GONUTS has been updated to MW1.31 Most things seem to be working but be sure to report problems.
TableEdit
PMID:18794125
You don't have sufficient rights on this wiki to edit tables. Perhaps you need to log in. Changes you make in the Table editor will not be saved back to the wiki
See Help for Help on this wiki. See the documentation for how to use the table editor
Citation |
Holmes, KA, Song, JS, Liu, XS, Brown, M and Carroll, JS (2008) Nkx3-1 and LEF-1 function as transcriptional inhibitors of estrogen receptor activity. Cancer Res. 68:7380-5 |
---|---|
Abstract |
Estrogen receptor (ER)-associated cofactors and cooperating transcription factors are one of the primary components determining transcriptional activity of estrogen target genes and may constitute potential therapeutic targets. Recent mapping of ER-binding sites on a genome-wide scale has provided insight into novel cooperating factors based on the enrichment of transcription factor motifs within the ER-binding sites. We have used the ER-binding sites in combination with sequence conservation to identify the statistical enrichment of Nkx and LEF motifs. We find that Nkx3-1 and LEF-1 bind to several ER cis-regulatory elements in vivo, but they both function as transcriptional repressors of estrogen signaling. We show that Nkx3-1 and LEF-1 can inhibit ER binding to chromatin, suggesting competition for common chromatin-binding regions. These data provide insight into the role of Nkx3-1 and LEF-1 as potential regulators of the hormone response in breast cancer. |
Links |
PubMed Online version:10.1158/0008-5472.CAN-08-0133 |
Keywords |
Animals; Binding Sites; Breast Neoplasms/genetics; Cell Line, Tumor; Chromatin/genetics; Chromatin/metabolism; Homeodomain Proteins/biosynthesis; Homeodomain Proteins/genetics; Homeodomain Proteins/metabolism; Humans; Lymphoid Enhancer-Binding Factor 1/biosynthesis; Lymphoid Enhancer-Binding Factor 1/genetics; Lymphoid Enhancer-Binding Factor 1/metabolism; Mice; Plasmids/genetics; Protein Binding; RNA, Small Interfering/genetics; Receptors, Estrogen/antagonists & inhibitors; Receptors, Estrogen/genetics; Receptors, Estrogen/metabolism; Transcription Factors/biosynthesis; Transcription Factors/genetics; Transcription Factors/metabolism; Transcription, Genetic; Transfection |
public |
Cancel |