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.
journal_name
Int J Exp Patholjournal_title
International journal of experimental pathologyauthors
Lee J,Kim HJ,Moon JA,Sung YH,Baek IJ,Roh JI,Ha NY,Kim SY,Bahk YY,Lee JE,Yoo TH,Lee HWdoi
10.1111/j.1365-2613.2011.00762.xsubject
Has Abstractpub_date
2011-08-01 00:00:00pages
251-9issue
4eissn
0959-9673issn
1365-2613journal_volume
92pub_type
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journal_title：International journal of experimental pathology
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journal_title：International journal of experimental pathology
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journal_title：International journal of experimental pathology
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journal_title：International journal of experimental pathology
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journal_title：International journal of experimental pathology
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