DNA damage-induced RORα Is crucial for p53 stabilization and increased apoptosis

Hyunkyung Kim, Ji Min Lee, Gina Lee, Jinhyuk Bhin, Se Kyu Oh, Kyeongkyu Kim, Ki Eun Pyo, Jason S. Lee, Hwa Young Yim, Keun Il Kim, Daehee Hwang, Jongkyeong Chung, Sung Hee Baek

Research output: Contribution to journalArticlepeer-review

64 Citations (Scopus)


A critical component of the DNA damage response is the p53 tumor suppressor, and aberrant p53 function leads to uncontrolled cell proliferation and malignancy. Several molecules have been shown to regulate p53 stability; however, genome-wide systemic approaches for determining the affected, specific downstream target genes have not been extensively studied. Here, we first identified an orphan nuclear receptor, RORα, as a direct target gene of p53, which contains functional p53 response elements. The functional consequences of DNA damage-induced RORα are to stabilize p53 and activate p53 transcription in a HAUSP/Usp7-dependent manner. Interestingly, microarray analysis revealed that RORα-mediated p53 stabilization leads to the activation of a subset of p53 target genes that are specifically involved in apoptosis. We further confirmed that RORα enhances p53-dependent, in vivo apoptotic function in the Drosophila model system. Together, we determined that RORα is a p53 regulator that exerts its role in increased apoptosis via p53.

Original languageEnglish
Pages (from-to)797-810
Number of pages14
JournalMolecular Cell
Issue number5
Publication statusPublished - 2011 Dec 9
Externally publishedYes

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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