ARDent about acetylation and deacetylation in hypoxia signalling

被引：31

作者：

Bilton, Rebecca ^{[1
]}

Trottier, Eric ^{[1
]}

Pouyssegur, Jacques ^{[1
]}

Brahimi-Horn, M. Christiane ^{[1
]}

机构：

[1] Univ Nice, CNRS UMR 6543, Inst Signaling Dev Biol & Canc Res, Ctr Antoine Lacassagne, F-06189 Nice, France

来源：

TRENDS IN CELL BIOLOGY | 2006年 / 16卷 / 12期

关键词：

D O I：

10.1016/j.tcb.2006.10.002

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Given the key role that the a subunit of the cep 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.

引用

收藏

页码：616 / 621

页数：6

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