Cortexolone: binding to glucocorticoid receptors in rat thymocytes and mechanism of its antiglucocorticoid action |
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| Authors: | N Kaiser R J Milholland R W Turnell F Rosen |
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| Affiliation: | 1. Collaborative Innovation Center of Yangtze River Delta Region Green Pharmaceuticals, College of Pharmaceutical Sciences, Zhejiang University of Technology, Hangzhou, 310014, China;2. Department of Medical Oncology, Cancer Hospital of China Medical University, China Medical University, Shenyang, 110001, China;1. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA;2. Center for Computational and Integrative Biology, Department of Molecular Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA;3. Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Blavatnik Institute, Boston, MA 02115, USA;1. Departamento de Farmácia, Universidade Federal de Sergipe, Avenida Marechal Rondon, s/n, Cidade Universitária, CEP 49100-000 São Cristóvão, SE, Brazil;2. Nutrition and Dietetics School, University of Atlántico, Atlántico, Colombia;3. Institute of Technology and Research of Sergipe, Rua Campo do Brito, 371, 49.020-380 Aracaju, Brazil;1. Sino-Norway Joint Lab on Fish Gut Microbiota, Institute of Feed Research, Chinese Academy of Agricultural Sciences, Beijing, 100081, China;2. Key Laboratory for Feed Biotechnology of the Ministry of Agriculture and Rural Affairs, Institute of Feed Research, Chinese Academy of Agricultural Sciences, Beijing, 100081, China;3. Norway-China Joint Lab on Fish Gastrointestinal Microbiota, Institute of Biology, Norwegian University of Science and Technology, Trondheim, 7491, Norway;1. Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China;2. China Academy of Chinese Medical Sciences, Beijing, China;3. Graduate School, Beijing University of Chinese Medicine, Beijing, China |
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| Abstract: | In rat thymocytes, cortexolone (11-deoxycortisol) competes for binding to glucocorticoid receptors, as identified on sucrose density gradients, and blocks the effect of triamcinolone acetonide (TA) on 2-deoxyglucose uptake. The cellular distribution and sedimentation coefficients of 3H-TA-receptor complexes are dependent on the incubation temperature and ionic strength of the extraction buffer. In contrast, the single receptor complex formed by 3H-cortexolone has a sedimentation coefficient of 3.5S, and is unaffected by changes in temperature and salt concentration. |
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