File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Molecular cloning and functional analysis of the promoter region of rat nonmuscle myosin heavy chain-B gene

TitleMolecular cloning and functional analysis of the promoter region of rat nonmuscle myosin heavy chain-B gene
Authors
Issue Date2000
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, 2000, v. 276 n. 3, p. 1203-1209 How to Cite?
AbstractRat nonmuscle myosin heavy chain-B (r-nmMHC-B) mRNA was previously found downregulated in Rat 6 fibroblasts transformed by mutant p53(val135) [J. W. P. Yam, J. Y. Zheng, and W. L. W. Hsiao (1987) Biochem. Biophys. Res. Commun. 266, 472-480]. Overexpression of exogenous r-nmMHC-B could partially reverse the transforming phenotypes both in vitro and in vivo. The downregulation of r-nmMHC-B was also observed in Rat 6 transformed by c-H-ras and v-myc oncogenes. We cloned a 5.2-kb r-nmMHC-B promoter region. Sequence analysis of -1248 to +1 revealed no TATA box, but did show that it contained CAAT boxes, E12/E47, MyoD, MEF, E2F, CREB, and SP1 binding sites. Based on transient reporter assays, the promoter/enhancer activities were unusually extended to the entire 5.2 kb region in normal Rat 6 cultures, but markedly suppressed in p53(val135)-, and c-H-ras-transformed cells. The activity detected by the reporter assay corresponded to levels of mRNA as analyzed previously by Northern blots in each respective cell line. Thus, the switch-off of the r-nmMHC-B in the transformed cells is very likely controlled by upstream transcriptional factors, which might have been altered in the course of neo-plastic transformation. (C) 2000 Academic Press.
Persistent Identifierhttp://hdl.handle.net/10722/88340
ISSN
2015 Impact Factor: 2.371
2015 SCImago Journal Rankings: 1.152
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYam, JWPen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorLi, Nen_HK
dc.contributor.authorHsiao, WLWendyen_HK
dc.date.accessioned2010-09-06T09:42:06Z-
dc.date.available2010-09-06T09:42:06Z-
dc.date.issued2000en_HK
dc.identifier.citationBiochemical And Biophysical Research Communications, 2000, v. 276 n. 3, p. 1203-1209en_HK
dc.identifier.issn0006-291Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/88340-
dc.description.abstractRat nonmuscle myosin heavy chain-B (r-nmMHC-B) mRNA was previously found downregulated in Rat 6 fibroblasts transformed by mutant p53(val135) [J. W. P. Yam, J. Y. Zheng, and W. L. W. Hsiao (1987) Biochem. Biophys. Res. Commun. 266, 472-480]. Overexpression of exogenous r-nmMHC-B could partially reverse the transforming phenotypes both in vitro and in vivo. The downregulation of r-nmMHC-B was also observed in Rat 6 transformed by c-H-ras and v-myc oncogenes. We cloned a 5.2-kb r-nmMHC-B promoter region. Sequence analysis of -1248 to +1 revealed no TATA box, but did show that it contained CAAT boxes, E12/E47, MyoD, MEF, E2F, CREB, and SP1 binding sites. Based on transient reporter assays, the promoter/enhancer activities were unusually extended to the entire 5.2 kb region in normal Rat 6 cultures, but markedly suppressed in p53(val135)-, and c-H-ras-transformed cells. The activity detected by the reporter assay corresponded to levels of mRNA as analyzed previously by Northern blots in each respective cell line. Thus, the switch-off of the r-nmMHC-B in the transformed cells is very likely controlled by upstream transcriptional factors, which might have been altered in the course of neo-plastic transformation. (C) 2000 Academic Press.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/descriptionen_HK
dc.relation.ispartofBiochemical and Biophysical Research Communicationsen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshBinding Sitesen_HK
dc.subject.meshCell Line, Transformeden_HK
dc.subject.meshCell Transformation, Neoplastic - geneticsen_HK
dc.subject.meshCloning, Molecularen_HK
dc.subject.meshConserved Sequence - geneticsen_HK
dc.subject.meshFibroblasts - metabolismen_HK
dc.subject.meshGene Expression Regulationen_HK
dc.subject.meshGenes, Reporter - geneticsen_HK
dc.subject.meshGenes, myc - geneticsen_HK
dc.subject.meshGenes, p53 - geneticsen_HK
dc.subject.meshGenes, ras - geneticsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMolecular Sequence Dataen_HK
dc.subject.meshMutation - geneticsen_HK
dc.subject.meshMyosin Heavy Chains - geneticsen_HK
dc.subject.meshNonmuscle Myosin Type IIBen_HK
dc.subject.meshPromoter Regions, Genetic - geneticsen_HK
dc.subject.meshRNA, Messenger - analysis - geneticsen_HK
dc.subject.meshRatsen_HK
dc.subject.meshResponse Elements - geneticsen_HK
dc.subject.meshSequence Alignmenten_HK
dc.subject.meshTranscription, Genetic - geneticsen_HK
dc.subject.meshTumor Suppressor Protein p53 - genetics - metabolismen_HK
dc.titleMolecular cloning and functional analysis of the promoter region of rat nonmuscle myosin heavy chain-B geneen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0006-291X&volume=276&spage=1203&epage=1209&date=2000&atitle=Molecular+cloning+and+functional+analysis+of+the+promoter+region+of+rat+nonmuscle+myosin+heavy+chain-B+geneen_HK
dc.identifier.emailYam, JWP:judyyam@pathology.hku.hken_HK
dc.identifier.authorityYam, JWP=rp00468en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1006/bbrc.2000.3614en_HK
dc.identifier.pmid11027611-
dc.identifier.scopuseid_2-s2.0-0034609949en_HK
dc.identifier.hkuros56449en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034609949&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume276en_HK
dc.identifier.issue3en_HK
dc.identifier.spage1203en_HK
dc.identifier.epage1209en_HK
dc.identifier.isiWOS:000089794300060-
dc.publisher.placeUnited Statesen_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats