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Cancer Science Institute, Department of Pathology, Biostatistics Unit, Department of Urology, Plunkett Chair of Molecular Biology (Medicine), National University Health System, National University of Singapore, 28 Medical Drive, Singapore, Singapore 117456
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Cancer Science Institute, Department of Pathology, Biostatistics Unit, Department of Urology, Plunkett Chair of Molecular Biology (Medicine), National University Health System, National University of Singapore, 28 Medical Drive, Singapore, Singapore 117456
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testosterone directly to activate ARs. The DHT–AR complex then binds to nuclear DNA sequences known as androgen response elements, which promote transcription of the target genes involved in prostate cell homeostasis, angiogenesis, differentiation, and
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the recruitment of repressor proteins to the androgen-response element of the AR promoter in UMUC3 cells, thereby inhibiting its transcriptional complex. In the tissue specimens from patients with bladder cancer, we detected high levels of coactivator
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the nucleus, the ligand-AR complex binds to specific androgen response elements, interacts with coactivators and modulates the expression of androgen-regulated genes. Several mechanisms implicated in prostate cancer progression are AR-related. They
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luciferase reporter plasmid, pGL-5.8PSAp, driven by a 5.8 kb PSA promoter including androgen-response elements ( Mizokami et al . 2000 ). Twelve hours after transfection, LNCaP cells were cocultured with 5×10 4 stromal cells for 12 h, followed by the
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Veterans Affairs-Northern California Health System, Mather, California, USA
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Department of Urologic Surgery, School of Medicine, University of California Davis, Sacramento, California, USA
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Department of Biomedical Engineering, University of California Davis, Davis, California, USA
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translocate to the nucleus, where it binds to the promoters of target genes at sequences called the androgen response element (ARE). Both testosterone and dihydrotestosterone (DHT) stimulate OB precursors and may also promote OB differentiation. By
The Vancouver Prostate Centre, Department of Urologic Sciences, 2660 Oak Street, Vancouver, British Columbia, Canada V6H‐3Z6
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The Vancouver Prostate Centre, Department of Urologic Sciences, 2660 Oak Street, Vancouver, British Columbia, Canada V6H‐3Z6
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The Vancouver Prostate Centre, Department of Urologic Sciences, 2660 Oak Street, Vancouver, British Columbia, Canada V6H‐3Z6
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The Vancouver Prostate Centre, Department of Urologic Sciences, 2660 Oak Street, Vancouver, British Columbia, Canada V6H‐3Z6
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of tumors. Targeting androgen response-driven cellular plasticity to improve patient outcomes Suppressing AR signaling remains the focus of therapeutic strategies for advanced PCa, which is justified given the success of second-generation anti
UVA Cancer Center University of Virginia, PO Box 800734, Charlottesville, Virginia 22908, USA
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UVA Cancer Center University of Virginia, PO Box 800734, Charlottesville, Virginia 22908, USA
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UVA Cancer Center University of Virginia, PO Box 800734, Charlottesville, Virginia 22908, USA
Department of Microbiology Immunology, and Cancer Biology
UVA Cancer Center University of Virginia, PO Box 800734, Charlottesville, Virginia 22908, USA
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in LNCaP cells showed that phosphorylated S81 AR binds to chromatin. However, phosphorylation on this site is not required for chromatin binding; sequential rounds of ChIP suggest that the non-phosphorylated S81 AR also binds to androgen-response
Biomarker Initiative, Cancer Research UK Cambridge Institute, Robinson Way, Cambridge, UK
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Biomarker Initiative, Cancer Research UK Cambridge Institute, Robinson Way, Cambridge, UK
Molecular Diagnostics and Therapeutics Group, University College London, London, UK
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Astra Zeneca, 2 Riverside, Granta Park, Cambridge, UK
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Astra Zeneca, 2 Riverside, Granta Park, Cambridge, UK
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Molecular Diagnostics and Therapeutics Group, University College London, London, UK
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Biomarker Initiative, Cancer Research UK Cambridge Institute, Robinson Way, Cambridge, UK
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Molecular and Computational Diagnostics Group, Cancer Research UK Cambridge Institute, Robinson Way, Cambridge, UK
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University College Hospital at Westmoreland Street, London, UK
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Nuffield Department of Surgical Sciences, John Radcliffe Hospital, Headington, Oxford, UK
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Biomarker Initiative, Cancer Research UK Cambridge Institute, Robinson Way, Cambridge, UK
Molecular Diagnostics and Therapeutics Group, University College London, London, UK
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binding to DNA via androgen response elements where it regulates the transcription of androgen-regulated genes ( Claessens et al . 2014 ). Due to the importance of the AR signalling axis, treatment for prostate cancer relies upon blocking the production
Veterans Affairs‐Northern California Health Care System, Department of Medical Microbiology and Immunology, Biochemistry, Mather, California, USA
Veterans Affairs‐Northern California Health Care System, Department of Medical Microbiology and Immunology, Biochemistry, Mather, California, USA
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Veterans Affairs‐Northern California Health Care System, Department of Medical Microbiology and Immunology, Biochemistry, Mather, California, USA
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AR is released from heat shock proteins (HSP), becomes phosphorylated, forms a homodimer, and translocates from the cytoplasm to the nucleus. In the nucleus, the AR binds to androgen response elements in the genome, and along with co
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Department of Microbiology, UVA Cancer Center, Immunology, and Cancer Biology
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acts as a transcription factor ( Evans 1988 , Mangelsdorf et al . 1995 , Gelmann 2002 ). Upon androgen binding, there is a change in the complement of AR-associated proteins as the AR shuttles to the nucleus and binds as homodimers to androgen-response