ArticlePloS one2008
Genomic androgen receptor-occupied regions with different functions, defined by histone acetylation, coregulators and transcriptional capacity.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
87 citing papers in PubMed, 149 citations in OpenAlex.
- Increased nuclear factor I-mediated chromatin access drives transition to androgen receptor splice variant dependence in prostate cancer.Cell reports · 2025Article
- A role for androgen receptor variant 7 in sensitivity to therapy: Involvement of IGFBP-2 and FOXA1.Translational oncology · 2023Article
- The testosterone paradox of advanced prostate cancer: mechanistic insights and clinical implications.Nature reviews. Urology · 2023Review
- Androgen receptor-mediated transcriptional repression targets cell plasticity in prostate cancer.Molecular oncology · 2022Article
- Epigenetic Editing in Prostate Cancer: Challenges and Opportunities.Epigenetics · 2022Review
- The role of ubiquitination in spinal and bulbar muscular atrophy.Frontiers in molecular neuroscience · 2022Review
- Post-Translational Modifications That Drive Prostate Cancer Progression.Biomolecules · 2021Review
- Increased nuclear factor I/B expression in prostate cancer correlates with AR expression.The Prostate · 2020Article
- AIB1 sequestration by androgen receptor inhibits estrogen-dependent cyclin D1 expression in breast cancer cells.BMC cancer · 2019Article
- FOXA1 and AR in invasive breast cancer: new findings on their co-expression and impact on prognosis in ER-positive patients.BMC cancer · 2018Article
- Androgen receptor splice variants bind to constitutively open chromatin and promote abiraterone-resistant growth of prostate cancer.Nucleic acids research · 2018Article
- Endogenous androgen receptor proteomic profiling reveals genomic subcomplex involved in prostate tumorigenesis.Oncogene · 2018Article
- Differential impact of RB status on E2F1 reprogramming in human cancer.The Journal of clinical investigation · 2018Article
- Epigenetic Regulation in Prostate Cancer Progression.Current molecular biology reports · 2018Review
- Exploiting Epigenetic Alterations in Prostate Cancer.International journal of molecular sciences · 2017Review
- IκB-Kinase-epsilon (IKKε) over-expression promotes the growth of prostate cancer through the C/EBP-β dependent activation of IL-6 gene expression.Oncotarget · 2017Article
- Review
- Androgen suppresses protein kinase D1 expression through fibroblast growth factor receptor substrate 2 in prostate cancer cells.Oncotarget · 2017Article
- Nfib Regulates Transcriptional Networks That Control the Development of Prostatic Hyperplasia.Endocrinology · 2016Article
- CCAAT/Enhancer binding protein β controls androgen-deprivation-induced senescence in prostate cancer cells.Oncogene · 2015Article
27 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe androgen receptor (AR) is a steroid-activated transcription factor that binds at specific DNA locations and plays a key role in the etiology of prostate cancer. While numerous studies have identified a clear connection between AR binding and expression of target genes for a limited number of loci, high-throughput elucidation of these sites allows for a deeper understanding of the complexities of this process. METHODOLOGY/PRINCIPAL
findingsWe have mapped 189 AR occupied regions (ARORs) and 1,388 histone H3 acetylation (AcH3) loci to a 3% continuous stretch of human genomic DNA using chromatin immunoprecipitation (ChIP) microarray analysis. Of 62 highly reproducible ARORs, 32 (52%) were also marked by AcH3. While the number of ARORs detected in prostate cancer cells exceeded the number of nearby DHT-responsive genes, the AcH3 mark defined a subclass of ARORs much more highly associated with such genes -- 12% of the genes flanking AcH3+ARORs were DHT-responsive, compared to only 1% of genes flanking AcH3-ARORs. Most ARORs contained enhancer activities as detected in luciferase reporter assays. Analysis of the AROR sequences, followed by site-directed ChIP, identified binding sites for AR transcriptional coregulators FoxA1, CEBPbeta, NFI and GATA2, which had diverse effects on endogenous AR target gene expression levels in siRNA knockout experiments. CONCLUSIONS/SIGNIFICANCE: We suggest that only some ARORs function under the given physiological conditions, utilizing diverse mechanisms. This diversity points to differential regulation of gene expression by the same transcription factor related to the chromatin structure.
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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.