ArticleBiochimica et biophysica acta2010
Mechanisms of p53-mediated repression of the human polycystic kidney disease-1 promoter.
Article in Biochimica et biophysica acta, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
- SALL2 represses cyclins D1 and E1 expression and restrains G1/S cell cycle transition and cancer-related phenotypes.Molecular oncology · 2018Article
- Epigenetics of Renal Development and Disease.The Yale journal of biology and medicine · 2016Review
- The transcription factor p53: not a repressor, solely an activator.Cell cycle (Georgetown, Tex.) · 2014Article
- Genome-wide analysis of the p53 gene regulatory network in the developing mouse kidney.Physiological genomics · 2013Article
- Wild type p53 transcriptionally represses the SALL2 transcription factor under genotoxic stress.PloS one · 2013Article
- Article
- One function--multiple mechanisms: the manifold activities of p53 as a transcriptional repressor.Journal of biomedicine & biotechnology · 2011Review
- MAP/ERK kinase kinase 1 (MEKK1) mediates transcriptional repression by interacting with polycystic kidney disease-1 (PKD1) promoter-bound p53 tumor suppressor protein.The Journal of biological chemistry · 2010Article
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4 authors at 1 institution in 1 country.
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Abstract
We previously reported that the tumor suppressor protein p53 participates in a negative feedback loop to fine-tune PKD1 gene expression. This physiological pathway is believed to prevent polycystin-1 overexpression and thus renal cysts. The present study examined the mechanisms of p53-mediated repression of PKD1. The 5'-upstream region of the human PKD1 gene is TATA-less, GC-rich, and contains four consensus p53 binding sites at positions -2.7 kb (BS4), -1.2 kb (BS3), -0.8 kb (BS2), and -0.2 kb (BS1), respectively. PKD1BS1-4 are bound to endogenous p53 in vivo and in vitro. Transient transfection assays in inner medullary collecting duct cells revealed that disruption of PKD1BS1 enhances baseline PKD1 promoter activity; in contrast, disruption of PKD1BS4 suppressed PKD1 transcription. PKD1BS1 confers p53-mediated repression when substituted for the p53 enhancer element in the bradykinin B2 receptor gene, indicating that PKD1BS1 is a bona fide p53 repressor element. Moreover, PKD1BS1 requires intact BS2-4 and cellular histone deacetylase activity for full functional activity. Indeed, the PKD1BS1/4 regions are occupied by a complex containing HDAC1/2 and mSin3. These findings suggest a model whereby p53 exerts a biphasic control on PKD1 gene transcription, depending on cellular context and the cognate cis-acting element.
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