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ATF4 differentially regulates transcriptional activation of myeloid-specific genes by C/EBPepsilon and C/EBPalpha.激活转录因子4（ATF4）通过C/EBPε和C/EBPα对髓系特异性基因的转录激活进行差异调节。
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通过异源二聚体形成以及与核因子κB信号通路的相互作用对CCAAT/增强子结合蛋白ε的DNA结合特性进行调控。

Modulation of DNA binding properties of CCAAT/enhancer binding protein epsilon by heterodimer formation and interactions with NFkappaB pathway.

作者信息

Chumakov Alexey M, Silla Agnes, Williamson Elizabeth A, Koeffler H Phillip

机构信息

Department of Medicine, Cedars-Sinai Medical Center, University of California at Los Angeles, CA 90048, USA.

出版信息

Blood. 2007 May 15;109(10):4209-19. doi: 10.1182/blood-2005-09-031963. Epub 2007 Jan 25.

DOI:10.1182/blood-2005-09-031963
PMID:17255362
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1885488/
Abstract

C/EBP epsilon is a transcription factor involved in myeloid cell differentiation. Along with C/EBP-alpha, -beta, -gamma, -delta, and -zeta, C/EBP-epsilon belongs to the family of CCAAT/enhancer binding proteins that are implicated in control of growth and differentiation of several cell lineages in inflammation and stress response. We have previously shown that C/EBP-epsilon preferentially binds DNA as a heterodimer with other C/EBP family members such as C/EBP-delta, CHOP (C/EBP-zeta), and the b-zip family protein ATF4. In this study, we define the consensus binding sites for C/EBP-epsilon dimers and C/EBP-epsilon-ATF4 heterodimers. We show that the activated NFkappaB pathway promotes interaction of the C/EBP-epsilon subunit with its cognate DNA binding site via interaction with RelA. RelA-C/EBP interaction is enhanced by phosphorylation of threonine at amino acid 75 and results in increased DNA binding compared with the wild-type nonphosphorylated C/EBP both in vitro and in vivo. We suggest that interaction of the activated NFkappaB pathway and C/EBP-epsilon may be important in selective activation of a subset of C/EBP-epsilon-responsive genes.

摘要

C/EBPε是一种参与髓样细胞分化的转录因子。与C/EBPα、β、γ、δ和ζ一起，C/EBPε属于CCAAT/增强子结合蛋白家族，该家族与炎症和应激反应中几种细胞谱系的生长和分化控制有关。我们之前已经表明，C/EBPε作为异二聚体与其他C/EBP家族成员（如C/EBPδ、CHOP（C/EBPζ）和b-zip家族蛋白ATF4）优先结合DNA。在本研究中，我们定义了C/EBPε二聚体和C/EBPε-ATF4异二聚体的共有结合位点。我们表明，活化的NFκB途径通过与RelA相互作用促进C/EBPε亚基与其同源DNA结合位点相互作用。与野生型未磷酸化的C/EBP相比，RelA-C/EBP相互作用通过苏氨酸75位的磷酸化增强，并且在体外和体内均导致DNA结合增加。我们认为活化的NFκB途径与C/EBPε的相互作用可能在C/EBPε反应性基因子集的选择性激活中起重要作用。