Acetylation and deacetylation regulate CCAAT/enhancer binding protein β at K39 in mediating gene transcription
- 作者：Teresa I. Ceseñ ; a ; Tracy X. Cui ; Lalitha Subramanian ; Christina T. Fulton ; Jorge A. Iñ ; iguez-Lluhí ; Rol ; P.S. Kwok ; Jessica Schwartz
- 关键词：C/EBPβ ; Acetylation ; Deacetylation ; Transcription ; p300 ; HDAC1 ; PPARγ ; C/EBP
//www.sciencedirect.com/scidirimg/entities/204e.gif" alt="greek small letter alpha" title="greek small letter alpha" border="0"> ; c-fos ; Glut4 ; L
- 刊名：Molecular and Cellular Endocrinology
- 出版年：2008
- 期刊代码：109_03037207
- 类别：bio
- 出版时间：16 July 2008
- 卷：289
- 期：1-2
- 页码：94-101
- 文件大小：719 K
摘要
The transcription factor CCAAT/enhancer binding protein β (C/EBPβ) contains multiple acetylation sites, including lysine (K) 39. Mutation of C/EBPβ at K39, an acetylation site in the transcriptional activation domain, impairs transcription of C/EBPβ target genes in a dominant-negative fashion. Further, K39 of C/EBPβ can be deacetylated by HDAC1, and HDAC1 may decrease C/EBPβ-mediated transcription, suggesting that acetylation of C/EBPβ at K39 is dynamically regulated in mediating gene transcription. Acetylation of endogenous C/EBPβ at K39 is detected in adipose tissue, and also occurs in 3T3-L1 cells undergoing adipocyte conversion. In addition, mutation of K39 in C/EBPβ impairs activation of its target genes encoding C/EBP
and PPARγ, essential mediators of adipogenesis, as well as adipocyte genes for leptin and Glut4. These findings suggest that acetylation of C/EBPβ 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.
and PPARγ, essential mediators of adipogenesis, as well as adipocyte genes for leptin and Glut4. These findings suggest that acetylation of C/EBPβ 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.