Publication: Genome-wide analysis of ChREBP binding sites on male mouse liver and white adipose chromatin
5
Issued Date
2015-06-01
Resource Type
ISSN
19457170
00137227
00137227
Other identifier(s)
2-s2.0-84930449863
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Endocrinology. Vol.156, No.6 (2015), 1982-1994
Suggested Citation
Naravat Poungvarin, Benny Chang, Minako Imamura, Junsheng Chen, Kanya Moolsuwan, Chanachai Sae-Lee, Wei Li, Lawrence Chan Genome-wide analysis of ChREBP binding sites on male mouse liver and white adipose chromatin. Endocrinology. Vol.156, No.6 (2015), 1982-1994. doi:10.1210/en.2014-1666 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/35445
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Genome-wide analysis of ChREBP binding sites on male mouse liver and white adipose chromatin
Other Contributor(s)
Abstract
Copyright © 2015 by the Endocrine Society. Glucose is an essential nutrient that directly regulates the expression of numerous genes in liver and adipose tissue. The carbohydrate response element-binding protein (ChREBP) links glucose as a signaling molecule to multiple glucose-dependent transcriptional regulatory pathways, particularly genes involved in glycolytic and lipogenic processes. In this study, we used chromatin immunoprecipitation followed by next-generation sequencing to identify specific ChREBP binding targets in liver and white adipose tissue. We found a large number of ChREBP binding sites, which are attributable to 5825 genes in the liver, 2418 genes in white adipose tissue, and 5919 genes in both tissues. The majority of these target genes were involved in known metabolic processes. Pathways in insulin signaling, the adherens junction, and cancers were among the top 5 pathways in both tissues. Motif analysis revealed a consensus sequence CAYGYGnnnnnCRCRTG that was commonly shared by ChREBP binding sites. Putative ChREBP binding sequences were enriched on promoters of genes involved in insulin signaling pathway, insulin resistance, and tumorigenesis.