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Genomics Research Centre, Institute of Health and Biomedical Innovation, Faculty of Health, Queensland University of Technology, Brisbane, Queensland, Australia
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(CREB1) . American Journal of Translational Research 7 2053 – 2059 . Lin X Li HR Lin XF Yu ME Tu XW Hua ZD Lin M Xu NL Han LL Chen YS 2015 Silencing of Livin inhibits tumorigenesis and metastasis via VEGF and MMPs pathway in lung cancer
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Department of Hematology and Medical Oncology, Department of Pathology and Laboratory Medicine, Emory Winship Cancer Institute, Department of Surgery, Department of Medicine, Department of Oncology, Emory University School of Medicine, Atlanta, Georgia 30322, USA
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increases E-cadherin expression via enhancing CREB-DNA and Sp1-DNA binding activity to E-cadherin promoter and modulates homotypic tumor cell adhesion and proliferation ( Mauro et al . 2007 ). Thus, uncontrolled leptin-induced signaling could contribute to
Division of Endocrinology, Department of Endocrinology and Metabolism, Diabetes, and Metabolism, Laboratory for Cellular and Molecular Thyroid Research, Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 333, Baltimore, Maryland 21287, USA
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TATA box, TTF1,AP1, AP2, Sp1, and cAMP response element-binding protein (CREB) binding sites in human NIS promoter ( Ryu et al . 1998 ). The regions P1 (−297/−107), P2 (−477/−277), and P3 (−678/−452) harbor many of these transcription factor
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Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, Athens, Greece
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extracellular signals that increase the content of Ca 2+ and/or cAMP lead to the activation of ERK and CREB, and thereby activate the CRE-mediated PER1 expression. In mammals the circadian clock regulation is made up of two main interlocking
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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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various published ChIP-seq data sets ( Cheneby et al . 2018 ), we found a number of transcription factors whose binding sites overlapped with XBP1s, including other bZIP transcription factors (e.g. FOS, JUN, CREB3), AR and FOXA1 (Supplementary Fig. 6A and
Institut Cochin, Inserm, Department of Endocrinology, Université Paris Descartes, CNRS (UMR 8104), 75014 Paris, France
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Institut Cochin, Inserm, Department of Endocrinology, Université Paris Descartes, CNRS (UMR 8104), 75014 Paris, France
Institut Cochin, Inserm, Department of Endocrinology, Université Paris Descartes, CNRS (UMR 8104), 75014 Paris, France
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Institut Cochin, Inserm, Department of Endocrinology, Université Paris Descartes, CNRS (UMR 8104), 75014 Paris, France
Institut Cochin, Inserm, Department of Endocrinology, Université Paris Descartes, CNRS (UMR 8104), 75014 Paris, France
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′-monophosphate-responsive element-binding protein (CREB) is decreased during human adrenal cortex tumorigenesis and fetal development . Journal of Clinical Endocrinology and Metabolism 88 3958 – 3965 doi:10.1210/jc.2003-030070 . Shimizu M Takai K
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stress, including Twist1 ( Shiota et al . 2010 ), YB-1 ( Shiota et al . 2011 c ), NF-κB ( Zhang et al . 2009 ), Sp1 ( Faber et al . 1993 , Yuan et al . 2005 ), Myc ( Grad et al . 1999 , Lee et al . 2009 ), CREB ( Mizokami et al . 1994 ), and
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expression of cofactors which potentiate agonistic effects of hydroxyflutamide, such as CREB-binding protein (CBP) or gelsolin ( Culig et al . 2005 ). For this reason, a novel AR antagonist, such as MDV3100, which acts by a different mechanism in comparison
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Department of Biomedical, Experimental and Clinical Sciences, University of Florence, Florence, Italy
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Molecular Endocrinology Laboratory, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium
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(CREB binding protein) that show elevated expression in advanced PCa and have oncogenic potential ( Debes et al. 2003 , Comuzzi et al. 2004 ). While these coactivators show high levels of homology, they play distinctive roles in PCa and other
Department of Internal Medicine, CHA Bundang Medical Center, CHA University, Seongnam, Korea
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Department of Surgery, Seoul National University College of Medicine, Seoul, Korea
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Genomic Medicine Institute, Medical Research Center, Seoul National University, Seoul, Korea
Center for Medical Innovation, Seoul National University Hospital, Seoul, Korea
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significant difference but with modest changes (fold changes, 2.0–2.7): CILP , SFTPA1 , SFTPA2 , PODNL1 , TSPAN11 , CREB3L1 , EGLN3 , WISP2 , GAS1 , SLC38A3 , MFAP5 and TFF3 (Supplementary Table 8). In the analysis of the SNU dataset, a similar