. The binding of hypoxia inducible factor (HIF-1) protein to the HREs was confirmed by gel shift and chromatin immunoprecipitation (ChIP) assays. These results indicate that HRE motifs are directly involved in the activation of the CYGB transcription under hypoxia. © 2007 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/179015
ISSN
2015 Impact Factor: 2.371
2015 SCImago Journal Rankings: 1.152
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorGuo, Xen_US
dc.contributor.authorPhilipsen, Sen_US
dc.contributor.authorTanUn, KCen_US
dc.date.accessioned2012-12-19T09:51:25Z-
dc.date.available2012-12-19T09:51:25Z-
dc.date.issued2007en_US
dc.identifier.citationBiochemical And Biophysical Research Communications, 2007, v. 364 n. 1, p. 145-150en_US
dc.identifier.issn0006-291Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/179015-
dc.description.abstractCytoglobin (CYGB) is ubiquitously expressed in all tissues and has been characterized as a respiratory protein in connective tissues. CYGB is up-regulated during hypoxia, implicating its function in maintaining the homeostasis redox of the cell. Here, we study the underlying molecular mechanisms by which hypoxia regulates human CYGB gene expression. When cells were subjected to hypoxia, the expression of endogenous CYGB was up-regulated ∼1.7-fold in BEAS-2B cells (p ≤ 0.05) and ∼1.6-fold in HeLa cells (p ≤ 0.05). Dual-luciferase assays and site directed mutagenesis showed the presence of hypoxia responsive elements (HREs) at positions -141, -144 and -448 that were essential for activation of CYGB expression under hypoxic conditions. The binding of hypoxia inducible factor (HIF-1) protein to the HREs was confirmed by gel shift and chromatin immunoprecipitation (ChIP) assays. These results indicate that HRE motifs are directly involved in the activation of the CYGB transcription under hypoxia. © 2007 Elsevier Inc. All rights reserved.en_US
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/descriptionen_US
dc.relation.ispartofBiochemical and Biophysical Research Communicationsen_US
dc.subject.meshAnoxia - Physiopathologyen_US
dc.subject.meshCell Lineen_US
dc.subject.meshChromatin Immunoprecipitationen_US
dc.subject.meshElectrophoretic Mobility Shift Assayen_US
dc.subject.meshGene Expression Regulationen_US
dc.subject.meshGlobins - Geneticsen_US
dc.subject.meshHela Cellsen_US
dc.subject.meshHumansen_US
dc.subject.meshHypoxia-Inducible Factor 1 - Metabolismen_US
dc.subject.meshMutagenesis, Site-Directeden_US
dc.subject.meshPromoter Regions, Geneticen_US
dc.subject.meshUp-Regulationen_US
dc.titleStudy of the hypoxia-dependent regulation of human CYGB geneen_US
dc.typeArticleen_US
dc.identifier.emailTanUn, KC: kctanun@hkucc.hku.hken_US
dc.identifier.authorityTanUn, KC=rp00787en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.bbrc.2007.09.108en_US
dc.identifier.pmid17936249-
dc.identifier.scopuseid_2-s2.0-35348964146en_US
dc.identifier.hkuros139815-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-35348964146&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume364en_US
dc.identifier.issue1en_US
dc.identifier.spage145en_US
dc.identifier.epage150en_US
dc.identifier.isiWOS:000250661500023-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridGuo, X=36725898900en_US
dc.identifier.scopusauthoridPhilipsen, S=7003745052en_US
dc.identifier.scopusauthoridTanUn, KC=6602914262en_US

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