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Transgenic overexpression of p23 induces spontaneous hydronephrosis in mice

Authors
 Jaehoon Lee  ;  Hye Jin Kim  ;  Jung Ah Moon  ;  Young Hoon Sung  ;  In-Jeoung Baek  ;  Jae-il Roh  ;  Na Young Ha  ;  Seung-Yeon Kim  ;  Young Yil Bahk  ;  Jong Eun Lee  ;  Tae Hyun Yoo  ;  Han-Woong Lee 
Citation
 International Journal of Experimental Pathology, Vol.92(4) : 251-259, 2011 
Journal Title
 International Journal of Experimental Pathology 
ISSN
 0959-9673 
Issue Date
2011
Abstract
p23 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.
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DOI
10.1111/j.1365-2613.2011.00762.x
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
Yonsei Authors
Yoo, Tae Hyun(유태현) ORCID logo https://orcid.org/0000-0002-9183-4507
Lee, Jong Eun(이종은) ORCID logo https://orcid.org/0000-0001-6203-7413
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URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/94002
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