Genome-wide analysis of estrogen receptor binding sites

By Jason S. Carroll, Clifford A. Meyer, Jun S. Song, T. Geistlinger, J. Eeckhoute, A. Brodsky, E. Keeton, K. Fertuck, Giles Hall, Qianben Wang and 7 more. Nature Genetics, 2006

1,425 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/1915d5dc782c65ab0666b9a9d805fd810080de57

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Citations in the corpus

Estrogen receptor β causes a G2 cell cycle arrest by inhibiting CDK1 activity through the regulation of cyclin B1, GADD45A, and BTG2 (2011, background): “We focused on these genes, because ERa binding sites have been identified in the BTG2 promoter [29] and both genes contain binding sites for AP1, which is known to be involved in ERa-mediated regulation of gene transcription [38, 39].”
Remodeling of the enhancer landscape during macrophage activation is coupled to enhancer transcription (2013, background): “…of their binding sites are in distal intra- and intergenic locations that exhibit epigenomic features associatedwith enhancers (Barish et al., 2010; Carroll et al., 2006; Heinz et al., 2010; John et al., 310 Molecular Cell 51, 310–325, August 8, 2013 ª2013 Elsevier Inc. 2011; Lefterova et al.,…”
The androgen receptor fuels prostate cancer by regulating central metabolism and biosynthesis (2011, background): “…(Margiotti et al, 2007; Prescott et al, 2007), that only a proportion of transcription factor binding sites are active in a given cellular context (Carroll et al, 2006) and that RNAP II enriched regions of the genome include both sites of active transcription and also sites where…”
Fibroblast growth factor signalling: from development to cancer (2010, background): “Binding sites for ER and OCT1 often cluster togethe”
Distinguishing protein-coding and noncoding genes in the human genome (2007, neutral): “1C; Yoder and Carroll 2006).”
PPARgamma and C/EBP factors orchestrate adipocyte biology via adjacent binding on a genome-wide scale. (2008, methodology): “This distribution is consistent with what has been shown for other transcription factors, including estrogen receptor (Carroll et al. 2006), androgen receptor (Bolton et al.”
The properties of high-dimensional data spaces: implications for exploring gene and protein expression data (2008, background): “Amplification of the transcription factor oestrogen receptor α (ER α ; encoded by ESR1 ) is a common event in breast cancers and benign lesions59 and ER α occupies over 3,500 unique sites in the human genome 60 .”
Differential oestrogen receptor binding is associated with clinical outcome in breast cancer (2012, neutral): “Reduced ER binding (1,805) ChIP-seq Treatment Replicate”
A brassinosteroid transcriptional network revealed by genome-wide identification of BESI target genes in Arabidopsis thaliana. (2011, background): “On the other hand, only 4% of the estrogen receptor binding sites are located in promoter-proximal regions in human cells (Carroll et al., 2006).”
Hormones and endocrine-disrupting chemicals: low-dose effects and nonmonotonic dose responses. (2012, neutral): “The majority of the changes are indirect, through chromatin rearrangements (510, 511).”
A hierarchical network of transcription factors governs androgen receptor-dependent prostate cancer growth. (2007, methodology): “ChIP combined with tiled DNA oligonucleotide microarray analysis (ChIP-on-chip) has recently evolved as an unbiased technique for mapping the in vivo binding sites of transcription factors in the genome (Carroll et al., 2005, 2006).”
The different roles of ER subtypes in cancer biology and therapy (2011, background): “During this interaction, ERs can bind to full or imperfect ERE motifs, such as ERE half-sites, or can indirectly interact with chromatin through a tethering mechanism that involves a partner transcription facto”
Overcoming Endocrine Resistance in Breast Cancer (2020, positive): “The pioneer factor FOXA1 opens up densely packed chromatin to make it transcriptionally accessible to ER (Carroll et al., 2006) and other lineage-specific transcription factors.”