Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands
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Department of Pediatric Neuro-Oncology, Prinses Máxima Centrum, Utrecht, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands
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study the biological mechanisms of action that underlie them, and this might help to decrease these adverse effects during glucocorticoid therapy. Synthetic glucocorticoids target the glucocorticoid receptor (GR), one of the two receptor types for the
Instituto de Investigación en Biomedicina de Buenos Aires – CONICET, Departamento de Fisiología, Partner Institute of the Max Planck Society, Buenos Aires, Argentina
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Instituto de Investigación en Biomedicina de Buenos Aires – CONICET, Departamento de Fisiología, Partner Institute of the Max Planck Society, Buenos Aires, Argentina
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Instituto de Investigación en Biomedicina de Buenos Aires – CONICET, Departamento de Fisiología, Partner Institute of the Max Planck Society, Buenos Aires, Argentina
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action during inflammation (23, 24) . GCs exert their biological effects binding to the glucocorticoid receptor (GR), which is a ligand-activated TF that regulates the expression of target genes, either positively or negatively (18, 25) . In an
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Introduction Polymorphisms of the glucocorticoid receptor (GR) may influence the sensitivity to glucocorticoids by altering the GR expression (e.g. reducing transcription) and influencing transactivation and transrepression of target genes
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signalling, often resulting in various peripheral effects, one of which is the tissue-specific reductions in the glucocorticoid receptor α (GRα) functional pool. This reduction in the GRα functional pool may ultimately drive the development of acquired GC
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dysfunctional humoral immune response. In general, BD might be regarded an immune-mediated inflammatory disease. Glucocorticoids (GC) play a key role in mediating a balanced inflammatory response. GCs exert their effects via interaction with the GC receptor (GR
Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, California, USA
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Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, California, USA
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Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, California, USA
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pituitary gland, which bind tissue-specific isoforms of their cognate receptor, the glucocorticoid receptor (GR), and activate cell-specific stress–response pathways ( 46 ). The primary forms of glucocorticoids in humans and rodents are cortisol and
Department of Rheumatology and Clinical Immunology, Charité-University Medicine, Berlin, Germany
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Bone Research Program, ANZAC Research Institute, University of Sydney, Sydney, NSW, Australia
Concord Clinical School, The University of Sydney, Sydney, Australia
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Key Laboratory for Space Bioscience and Biotechnology, Institute of Special Environmental Biophysics, School of Life Sciences, Northwestern Polytechnical University, Shaanxi, China
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Concord Clinical School, The University of Sydney, Sydney, Australia
Department of Endocrinology & Metabolism, Concord Hospital, Sydney, Australia
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Concord Clinical School, The University of Sydney, Sydney, Australia
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Concord Clinical School, The University of Sydney, Sydney, Australia
Department of Endocrinology & Metabolism, Concord Hospital, Sydney, Australia
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then blocked with 5% goat serum for 30 min and incubated overnight with the primary antibody for 11β-HSD1 (1:100, Cayman Chemicals) and glucocorticoid receptor (GR) (1:400, sc-1004, Santa Cruz Biotechnology). A biotinylated secondary antibody was
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M Burmester GR Cutolo M Jacobs J Kirwan J Köhler L Riel Van P Vischer T et al . Standardised nomenclature for glucocorticoid dosages and glucocorticoid treatment regimens: current questions and tentative answers in rheumatology
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development of corticosteroid side effects between patients ( 7 ). Interestingly, when the endogenous glucocorticoid, cortisol (hydrocortisone), is compared with prednisolone at the isolated human glucocorticoid receptor (GR), the transactivation activity of
Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany
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Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany
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Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany
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Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany
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DFG Research Center and Cluster of Excellence for Regenerative Therapies, Technical University, Dresden, Germany
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Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany
DFG Research Center and Cluster of Excellence for Regenerative Therapies, Technical University, Dresden, Germany
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Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany
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). Figure 4 Sclerostin ( SOST ) expression depends on the presence of the glucocorticoid receptor (GR). The GR was overexpressed in human mesenchymal stromal cells (HMSCs) using pCMX-HA-hGRalpha and then left untreated or treated with dexamethasone (DEX