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Cancer Biology and Therapeutics Laboratory, UCD Conway Institute of Biomolecular and Biomedical Science, University College Dublin, Belfield, Dublin, Ireland
Systems Biology Ireland, University College Dublin, Belfield, Dublin, Ireland
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), SMAD3 (Abcam, ab28379), SMAD3 phospho-Ser423/425 (Abcam, ab52903) and XBP1 (Abcam, ab198999). Mouse xenograft model Six-to-seven-week-old female C.B. 17- SCID mice (Animal Resources Centre, Perth, Australia) either had a 0.72mg/pellet 90-day
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Smad3 and this causes a redistribution of the cell cycle into G 0 /G 1 arrest ( Liu et al. 1996 , Ying & Zhang 1996 , Cocolakis et al. 2001 , Burdette et al. 2005 ). Activins A and B reduce proliferation of cultured rat acini isolated during
Institute of Pathology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
Institute for Pathology University Hospital Basel, Basel, Switzerland
Department of Urology St. Claraspital, Basel, Switzerland
Department of Urology University Hospital Basel, Basel, Switzerland
Department of Urology University Hospital of Örebro, Örebro, Sweden
School of Health and Medical Sciences Örebro University, Örebro, Sweden
Center for Genomics and Transcriptomics CeGaT GmbH, Tuebingen, Germany
Clinic for Urology and Pediatric Urology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
Section of Molecular Urooncology Department of Urology, School of Medicine, University of Heidelberg, Heidelberg, Germany
Department of Prostate Cancer Research
Institute of Pathology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
Institute for Pathology University Hospital Basel, Basel, Switzerland
Department of Urology St. Claraspital, Basel, Switzerland
Department of Urology University Hospital Basel, Basel, Switzerland
Department of Urology University Hospital of Örebro, Örebro, Sweden
School of Health and Medical Sciences Örebro University, Örebro, Sweden
Center for Genomics and Transcriptomics CeGaT GmbH, Tuebingen, Germany
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Institute of Pathology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
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Department of Urology University Hospital Basel, Basel, Switzerland
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Clinic for Urology and Pediatric Urology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
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Department of Urology University Hospital Basel, Basel, Switzerland
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Institute of Pathology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
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Clinic for Urology and Pediatric Urology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
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Institute of Pathology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
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Institute of Pathology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
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Institute of Pathology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
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Department of Urology University Hospital Basel, Basel, Switzerland
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Institute of Pathology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
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Institute of Pathology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
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Institute of Pathology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
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Institute of Pathology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
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Institute of Pathology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
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Institute of Pathology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
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Institute of Pathology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
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Department of Urology University Hospital Basel, Basel, Switzerland
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Center for Genomics and Transcriptomics CeGaT GmbH, Tuebingen, Germany
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Institute of Pathology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
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Department of Urology University Hospital Basel, Basel, Switzerland
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Institute of Pathology University Hospital of Bonn, Sigmund‐Freud Strasse 25, 53127 Bonn, Germany
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Department of Urology University Hospital Basel, Basel, Switzerland
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Department of Urology University Hospital Basel, Basel, Switzerland
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Center for Genomics and Transcriptomics CeGaT GmbH, Tuebingen, Germany
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-phospho (S423+S425)-SMAD3 rabbit MAB (1:1000, EP823Y, Abcam, Cambridge, UK), anti-β-actin MAB (1:5000, A1978, Sigma Aldrich, St Louis, MO, USA), and anti-Vimentin rabbit monoclonal (1:1000, 3932, Cell Signaling) primary antibodies at 4 °C overnight. The
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Laboratory of Cancer Genetics, Veterans Affairs Medical Center, Digestive Diseases, and GI Developmental Biology, Department of Surgery, Medicine and Lombardi Cancer Center, Georgetown University Medical Center, Medical/Dental Building, NW 213, 3900 Reservoir Road, NW, Washington, District of Columbia 20007, USA
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) falling into three functional classes: i) receptor-activated Smads (R-Smads): Smad1, Smad2, Smad3, Smad5, and Smad8; ii) co-mediator Smads: Smad4 and Smad 10; and iii) inhibitory Smads (I-Smads): Smad6 and Smad7. Activation of the TGF-β receptor complex by
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. 1994 , Massague 1998 , Derynck et al. 2001 ). Activated SMAD2 and SMAD3 form heterotrimeric complexes with the signal mediator SMAD4. The complex translocates to the nucleus to modulate transcription of target genes. Inhibitory SMADs, such as SMAD6
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subsequent phosphorylation of TGFBR2 receptor to the TGFBR1 kinase to SMAD activation ( Zhu & Kyprianou 2005 ). Interaction of SMAD4, (alone or together with SMAD3), with the AR in the DNA-binding and ligand-binding domains, may result in the modulation of
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Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China
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Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China
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Shanghai Clinical Center for Endocrine and Metabolic Diseases,, Laboratory for Endocrine and Metabolic Diseases,, Department of Radiological Medicine,, Laboratoire Genetique et Cancer,, Shanghai Key Laboratory for Endocrine Tumours,, Shanghai Institute of Endocrinology and Metabolism and Chinese-French Laboratory of Genomics and Life Sciences, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China
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interacting domain for Smad3 binding, possibly affects Smad3 signalling ( Kaji et al . 2001 ), which is a crucial player in transforming growth factor-β (TGF-β) signalling pathway. In vitro study has confirmed that amino acid substitution in Smad3-binding
Université Claude Bernard Lyon, CNRS UMR5201, INSERM-INRA U418, INSERM, Groupe d'Etude Recherche, Lyon, France; Faculté de Médecine, Université Lyon 1, Lyon F-69003, France; Laboratoire Génétique Moléculaire, Signalisation et Cancer, 8 Avenue Rockefeller, Lyon F-69373, France
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Université Claude Bernard Lyon, CNRS UMR5201, INSERM-INRA U418, INSERM, Groupe d'Etude Recherche, Lyon, France; Faculté de Médecine, Université Lyon 1, Lyon F-69003, France; Laboratoire Génétique Moléculaire, Signalisation et Cancer, 8 Avenue Rockefeller, Lyon F-69373, France
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Université Claude Bernard Lyon, CNRS UMR5201, INSERM-INRA U418, INSERM, Groupe d'Etude Recherche, Lyon, France; Faculté de Médecine, Université Lyon 1, Lyon F-69003, France; Laboratoire Génétique Moléculaire, Signalisation et Cancer, 8 Avenue Rockefeller, Lyon F-69373, France
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Université Claude Bernard Lyon, CNRS UMR5201, INSERM-INRA U418, INSERM, Groupe d'Etude Recherche, Lyon, France; Faculté de Médecine, Université Lyon 1, Lyon F-69003, France; Laboratoire Génétique Moléculaire, Signalisation et Cancer, 8 Avenue Rockefeller, Lyon F-69373, France
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Université Claude Bernard Lyon, CNRS UMR5201, INSERM-INRA U418, INSERM, Groupe d'Etude Recherche, Lyon, France; Faculté de Médecine, Université Lyon 1, Lyon F-69003, France; Laboratoire Génétique Moléculaire, Signalisation et Cancer, 8 Avenue Rockefeller, Lyon F-69373, France
Université Claude Bernard Lyon, CNRS UMR5201, INSERM-INRA U418, INSERM, Groupe d'Etude Recherche, Lyon, France; Faculté de Médecine, Université Lyon 1, Lyon F-69003, France; Laboratoire Génétique Moléculaire, Signalisation et Cancer, 8 Avenue Rockefeller, Lyon F-69373, France
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Université Claude Bernard Lyon, CNRS UMR5201, INSERM-INRA U418, INSERM, Groupe d'Etude Recherche, Lyon, France; Faculté de Médecine, Université Lyon 1, Lyon F-69003, France; Laboratoire Génétique Moléculaire, Signalisation et Cancer, 8 Avenue Rockefeller, Lyon F-69373, France
Université Claude Bernard Lyon, CNRS UMR5201, INSERM-INRA U418, INSERM, Groupe d'Etude Recherche, Lyon, France; Faculté de Médecine, Université Lyon 1, Lyon F-69003, France; Laboratoire Génétique Moléculaire, Signalisation et Cancer, 8 Avenue Rockefeller, Lyon F-69373, France
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. 2003 a ), using antibodies against menin (C19, 1:500), anti-p18 (1:3000), anti-p27 (1:1000), anti-pSmad1 (1:1000), anti-Smad1 (1:1000), anti-Smad3 (1:1000), anti-Smad4 (1:1000), anti-Smad5 polyclonal (1:1000) and anti-Cdk4 (1:1000, Santa
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Departments of, Experimental Medicine, Molecular Medicine, Radiological Sciences, Oncology and Anatomical Pathology, Sapienza University of Rome, Viale Regina Elena 324, 00161 Rome, Italy
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1998 ). TGFβ ligands bind to heterotetrameric complexes of receptors with serine–threonine kinase activity, leading to an increase in their ability to phosphorylate receptor-regulated Smads (R-Smads). The phosphorylation of R-Smads (Smad2 and Smad3) by
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-β signaling is integrated with signaling from other growth factors ( Zhang & Derynck 1999 , Attisano & Wrana 2000 , Massague & Chen 2000 ). Specific R-Smads transduce distinct signals for members of the TGF-β superfamily. Smad2 and Smad3 mediate signaling by