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Journal of Cancer Prevention

Original

Cancer prevention research 2006; 11(4): 284-290

Published online December 30, 2006

© Korean Society of Cancer Prevention

Decreased ARD1 Expression Stabilizes the HIF-1α
Stability Under Hypoxia

Joo-Won Jeong

Received: October 27, 2006; Accepted: December 6, 2006

Abstract

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The stability and activity of HIF-1α are regulated by various post-translational modifications, hydroxylation,
acetylation, and phosphorylation. Therefore, HIF-1α interacts with several protein factors
including PHD, pVHL, ARD1, and p300/CBP. Under normoxia, the HIF-1α subunit is rapidly degraded
via the von Hippel-Lindau tumor suppressor gene product (pVHL)-mediated ubiquitin-proteasome
pathway. Mouse ARD1 has been reported to negatively regulate the hypoxia-inducible factor 1α (HIF-1
α) protein by acetylating a lysine residue and enhancing HIF-1α ubiquitination and degradation. Herein,
it is demonstrated that ARD1 cannot affect the hydroxylation of HIF-1α, which is the major regulatory
modification for the stability. Moreover, the ARD1 expression level is downregulated by hypoxic
exposure.

Keywords: ARD1, HIF-1α, Hypoxia

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