ArticleCancer research2015
Androgen Receptor Splice Variants Dimerize to Transactivate Target Genes.
Article in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 2 of them syntheses that pooled it.
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Who cites it
123 citing papers in PubMed, 2 syntheses or guidelines pooled it, 189 citations in OpenAlex.
- Development and prevalence of castration-resistant prostate cancer subtypes.Neoplasia (New York, N.Y.) · 2020Pooled it
- Androgen receptor variant-driven prostate cancer II: advances in laboratory investigations.Prostate cancer and prostatic diseases · 2020Pooled it
- Single-cell imaging analysis, therapeutic modeling and a Phase Ib trial validate BCL-2 as a target across heterogeneous castration-resistant prostate cancer.Signal transduction and targeted therapy · 2026Trial
- Targeting the ELF1/EGFR/ERK positive feedback loop overcomes resistance to androgen receptor inhibition in AR-Vs positive prostate cancer.Neoplasia (New York, N.Y.) · 2026Article
- Drugging the intrinsically disordered transactivation domain of androgen receptor.Signal transduction and targeted therapy · 2026Article
- Androgen Receptor Point Mutations: A Mechanism of Therapeutic Resistance and a Framework for Rational Drug Design.Cancers · 2026Review
- Emerging therapies to overcome antiandrogen resistance and beyond in lethal prostate cancer.Journal of the National Cancer Center · 2026Review
- Alterations in AR-FOXA1 signaling in prostate cancer progression and therapeutic resistance.Journal of the National Cancer Center · 2026Review
- The interconnection between androgen receptor and DNA damage response pathways in prostate cancer.Current urology · 2025Review
- Reprogramming of Androgen Receptor Activity in Castration-resistant Prostate Cancer is Shaped by Truncated Variants.European urology focus · 2025Article
- Deciphering Complexity: The Molecular Landscape of Castration-Resistant Prostate Cancer.Surgical pathology clinics · 2025Review
- Aryl hydrocarbon receptor as a drug target in advanced prostate cancer therapy - obstacles and perspectives.Transcription · 2025Review
- Increased nuclear factor I-mediated chromatin access drives transition to androgen receptor splice variant dependence in prostate cancer.Cell reports · 2025Article
- Looking beyond the ER, PR, and HER2: what's new in the ARsenal for combating breast cancer?Reproductive biology and endocrinology : RB&E · 2025Review
- An Autophagy-Targeting Chimera Induces Degradation of Androgen Receptor Mutants and AR-v7 in Castration-Resistant Prostate Cancer.Cancer research · 2025Article
- Prognostic role of Androgen Receptor splice variant 7 (AR-V7) in the pathogenesis of breast cancer.BMC cancer · 2024Article
- Nodularin-R Synergistically Enhances Abiraterone Against Castrate- Resistant Prostate Cancer via PPP1CA Inhibition.Journal of cellular and molecular medicine · 2024Article
- Androgen receptor and estrogen receptor variants in prostate and breast cancers.The Journal of steroid biochemistry and molecular biology · 2024Review
- Article
- Inhibition of N-myristoyltransferase activity promotes androgen receptor degradation in prostate cancer.The Prostate · 2024Article
63 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
Constitutively active androgen receptor splice variants (AR-V) lacking the ligand-binding domain have been implicated in the pathogenesis of castration-resistant prostate cancer and in mediating resistance to newer drugs that target the androgen axis. AR-V regulates expression of both canonical AR targets and a unique set of cancer-specific targets that are enriched for cell-cycle functions. However, little is known about how AR-V controls gene expression. Here, we report that two major AR-Vs, termed AR-V7 and AR(v567es), not only homodimerize and heterodimerize with each other but also heterodimerize with full-length androgen receptor (AR-FL) in an androgen-independent manner. We found that heterodimerization of AR-V and AR-FL was mediated by N- and C-terminal interactions and by the DNA-binding domain of each molecule, whereas AR-V homodimerization was mediated only by DNA-binding domain interactions. Notably, AR-V dimerization was required to transactivate target genes and to confer castration-resistant cell growth. Our results clarify the mechanism by which AR-Vs mediate gene regulation and provide a pivotal pathway for rational drug design to disrupt AR-V signaling as a rational strategy for the effective treatment of advanced prostate cancer.
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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.