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Université de Paris, Cochin Institute, Inserm U1016, CNRS 8104, Paris, France
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Centre of Membrane Proteins and Receptors (COMPARE), Universities of Nottingham and Birmingham, Birmingham, UK
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Center for Rare Adrenal Diseases, Endocrinology Department, Cochin Hospital, Assistance Publique Hôpitaux de Paris, Paris, France
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University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA
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variant expressed higher PRKACB protein with significant presence of phosphorylated CREB (p-CREB) compared to the adrenal gland from a PPNAD without PRKAR1A mutation. Magnification x40 of another immunostaining of PRKACB (D) and p-CREB presence (E) in
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several well-known Akt substrates. As measured by western blot, perifosine significantly decreased GSK3α/β, p70S6K, and MDM2 ( Fig. 3 A), while strongly inducing CREB phosphorylation ( Fig. 3 B). In order to identify whether CREB phosphorylation in
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adenylyl cylase. cAMP binds to the PKA heterotetramer, releasing PKAR subunit dimers and free PKAC subunits (red squares). The catalytic subunits phosphorylate both cytoplasmic and nuclear targets (for e.g. CREB), leading to the downstream effects of this
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with nuclear factor Y, signal transducer and activator of transcription 5 (STAT5), or nuclear factor κB (NF-κB), and drives target gene promoters via other elements such as CAAT box, STAT5 motif, CREB, or NF-κB-binding sites ( Boulon et al . 2002
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Hereditary Endocrine Cancer Group, Familial Cancer Clinic, Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Confocal Microscopy Unit, Proteomics Unit, Endocrinology and Nutrition Service, Endocrinology and Nutrition Service, Department of Medical and Surgical Sciences, Human Cancer Genetics Programme, Spanish National Cancer Research Centre, Centro Nacional de Investigaciones Oncológicas, Melchor Fernández Almagro 3, 28029 Madrid, Spain
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Hereditary Endocrine Cancer Group, Familial Cancer Clinic, Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Confocal Microscopy Unit, Proteomics Unit, Endocrinology and Nutrition Service, Endocrinology and Nutrition Service, Department of Medical and Surgical Sciences, Human Cancer Genetics Programme, Spanish National Cancer Research Centre, Centro Nacional de Investigaciones Oncológicas, Melchor Fernández Almagro 3, 28029 Madrid, Spain
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Hereditary Endocrine Cancer Group, Familial Cancer Clinic, Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Confocal Microscopy Unit, Proteomics Unit, Endocrinology and Nutrition Service, Endocrinology and Nutrition Service, Department of Medical and Surgical Sciences, Human Cancer Genetics Programme, Spanish National Cancer Research Centre, Centro Nacional de Investigaciones Oncológicas, Melchor Fernández Almagro 3, 28029 Madrid, Spain
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Hereditary Endocrine Cancer Group, Familial Cancer Clinic, Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Confocal Microscopy Unit, Proteomics Unit, Endocrinology and Nutrition Service, Endocrinology and Nutrition Service, Department of Medical and Surgical Sciences, Human Cancer Genetics Programme, Spanish National Cancer Research Centre, Centro Nacional de Investigaciones Oncológicas, Melchor Fernández Almagro 3, 28029 Madrid, Spain
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Hereditary Endocrine Cancer Group, Familial Cancer Clinic, Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Confocal Microscopy Unit, Proteomics Unit, Endocrinology and Nutrition Service, Endocrinology and Nutrition Service, Department of Medical and Surgical Sciences, Human Cancer Genetics Programme, Spanish National Cancer Research Centre, Centro Nacional de Investigaciones Oncológicas, Melchor Fernández Almagro 3, 28029 Madrid, Spain
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Hereditary Endocrine Cancer Group, Familial Cancer Clinic, Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Confocal Microscopy Unit, Proteomics Unit, Endocrinology and Nutrition Service, Endocrinology and Nutrition Service, Department of Medical and Surgical Sciences, Human Cancer Genetics Programme, Spanish National Cancer Research Centre, Centro Nacional de Investigaciones Oncológicas, Melchor Fernández Almagro 3, 28029 Madrid, Spain
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as MAX -mutant tumors. Some examples for the latter included brain-derived neurotrophic factor ( BDNF ) targeted by miRs-370/381/382/495, CREB5 by miRs-539/543/495, PIK3R1 by miRs-376a/376b/495, and sortilin-related VPS10 domain containing
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State Key Laboratory of Veterinary Biotechnology Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, Heilongjiang, China
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) response element-binding protein (CREB), likely through PRMT5 or PRMT5-like enzyme-mediated methylation of FOXO1 and CREB ( Muhammad et al. 2017 ). Second, menin recruits PRMT5 to the promoter of the Gas1 gene, increases repressive H4R3me2s and
Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
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Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
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Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
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Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
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Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
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Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
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Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
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Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
Department of Structural and Cellular Biology, Department of Surgery, Tulane Cancer Center and Louisiana Cancer Research Consortium, Circadian Cancer Biology Group, Tulane Center for Circadian Biology, Tulane University School of Medicine, 1430 Tulane Avenue, SL-49, New Orleans, Louisiana 70112, USA
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Gα i proteins ( Dinet & Korf 2007 , Lai et al . 2008 ). Activation of the MT 1 receptor promotes the inhibition of forskolin-stimulated cAMP formation, the suppression of protein kinase A (PKA) activity, and the phosphorylation of the CREB
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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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-cadherin was from Immunological Sciences (Rome, Italy), Smad2/3 from BD Biosciences PharMingen (San Diego, CA, USA), and GAPDH and cAMP response element-binding (CREB) were from Abcam. Texas-red–conjugated goat anti-mouse IgG was obtained from Jackson
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Department of Molecular, Center for Biostatistics, National Hormone and Peptide Program, Department of Veterinary Biosciences, Division of Endocrinology, Virology, Immunology, and Medical Genetics, The Ohio State University, 420 West 12th Avenue, Tzagournis Research Facility 544, Columbus, Ohio 43210, USA
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/2 (Mapk1, Mapk3) (9102), pErk Thr202/Tyr204 (9101), pStat3 Tyr705 (9145P), Stat3 (9132), pCreb Ser133 (9198), and Creb (9197) (Cell Signaling Technology); Pcna (sc-56) and Spot14 (Thrsp) (sc-137178) (Santa Cruz Biotechnology, Santa Cruz, CA, USA); β
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Division of Pathophysiology, National and Kapodistrian University of Athens Medical School, Athens, Greece
Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, UK
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of transcription 3 (STAT3) ( Akiyama et al. 2015 ). The EWSR1-CREB1 fusion gene detected in the tumour led to continuous activation of CREB1 and IL6 production because the promoter region of IL6 has a CREB binding site ( Akiyama et al. 2015