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Article: Transgenic mice expressing dominant-negative osmotic-response element-binding protein (OREBP) in lens exhibit fiber cell elongation defect associated with increased DNA breaks

TitleTransgenic mice expressing dominant-negative osmotic-response element-binding protein (OREBP) in lens exhibit fiber cell elongation defect associated with increased DNA breaks
Authors
Issue Date2005
PublisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
Citation
Journal Of Biological Chemistry, 2005, v. 280 n. 20, p. 19986-19991 How to Cite?
AbstractOsmotic-response element-binding protein (OREBP), also known as TonEBP or NFAT5, is thought to be responsible for the induction of osmolyte-accumulating genes when cells are under hypertonic stress. Recent studies suggest that OREBP also plays a role in water reabsorption in the kidney, T-cell proliferation, and embryonic development. We developed transgenic mice that express the dominant-negative OREBP (OREBPdn) specifically in the lens because our earlier studies showed that it is particularly sensitive to osmotic stress. The transgenic mice developed nuclear cataract soon after birth, suggesting defects in lens development. The developing transgenic lenses showed incomplete elongation of fiber cells and formation of vacuoles. This is accompanied by evidence of DNA strand breaks, activation of p53, and induction of checkpoint kinase, suggesting that the developing fiber cells lacking OREBP are in a similar physiological state as cells experiencing hypertonic stress. These results indicate that OREBP-mediated accumulation of osmolytes is essential during elongation of the lens fiber cells. © 2005 by The American Society for Biochemistry and Molecular Biology, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/88021
ISSN
2015 Impact Factor: 4.258
2015 SCImago Journal Rankings: 3.151
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Yen_HK
dc.contributor.authorKo, BCBen_HK
dc.contributor.authorYang, JYen_HK
dc.contributor.authorLam, TTLen_HK
dc.contributor.authorJiang, Zen_HK
dc.contributor.authorZhang, Jen_HK
dc.contributor.authorChung, SKen_HK
dc.contributor.authorChung, SSMen_HK
dc.date.accessioned2010-09-06T09:37:37Z-
dc.date.available2010-09-06T09:37:37Z-
dc.date.issued2005en_HK
dc.identifier.citationJournal Of Biological Chemistry, 2005, v. 280 n. 20, p. 19986-19991en_HK
dc.identifier.issn0021-9258en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88021-
dc.description.abstractOsmotic-response element-binding protein (OREBP), also known as TonEBP or NFAT5, is thought to be responsible for the induction of osmolyte-accumulating genes when cells are under hypertonic stress. Recent studies suggest that OREBP also plays a role in water reabsorption in the kidney, T-cell proliferation, and embryonic development. We developed transgenic mice that express the dominant-negative OREBP (OREBPdn) specifically in the lens because our earlier studies showed that it is particularly sensitive to osmotic stress. The transgenic mice developed nuclear cataract soon after birth, suggesting defects in lens development. The developing transgenic lenses showed incomplete elongation of fiber cells and formation of vacuoles. This is accompanied by evidence of DNA strand breaks, activation of p53, and induction of checkpoint kinase, suggesting that the developing fiber cells lacking OREBP are in a similar physiological state as cells experiencing hypertonic stress. These results indicate that OREBP-mediated accumulation of osmolytes is essential during elongation of the lens fiber cells. © 2005 by The American Society for Biochemistry and Molecular Biology, Inc.en_HK
dc.languageengen_HK
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/en_HK
dc.relation.ispartofJournal of Biological Chemistryen_HK
dc.rightsJournal of Biological Chemistry. Copyright © American Society for Biochemistry and Molecular Biology, Inc.en_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAnimals, Newbornen_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshCataract - genetics - metabolism - pathologyen_HK
dc.subject.meshDNA - geneticsen_HK
dc.subject.meshDNA Damage - geneticsen_HK
dc.subject.meshDNA-Binding Proteins - geneticsen_HK
dc.subject.meshGene Expression Regulation, Developmentalen_HK
dc.subject.meshGenetic Vectorsen_HK
dc.subject.meshLens, Crystalline - abnormalities - embryology - growth & development - metabolismen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred C57BLen_HK
dc.subject.meshMice, Transgenicen_HK
dc.subject.meshNFATC Transcription Factorsen_HK
dc.subject.meshOsmotic Pressureen_HK
dc.subject.meshPhenotypeen_HK
dc.subject.meshTranscription Factors - geneticsen_HK
dc.titleTransgenic mice expressing dominant-negative osmotic-response element-binding protein (OREBP) in lens exhibit fiber cell elongation defect associated with increased DNA breaksen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9258&volume=280&spage=19986&epage=199991&date=2005&atitle=Transgenic+mice+expressing+dominant-negative+osmotic-response+element-binding+protein+(OREBP)+in+lens+exhibit+fiber+cell+elongation+defect+associated+with+increased+DNA+breaksen_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1074/jbc.M501689200en_HK
dc.identifier.pmid15774462-
dc.identifier.scopuseid_2-s2.0-21244460386en_HK
dc.identifier.hkuros106609en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-21244460386&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume280en_HK
dc.identifier.issue20en_HK
dc.identifier.spage19986en_HK
dc.identifier.epage19991en_HK
dc.identifier.isiWOS:000229113700068-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWang, Y=34973744400en_HK
dc.identifier.scopusauthoridKo, BCB=7102833927en_HK
dc.identifier.scopusauthoridYang, JY=8915077600en_HK
dc.identifier.scopusauthoridLam, TTL=8915077700en_HK
dc.identifier.scopusauthoridJiang, Z=7404279744en_HK
dc.identifier.scopusauthoridZhang, J=7601342242en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK

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