The Galectin-3 Gene Promoter Binding Proteins in the Liver of Rats 48-h Post-treatment with Ccl4.
From: The Department of Biochemistry, Toyama Medical and Pharmaceutical University School of Medicine, 2630 Sugitani, Toyama 930-0194, Japan.
Gene
- Publish Date: Feb 2006
- ISSN: 0378-1119
- Volume: 367
- Issue:
- Pages: 46-55
- Medium: Print
- Language: English
- Citation (JAMA): Li Fang, Kato Ichiro, Kawaguchi Hiroshi, et al. The Galectin-3 Gene Promoter Binding Proteins in the Liver of Rats 48-h Post-treatment with Ccl4.. Gene Feb 2006;367:46-55
Abstract
The present study was undertaken to characterize structure-function relationships of the rat galectin-3 gene promoter especially focusing on the promoter binding proteins included in livers injured with CCl4. Transcription start site determination identified a 66-nucleotide-long exon 1 of this gene. Transient expression analysis using a reporter luciferase gene assigned a region between -161 and -15 to the proximal promoter within the 1-kb region flanking the 5’-end of exon 1. The rat galectin-3 gene promoter possesses a Runx2 binding site and inverted repeats of Sp1 binding motifs in separate regions downstream from -117 as structures resembling those of the mouse galectin-3 gene promoter. The -161/-118 region bound two different proteins. One is a novel protein, a rat version of Purbeta that binds to a guanine nucleotide pair at -145 and -144 to modulate constitutive galectin-3 gene transcription. Southwestern blot analysis using the -161/-118 ligand revealed a signal of a 50-kDa protein in liver nuclear extracts from rats 48-h post-treatment with CCl4, but not in those from Ac2F cells and normal rat livers. The inducible nature of this protein suggested its distinctive role in galectin-3 induction in a liver injured with CCl4. E-box and peroxisome proliferator response element-like motifs reside on separate DNA strands from -140 to -135. Contribution of this segment to the regulation of galectin-3 gene transcription under pathological conditions was suggested, since a DNA ligand with the two motifs simultaneously mutagenized at -136 and -137 was not bound by the 50-kDa protein.
Mesh Headings (Keywords): Animals, Base Sequence, Binding Sites, Carbon Tetrachloride, Carcinoma, Hepatocellular, Carrier Proteins, Cell Line, Tumor, DNA-Binding Proteins, Electrophoretic Mobility Shift Assay, Exons, Galectin 3, Genes, Reporter, Liver, Liver Neoplasms, Luciferases, Male, Molecular Sequence Data, Promoter Regions (Genetics), Rats, Rats, Wistar, Sequence Deletion, Sequence Homology, Amino Acid, Structure-Activity Relationship, Time Factors, Transcription Factors, Transcription Initiation Site, Transcription, Genetic
Check for Full Text / PubMed Unique Identifier (PMID): 16309856
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.
