167 173

Cited 4 times in

Transgenic overexpression of p23 induces spontaneous hydronephrosis in mice

DC FieldValueLanguage
dc.contributor.author유태현-
dc.contributor.author이종은-
dc.date.accessioned2014-12-20T17:07:19Z-
dc.date.available2014-12-20T17:07:19Z-
dc.date.issued2011-
dc.identifier.issn0959-9673-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/94002-
dc.description.abstractp23 is a cochaperone of heat shock protein 90 and also interacts functionally with numerous steroid receptors and kinases. However, the in vivo roles of p23 remain unclear. To explore its in vivo function, we generated the transgenic (TG) mice ubiquitously overexpressing p23. The p23 TG mice spontaneously developed kidney abnormalities closely resembling human hydronephrosis. Consistently, kidney functions deteriorate significantly in the p23 TG mice compared to their wild-type (WT) littermates. Furthermore, the expression of target genes for aryl hydrocarbon receptor (AhR), such as cytochrome P450, family 1, subfamily A, polypeptide 1 (Cyp1A1) and cytochrome P450, family 1, subfamily B, polypeptide 1 (Cyp1B1), were induced in the kidneys of the p23 TG mice. These results indicate that the overexpression of p23 contributes to the development of hydronephrosis through the upregulation of the AhR pathway in vivo.-
dc.description.statementOfResponsibilityopen-
dc.format.extent251~259-
dc.relation.isPartOfINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHAryl Hydrocarbon Hydroxylases/metabolism-
dc.subject.MESHCytochrome P-450 CYP1A1/metabolism-
dc.subject.MESHCytochrome P-450 CYP1B1-
dc.subject.MESHDisease Models, Animal-
dc.subject.MESHFemale-
dc.subject.MESHGene Expression Regulation/physiology*-
dc.subject.MESHHydronephrosis/metabolism-
dc.subject.MESHHydronephrosis/physiopathology*-
dc.subject.MESHIntramolecular Oxidoreductases/genetics*-
dc.subject.MESHIntramolecular Oxidoreductases/physiology*-
dc.subject.MESHKidney/metabolism-
dc.subject.MESHKidney/physiopathology-
dc.subject.MESHMale-
dc.subject.MESHMice-
dc.subject.MESHMice, Transgenic-
dc.subject.MESHProstaglandin-E Synthases-
dc.subject.MESHReceptors, Aryl Hydrocarbon/metabolism-
dc.subject.MESHSignal Transduction/physiology-
dc.titleTransgenic overexpression of p23 induces spontaneous hydronephrosis in mice-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorJaehoon Lee-
dc.contributor.googleauthorHye Jin Kim-
dc.contributor.googleauthorJung Ah Moon-
dc.contributor.googleauthorYoung Hoon Sung-
dc.contributor.googleauthorIn-Jeoung Baek-
dc.contributor.googleauthorJae-il Roh-
dc.contributor.googleauthorNa Young Ha-
dc.contributor.googleauthorSeung-Yeon Kim-
dc.contributor.googleauthorYoung Yil Bahk-
dc.contributor.googleauthorJong Eun Lee-
dc.contributor.googleauthorTae Hyun Yoo-
dc.contributor.googleauthorHan-Woong Lee-
dc.identifier.doi10.1111/j.1365-2613.2011.00762.x-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02526-
dc.contributor.localIdA03146-
dc.relation.journalcodeJ01114-
dc.identifier.eissn1365-2613-
dc.identifier.pmid21323770-
dc.subject.keywordaryl hydrocarbon receptor-
dc.subject.keywordhydronephrosis-
dc.subject.keywordkidney-
dc.subject.keywordp23-
dc.subject.keywordTG mouse-
dc.contributor.alternativeNameYoo, Tae Hyun-
dc.contributor.alternativeNameLee, Jong Eun-
dc.contributor.affiliatedAuthorYoo, Tae Hyun-
dc.contributor.affiliatedAuthorLee, Jong Eun-
dc.rights.accessRightsfree-
dc.citation.volume92-
dc.citation.number4-
dc.citation.startPage251-
dc.citation.endPage259-
dc.identifier.bibliographicCitationINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Vol.92(4) : 251-259, 2011-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Anatomy (해부학교실) > 1. Journal Papers

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.