Histone acetyltransferase HBO1 inhibits NF-kappaB activity by coactivator sequestration

Détails

ID Serval
serval:BIB_D8925C4B9B42
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Histone acetyltransferase HBO1 inhibits NF-kappaB activity by coactivator sequestration
Périodique
Biochemical and Biophysical Research Communications
Auteur(s)
Contzler  R., Regamey  A., Favre  B., Roger  T., Hohl  D., Huber  M.
ISSN
0006-291X (Print)
Statut éditorial
Publié
Date de publication
11/2006
Volume
350
Numéro
1
Pages
208-13
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Nov 10
Résumé
The MYST acetyltransferase HBO1 is implicated in the regulation of DNA replication and activities of transcription factors such as the androgen receptor. Since the androgen receptor and NF-kappaB transcription factors crossmodulate their transcriptional activity, we investigated whether HBO1 regulates NF-kappaB signaling. Here, we report that in 293T cells HBO1 reduced dose-dependently NF-kappaB activity stimulated by TNFalpha, or by overexpressing p65/RelA, RelB, or cRel. Mutational analysis showed that the N-terminal serine-rich region of HBO1 but not the acetyltransferase function was required for inhibition. Electrophoretic mobility-shift assays demonstrated that HBO1 was neither perturbing the formation of p65/RelA DNA complexes nor binding itself to the kappaB consensus sequence or to p65/RelA, suggesting that HBO1 reduced NF-kappaB activity by squelching a cofactor. These data establish a novel function for HBO1 showing that it reduced NF-kappaB activity by sequestrating an essential coactivator from the NF-kappaB transcriptional complex.
Mots-clé
Cell Line Histone Acetyltransferases/genetics/*metabolism Humans NF-kappa B/*antagonists & inhibitors/*metabolism Receptors, Androgen/metabolism Signal Transduction Trans-Activation (Genetics) Tumor Necrosis Factor-alpha/pharmacology
Pubmed
Web of science
Création de la notice
25/01/2008 14:35
Dernière modification de la notice
03/03/2018 21:51
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