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Article: Oligodeoxynucleotide decoy therapy blocks type 1 procollagen transcription and the prolyl hydroxylase β subunit translation

TitleOligodeoxynucleotide decoy therapy blocks type 1 procollagen transcription and the prolyl hydroxylase β subunit translation
Authors
Issue Date2008
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/35503
Citation
Journal Of Cellular Biochemistry, 2008, v. 103 n. 4, p. 1066-1075 How to Cite?
AbstractPersistent transforming growth factor-β1 (TGF-β1) exposure to lungs increases type 1 collagen synthesis and deposition resulting in excess fibrosis which leads to morbidity and possibly death. We now report using human embryonic lung fibroblasts in the presence of TGF-β1, a novel double-stranded (ds) DNA decoy with phosphorothioate (PT) linkages, containing the TGF-β cis-element found in the distal promoter region of the COL1A1 gene which silences COL1A1 gene expression. In a cell-free protein translation system, we have previously reported that collagen synthesis was inhibited by disulfide isomerase, the prolyl-4-hydroxylase (P-4-H) β subunit. By comparative proteomics dsdecoy therapy increased the levels of disulfide isomerase, the P-4-H β subunit. These findings taken together support the notion that the dsdecoy inhibits type 1 collagen synthesis at both the transcriptional and translational levels. © 2007 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/168279
ISSN
2015 Impact Factor: 3.446
2015 SCImago Journal Rankings: 1.520
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLok, CNen_US
dc.contributor.authorEhrlich, HPen_US
dc.contributor.authorWhite, SLen_US
dc.contributor.authorButtolph, TRen_US
dc.contributor.authorCutroneo, KRen_US
dc.contributor.authorChiu, JFen_US
dc.date.accessioned2012-10-08T03:16:58Z-
dc.date.available2012-10-08T03:16:58Z-
dc.date.issued2008en_US
dc.identifier.citationJournal Of Cellular Biochemistry, 2008, v. 103 n. 4, p. 1066-1075en_US
dc.identifier.issn0730-2312en_US
dc.identifier.urihttp://hdl.handle.net/10722/168279-
dc.description.abstractPersistent transforming growth factor-β1 (TGF-β1) exposure to lungs increases type 1 collagen synthesis and deposition resulting in excess fibrosis which leads to morbidity and possibly death. We now report using human embryonic lung fibroblasts in the presence of TGF-β1, a novel double-stranded (ds) DNA decoy with phosphorothioate (PT) linkages, containing the TGF-β cis-element found in the distal promoter region of the COL1A1 gene which silences COL1A1 gene expression. In a cell-free protein translation system, we have previously reported that collagen synthesis was inhibited by disulfide isomerase, the prolyl-4-hydroxylase (P-4-H) β subunit. By comparative proteomics dsdecoy therapy increased the levels of disulfide isomerase, the P-4-H β subunit. These findings taken together support the notion that the dsdecoy inhibits type 1 collagen synthesis at both the transcriptional and translational levels. © 2007 Wiley-Liss, Inc.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/35503en_US
dc.relation.ispartofJournal of Cellular Biochemistryen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCollagen Type I - Biosynthesis - Geneticsen_US
dc.subject.meshEmbryo, Mammalian - Cytologyen_US
dc.subject.meshFibroblasts - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshLung - Cytologyen_US
dc.subject.meshOligonucleotides - Genetics - Pharmacologyen_US
dc.subject.meshOligonucleotides, Antisense - Genetics - Pharmacologyen_US
dc.subject.meshProcollagen-Proline Dioxygenase - Biosynthesisen_US
dc.subject.meshPromoter Regions, Geneticen_US
dc.subject.meshProtein Biosynthesisen_US
dc.subject.meshTranscription, Geneticen_US
dc.subject.meshTransforming Growth Factor Beta1 - Genetics - Pharmacologyen_US
dc.titleOligodeoxynucleotide decoy therapy blocks type 1 procollagen transcription and the prolyl hydroxylase β subunit translationen_US
dc.typeArticleen_US
dc.identifier.emailLok, CN:cnlok@hku.hken_US
dc.identifier.authorityLok, CN=rp00752en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/jcb.21477en_US
dc.identifier.pmid18027883-
dc.identifier.scopuseid_2-s2.0-40349113287en_US
dc.identifier.hkuros141592-
dc.identifier.volume103en_US
dc.identifier.issue4en_US
dc.identifier.spage1066en_US
dc.identifier.epage1075en_US
dc.identifier.isiWOS:000253873800004-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLok, CN=7006410829en_US
dc.identifier.scopusauthoridEhrlich, HP=7102414814en_US
dc.identifier.scopusauthoridWhite, SL=7404080473en_US
dc.identifier.scopusauthoridButtolph, TR=13104427200en_US
dc.identifier.scopusauthoridCutroneo, KR=7005730844en_US
dc.identifier.scopusauthoridChiu, JF=7201501692en_US

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