Molecular characterization of the Xenopus CCAAT-enhancer binding protein beta gene promoter

Citation
P. Foka et al., Molecular characterization of the Xenopus CCAAT-enhancer binding protein beta gene promoter, BIOC BIOP R, 285(2), 2001, pp. 430-436
Citations number
34
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Biochemistry & Biophysics
Journal title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
ISSN journal
0006-291X → ACNP
Volume
285
Issue
2
Year of publication
2001
Pages
430 - 436
Database
ISI
SICI code
0006-291X(20010713)285:2<430:MCOTXC>2.0.ZU;2-Z
Abstract
Transcription factors belonging to the CCAAT-enhancer binding protein (C/EB P) family play key roles in the regulation of genes implicated in the contr ol of growth, differentiation, metabolism, and inflammation, The recent lim ited studies on the promoter regions of C/EBP genes, particularly C/EBP alp ha, have indicated the potential existence of species-specific regulatory m echanisms. It is therefore essential that the promoter regions of different C/EBP genes from a wide range of species are investigated in detail. As an important step toward this goal, we report here the characterization of th e Xenopus laevis C/EBP beta gene promoter. Sequence analysis showed that th e 1.6-kb promoter region contained putative binding sites for several trans cription factors that have previously been implicated in the regulation of the C/EBPs, including C/EBP, CREB, Myb, STAT, and USF, The -288/+91 promote r region was capable of directing high levels of expression in the hepatoma Hep3B cell line. In addition, this minimal promoter could be autoregulated by both C/EBP alpha and C/EBP beta and activated by lipopolysaccharide, in terleukin-g and CREB, These results therefore demonstrate that several aspe cts of C/EBP beta regulation in mammals have been highly conserved in amphi bians. However, a comparison of C/EBP beta gene promoters characterized to date does indicate the existence of species-specific differences in autoreg ulation. (C) 2001 Academic Press.