Transgenic overexpression of p23 induces spontaneous hydronephrosis in mice

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

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)251-259
Number of pages9
JournalInternational Journal of Experimental Pathology
Issue number4
Publication statusPublished - 2011 Aug

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Cell Biology


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