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Foundation for the Finnish Cancer Institute, Helsinki, Finland
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Institute of Biomedicine, University of Eastern Finland, Kuopio, Finland
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Fimlab Laboratories Ltd, Tampere, Finland
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on the gene expression changes related to the activation of AR using our RNA-seq dataset. First, we used unsupervised hierarchical clustering of the HALLMARK ANDROGEN RESPONSE gene set to cluster the cell lines based on their transcriptional response
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full promoter activity (acting as an enhancer). Our analysis of the sequence proximal to the ATG revealed a putative androgen response element (ARE) which is further upstream of this minimal promoter region. We have previously observed a similar
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Department of Pathology, Department of Pathology, NYU Cancer Institute, Department of Urology, Department of Pharmacology, New York Harbor Healthcare System, New York University School of Medicine, New York, New York, USA
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Department of Pathology, Department of Pathology, NYU Cancer Institute, Department of Urology, Department of Pharmacology, New York Harbor Healthcare System, New York University School of Medicine, New York, New York, USA
Department of Pathology, Department of Pathology, NYU Cancer Institute, Department of Urology, Department of Pharmacology, New York Harbor Healthcare System, New York University School of Medicine, New York, New York, USA
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Department of Pathology, Department of Pathology, NYU Cancer Institute, Department of Urology, Department of Pharmacology, New York Harbor Healthcare System, New York University School of Medicine, New York, New York, USA
Department of Pathology, Department of Pathology, NYU Cancer Institute, Department of Urology, Department of Pharmacology, New York Harbor Healthcare System, New York University School of Medicine, New York, New York, USA
Department of Pathology, Department of Pathology, NYU Cancer Institute, Department of Urology, Department of Pharmacology, New York Harbor Healthcare System, New York University School of Medicine, New York, New York, USA
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factors that plays an important role in the regulation of genes controlling growth suppression/differentiation and growth of prostate cells. Androgens activate AR, facilitating its translocation to the nucleus, binding at androgen-response elements (ARE
VA Northern California Health Care System, Department of Urology, Division of Biostatistics, Department of Statistics, Department of Biochemistry and Molecular Medicine, Department of Medical Microbiology and Immunology, Mather, California, USA
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VA Northern California Health Care System, Department of Urology, Division of Biostatistics, Department of Statistics, Department of Biochemistry and Molecular Medicine, Department of Medical Microbiology and Immunology, Mather, California, USA
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VA Northern California Health Care System, Department of Urology, Division of Biostatistics, Department of Statistics, Department of Biochemistry and Molecular Medicine, Department of Medical Microbiology and Immunology, Mather, California, USA
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VA Northern California Health Care System, Department of Urology, Division of Biostatistics, Department of Statistics, Department of Biochemistry and Molecular Medicine, Department of Medical Microbiology and Immunology, Mather, California, USA
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VA Northern California Health Care System, Department of Urology, Division of Biostatistics, Department of Statistics, Department of Biochemistry and Molecular Medicine, Department of Medical Microbiology and Immunology, Mather, California, USA
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VA Northern California Health Care System, Department of Urology, Division of Biostatistics, Department of Statistics, Department of Biochemistry and Molecular Medicine, Department of Medical Microbiology and Immunology, Mather, California, USA
VA Northern California Health Care System, Department of Urology, Division of Biostatistics, Department of Statistics, Department of Biochemistry and Molecular Medicine, Department of Medical Microbiology and Immunology, Mather, California, USA
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the end of this article. Plasmids pCMV-FLNA, FLNA(16–24), and FLNA(1–15) plasmids were kindly provided by Dr E W Yong, National University of Singapore, Singapore, and human PSA-luciferase (hPSA-luc) construct containing two androgen response elements
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troglitazone at concentrations (≤10 μM) lower than that required for growth inhibition (≥20 μM) was able to down-regulate PSA expression in LNCaP prostate cancer cells through the inhibition of androgen activation of the androgen response elements in the
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Division of Molecular Carcinogenesis, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands
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Faculty of EEMCS, Delft University of Technology, Delft, The Netherlands
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Division of Medical Oncology, The Netherlands Cancer Institute, Amsterdam, The Netherlands
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Laboratory of Chemical Biology and Institute for Complex Molecular Systems, Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands
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-occupied by AR. Downregulation of androgen response genes and UPR genes upon knockdown of XBP1 By exploring gene expression of vehicle- and R1881-treated LNCaP cells, we identified 934 differentially expressed genes upon 24 h R1881 stimulation ( P
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regulation of TRPM8 in androgen-responsive prostate cancer cells has been addressed, and several putative androgen response elements have been detected ( Zhang & Barritt 2004 , Bidaux et al. 2005 ). Analysis of 5′ flank regions of the TRPM8 gene using
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regulating the binding of endogenous HuR to the AU-rich 3′UTRs, e.g. EGF mRNA ( Myers et al . 1999 , Torring et al . 2003 ). The ability of androgens to regulate the expression of androgen response element (ARE)-binding proteins that bind to these
Department of Urologic Sciences, Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada
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Department of Urology, Xiangya Hospital, Central South University, Changsha, China
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Department of Cardiothoracic Surgeries, Weill Cornell Medical College, Cornell University, New York, New York, USA
Institute for Academic Medicine, Houston Methodist Hospital, Houston, Texas, USA
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Department of Cardiothoracic Surgeries, Weill Cornell Medical College, Cornell University, New York, New York, USA
Institute for Academic Medicine, Houston Methodist Hospital, Houston, Texas, USA
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Department of Cardiothoracic Surgeries, Weill Cornell Medical College, Cornell University, New York, New York, USA
Institute for Academic Medicine, Houston Methodist Hospital, Houston, Texas, USA
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lipid metabolism gene sets are highly suppressed by HOXA10 ( P < 0.001) ( Fig. 4B ). Additionally, androgen response genes were also inhibited ( Fig. 4C ). Together, these results revealed an association of HOXA10 with both cell lipid metabolism and the
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Department of Urology, Cleveland Clinic, Cleveland, Ohio, USA
Department of Hematology/Medical Oncology, Cleveland Clinic, Cleveland, Ohio, USA
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undergo conformational changes, alter its association with chaperones and translocate to the nucleus. Inside the nucleus, ligand-bound AR binds to DNA recognition motifs known as androgen response elements (AREs) and recruits from a large array of