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Pubmed ID: 18486321
Publication Date: 2008/03/27

Acetylation and deacetylation regulate CCAAT/enhancer binding protein beta at K39 in mediating gene transcription.


The transcription factor CCAAT/enhancer binding protein beta (C/EBPbeta) contains multiple acetylation sites, including lysine (K) 39. Mutation of C/EBPbeta at K39, an acetylation site in the transcriptional activation domain, impairs transcription of C/EBPbeta target genes in a dominant-negative fashion. Further, K39 of C/EBPbeta can be deacetylated by HDAC1, and HDAC1 may decrease C/EBPbeta-mediated transcription, suggesting that acetylation of C/EBPbeta at K39 is dynamically regulated in mediating gene transcription. Acetylation of endogenous C/EBPbeta at K39 is detected in adipose tissue, and also occurs in 3T3-L1 cells undergoing adipocyte conversion. In addition, mutation of K39 in C/EBPbeta impairs activation of its target genes encoding C/EBPalpha and PPARgamma, essential mediators of adipogenesis, as well as adipocyte genes for leptin and Glut4. These findings suggest that acetylation of C/EBPbeta at K39 is an important and dynamic regulatory event that contributes to its ability to transactivate target genes, including those associated with adipogenesis and adipocyte function.
Authors: Ceseña Teresa I , Cui Tracy X , Subramanian Lalitha , Fulton Christina T , Iñiguez-Lluhí Jorge A , Kwok Roland P S , Schwartz Jessica ,

Reference:

  1. ncbi.nlm.nih.gov. [Last access 2008/03/27].

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