ArticleMolecular and cellular biology2011
Dynamic nucleosome-depleted regions at androgen receptor enhancers in the absence of ligand in prostate cancer cells.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- A meta-analysis of 87,040 individuals identifies 23 new susceptibility loci for prostate cancer.Nature genetics · 2014Pooled it
- Review
- Review
- Cellular specificity of androgen receptor, coregulators, and pioneer factors in prostate cancer.Endocrine oncology (Bristol, England) · 2022Review
- Epigenetic Coregulation of Androgen Receptor Signaling.Advances in experimental medicine and biology · 2022Article
- BRG1 knockdown inhibits proliferation through multiple cellular pathways in prostate cancer.Clinical epigenetics · 2021Article
- Steroid hormones regulate genome-wide epigenetic programming and gene transcription in human endometrial cells with marked aberrancies in endometriosis.PLoS genetics · 2020Article
- Endogenous androgen receptor proteomic profiling reveals genomic subcomplex involved in prostate tumorigenesis.Oncogene · 2018Article
- Androgen-dependent alternative mRNA isoform expression in prostate cancer cells.F1000Research · 2018Article
- Acetylated histone variant H2A.Z is involved in the activation of neo-enhancers in prostate cancer.Nature communications · 2017Article
- Androgen Receptor Deregulation Drives Bromodomain-Mediated Chromatin Alterations in Prostate Cancer.Cell reports · 2017Article
- Prediction of nucleosome positioning by the incorporation of frequencies and distributions of three different nucleotide segment lengths into a general pseudo k-tuple nucleotide composition.Bioinformatics (Oxford, England) · 2017Article
- Article
- Integration of Signaling Pathways with the Epigenetic Machinery in the Maintenance of Stem Cells.Stem cells international · 2016Review
- Intrauterine growth restriction perturbs nucleosome depletion at a growth hormone-responsive element in the mouse IGF-1 gene.Physiological genomics · 2015Article
- A medium-scale assay for enhancer validation in amniotes.Developmental dynamics : an official publication of the American Association of Anatomists · 2015Article
- Multiple novel prostate cancer susceptibility signals identified by fine-mapping of known risk loci among Europeans.Human molecular genetics · 2015Article
- Integration of multiethnic fine-mapping and genomic annotation to prioritize candidate functional SNPs at prostate cancer susceptibility regions.Human molecular genetics · 2015Article
- Research Resource: Androgen Receptor Activity Is Regulated Through the Mobilization of Cell Surface Receptor Networks.Molecular endocrinology (Baltimore, Md.) · 2015Article
- Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Nucleosome positioning at transcription start sites is known to regulate gene expression by altering DNA accessibility to transcription factors; however, its role at enhancers is poorly understood. We investigated nucleosome positioning at the androgen receptor (AR) enhancers of TMPRSS2, KLK2, and KLK3/PSA in prostate cancer cells. Surprisingly, a population of enhancer modules in androgen-deprived cultures showed nucleosome-depleted regions (NDRs) in all three loci. Under androgen-deprived conditions, NDRs at the TMPRSS2 enhancer were maintained by the pioneer AR transcriptional collaborator GATA-2. Androgen treatment resulted in AR occupancy, an increased number of enhancer modules with NDRs without changes in footprint width, increased levels of histone H3 acetylation (AcH3), and dimethylation (H3K4me2) at nucleosomes flanking the NDRs. Our data suggest that, in the absence of ligand, AR enhancers exist in an equilibrium in which a percentage of modules are occupied by nucleosomes while others display NDRs. We propose that androgen treatment leads to the disruption of the equilibrium toward a nucleosome-depleted state, rather than to enhancer de novo "remodeling." This allows the recruitment of histone modifiers, chromatin remodelers, and ultimately gene activation. The "receptive" state described here could help explain AR signaling activation under very low ligand concentrations.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.