Searching across hundreds of databases

Our searching services are busy right now. Your search will reload in five seconds.

Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Post-activation turn-off of NF-kappa B-dependent transcription is regulated by acetylation of p65.

NF-kappaB represents a family of eukaryotic transcription factors participating in the regulation of various cellular genes involved in the immediate early processes of immune, acute-phase, and inflammatory responses. Cellular localization and consequently the transcriptional activity of NF-kappaB is tightly regulated by its partner IkappaBalpha. Here, we show that the p65 subunit of NF-kappaB is acetylated by both p300 and PCAF on lysines 122 and 123. Both HDAC2 and HDAC3 interact with p65, although only HDAC3 was able to deacetylate p65. Acetylation of p65 reduces its ability to bind kappaBeta-DNA. Finally, acetylation of p65 facilitated its removal from DNA and consequently its IkappaBetaalpha-mediated export from the nucleus. We propose that acetylation of p65 plays a key role in IkappaBetaalpha-mediated attenuation of NF-kappaBeta transcriptional activity which is an important process that restores the latent state in post-induced cells.

Pubmed ID: 12419806 RIS Download

Mesh terms: Acetylation | Acetyltransferases | Cell Nucleus | Chromatin | DNA | Enzyme Activation | Gene Expression Regulation, Enzymologic | HeLa Cells | Histone Acetyltransferases | Histone Deacetylase 2 | Histone Deacetylases | Humans | Jurkat Cells | Lysine | Models, Biological | NF-kappa B | Nuclear Proteins | Plasmids | Precipitin Tests | Protein Binding | Protein Transport | Repressor Proteins | Saccharomyces cerevisiae Proteins | Trans-Activators | Transcription Factor RelA | Transcription, Genetic

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants


Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

We have not found any resources mentioned in this publication.