ArticleInternational journal of experimental pathology2011
Transgenic overexpression of p23 induces spontaneous hydronephrosis in mice.
Article in International journal of experimental pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- MicroRNA-1912 regulates cholesterol homeostasis by targeting PCSK9.Molecular therapy. Nucleic acids · 2025Article
- Implications of Genetic Factors Underlying Mouse Hydronephrosis: Cautionary Considerations on Phenotypic Interpretation in Genetically Engineered Mice.International journal of molecular sciences · 2024Article
- Effect of PIERCE1 on colorectal cancer.Experimental animals · 2020Article
- Investigation and identification of etiologies involved in the development of acquired hydronephrosis in aged laboratory mice with the use of high-frequency ultrasound imaging.Pathobiology of aging & age related diseases · 2014Article
- Cytosolic Bax: does it require binding proteins to keep its pro-apoptotic activity in check?The Journal of biological chemistry · 2012Article
- Chaperoning steroidal physiology: lessons from mouse genetic models of Hsp90 and its cochaperones.Biochimica et biophysica acta · 2012Review
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12 authors at 1 institution in 1 country.
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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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