C/EBP binding activity to site F of the rat GLUT2 glucose transporter gene promoter is attenuated by c-Jun in vitro.
- Author:
Jae Woo KIM
1
;
Yong Ho AHN
Author Information
1. Department of Biochemistry and Molecular Biology, Institute of Genetic Science, Yonsei University College of Medicine, Seoul, Korea. yha111@yumc.yonsei.ac.kr
- Publication Type:Research Support, Non-U.S. Gov't ; Original Article
- Keywords:
C/EBP;
c-jun;
DNA-protein binding;
GLUT2 promoter;
hepatocyte
- MeSH:
Animals;
Base Sequence;
Binding Sites;
CCAAT-Enhancer-Binding Proteins/*metabolism;
Cell Nucleus/metabolism;
Cells, Cultured;
Liver/cytology/metabolism;
Male;
Molecular Sequence Data;
Monosaccharide Transport Proteins/*genetics/metabolism;
Promoter Regions (Genetics)/*physiology;
Proto-Oncogene Proteins c-jun/genetics/*metabolism;
Rats;
Rats, Sprague-Dawley;
Recombinant Proteins/genetics/metabolism;
Transcription Factor AP-1/genetics/metabolism
- From:Experimental & Molecular Medicine
2002;34(5):379-384
- CountryRepublic of Korea
- Language:English
-
Abstract:
The expression of the GLUT2 glucose transporter gene in liver is suppressed in cultured hepatoma cell lines and primary cultured hepatocytes. Earlier report showed that CCAAT/enhancer binding protein (C/EBP) regulates the promoter activity of the rat GLUT2 glucose transporter gene in liver cells. C/EBPa and C/EBPb activated the promoter activity by binding to at least two regions of the promoter and one of the C/EBP binding sites, named as site F, also has the AP-1 binding consensus. In this study, we investigated whether the AP-1 can influence on C/EBP binding to this site. The addition of recombinant c-Jun protein with liver extract caused the attenuation of C/EBP binding to site F with the appearance of a new shifted band. The shifted band was competed out with the addition of unlabeled AP-1 consensus oligonucleotide, indicating that c-Jun also can bind to site F. Another C/EBP site on GLUT2 promoter, site H, did not bind AP-1. Analysis of the DNA-protein complex revealed that C/EBP and c-Jun bind to site F in mutually exclusive manner rather than form heterodimeric complex with each other. From these results, it is suggested that the transcriptional activation of C/EBP may be influenced by c-Jun protein in certain status of the liver cells, such as acute phase response, as well as hepatocarcinogenesis.
