ARDent about acetylation and deacetylation in hypoxia signalling
Date
2006
Authors
Bilton, Rebecca Louise
Trottier, Eric
Pouyssegur, Jacques
Brahimi-Horn, M. Christiane
Editors
Advisors
Journal Title
Journal ISSN
Volume Title
Type:
Journal article
Citation
Trends in Cell Biology, 2006; 16(12):616-621
Statement of Responsibility
Rebecca Bilton, Eric Trottier, Jacques Pouysségur and M. Christiane Brahimi-Horn
Conference Name
Abstract
Given the key role that the α subunit of the αβ heterodimeric transcription factor hypoxia-inducible factor-1 (HIF-1) has in tumourigenesis, and in particular in angiogenesis, a full understanding of its regulation is crucial to the development of cancer therapeutics. Posttranslational acetylation and deacetylation of this subunit by an acetyltransferase called Arrest-defective-1 (ARD1) and by different histone deacetylases (HDACs), respectively, has been suggested as a mechanism. However, conflicting data bring into question the foundations of this mechanism and at present it is not clear what the precise role of these proteins is with respect to HIF. Nonetheless, the observation that small-molecule inhibitors of HDACs have anti-angiogenic activity suggests that acetylation and deacetylation of HIF or HIF modifiers represents a potential target in cancer therapy.
School/Discipline
School of Molecular and Biomedical Science
Dissertation Note
Provenance
Description
Copyright © 2006 Elsevier Ltd All rights reserved.