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1. Full Text Glucocorticoid receptor physiology
by Heitzer, Marjet D and Wolf, Irene M and Sanchez, Edwin R and Witchel, Selma F and DeFranco, Donald B
Reviews in Endocrine and Metabolic Disorders, ISSN 1389-9155, 12/2007, Volume 8, Issue 4, pp. 321 - 330
Glucocorticoid action in cells is mediated by a specific receptor protein, the glucocorticoid receptor (GR). GR is a member of a superfamily of... 
Medicine & Public Health | Internal Medicine | Diabetes | NUCLEAR HORMONE RECEPTORS | DNA-BINDING | TRANSCRIPTIONAL ACTIVATION | IMMUNOPHILIN FKBP52 | ENDOCRINOLOGY & METABOLISM | TRANSACTIVATION DOMAIN | HISTONE ACETYLTRANSFERASE | DEPENDENT DOWN-REGULATION | TETRATRICOPEPTIDE REPEAT | HEAT-SHOCK-PROTEIN | MOLECULAR-MECHANISMS | Animals | Biological Transport | Glucocorticoids - metabolism | Models, Biological | Humans | Glucocorticoids - physiology | Protein Binding | Signal Transduction - physiology | Receptors, Glucocorticoid - metabolism | Receptors, Glucocorticoid - physiology | Physiological aspects | Corticosteroids
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2. Full Text Utilization of the allen gene expression atlas to gain further insight into glucocorticoid physiology in the adult mouse brain
by Kalafatakis, Konstantinos and Giannakeas, Nikolaos and Lightman, Stafford L and Charalampopoulos, Ioannis and Russell, Georgina M and Tsipouras, Markos and Tzallas, Alexandros
Neuroscience Letters, ISSN 0304-3940, 07/2019, Volume 706, pp. 194 - 200
The neuroanatomic variation of the genomic expression of 25 genes involved in the regulation of glucocorticoid dynamics has been highlighted across 96 regions... 
Glucocorticoid neurodynamics | Allen Brain Atlas-Driven Visualizations | Adult mouse brain | Anatomic Gene Expression Atlas | CORTICOSTERONE | MEMORY | BDNF | TISSUE | TRANSLOCATOR PROTEIN TSPO | RECEPTORS | STRESS | NEUROSCIENCES | Neurosciences | Corticosteroids | Animal behavior | Analysis | Genes | Physiological aspects | Information management | Gene expression
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3. Full Text Glucocorticoid Programming
by SECKL, JONATHAN R and MEANEY, MICHAEL J
Annals of the New York Academy of Sciences, ISSN 0077-8923, 12/2004, Volume 1032, Issue 1, pp. 63 - 84
: Epidemiological evidence suggests that an adverse fetal environment permanently programs physiology, leading to increased risks of cardiovascular, metabolic,... 
birth weight | 11β‐HSD‐2 | glucocorticoids | programming | Programming | 11β-HSD-2 | Birth weight | Glucocorticoids | CORTICOTROPIN-RELEASING HORMONE | APPARENT MINERALOCORTICOID EXCESS | LOW-BIRTH-WEIGHT | MULTIDISCIPLINARY SCIENCES | 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-2 | RECEPTOR GENE-EXPRESSION | BETA-HYDROXYSTEROID DEHYDROGENASE | PHOSPHOENOLPYRUVATE CARBOXYKINASE GENE | 11 beta-HSD-2 | PLASMA-CORTISOL CONCENTRATIONS | INTRAUTERINE GROWTH RESTRICTION | CARDIOVASCULAR RISK-FACTORS | Cardiovascular Physiological Phenomena | Prenatal Exposure Delayed Effects | Humans | Birth Weight - physiology | Stress, Physiological - physiopathology | Behavior - physiology | Metabolism - physiology | Central Nervous System - embryology | Central Nervous System - physiology | Pregnancy | Fetal Development - physiology | Infant, Premature | 11-beta-Hydroxysteroid Dehydrogenase Type 2 - metabolism | Glucocorticoids - physiology | Female | Infant, Newborn
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4. Full Text Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse
by McGowan, Patrick O and Sasaki, Aya and D'Alessio, Ana C and Dymov, Sergiy and Labonté, Benoit and Szyf, Moshe and Turecki, Gustavo and Meaney, Michael J
Nature Neuroscience, ISSN 1097-6256, 03/2009, Volume 12, Issue 3, pp. 342 - 348
Maternal care influences hypothalamic-pituitary-adrenal (HPA) function in the rat through epigenetic programming of glucocorticoid receptor expression. In... 
YOUNG-ADULTS | MATERNAL-CARE | STRESS RESPONSES | GENETIC-ANALYSIS | DNA METHYLATION | MESSENGER-RNA | MOOD DISORDERS | SCHIZOPHRENIA | MAJOR DEPRESSION | NEUROSCIENCES | LIFE | Cell Line | Adult Survivors of Child Abuse - psychology | Humans | Middle Aged | Receptors, Glucocorticoid - biosynthesis | Molecular Sequence Data | Male | DNA Methylation - genetics | Hippocampus - pathology | Receptors, Glucocorticoid - metabolism | Epigenesis, Genetic - physiology | Young Adult | Promoter Regions, Genetic - physiology | Base Sequence | Receptors, Glucocorticoid - genetics | Suicide - psychology | Adult | Female | Hippocampus - physiology | Receptors, Glucocorticoid - physiology | Hormone receptors | Child abuse | Physiological aspects | Genetic aspects | Research | Hippocampus (Brain) | Gene expression
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5. Full Text γ-secretase inhibitors reverse glucocorticoid resistance in T cell acute lymphoblastic leukemia
by Real, Pedro J and Tosello, Valeria and Palomero, Teresa and Castillo, Mireia and Hernando, Eva and De Stanchina, Elisa and Sulis, Maria Luisa and Barnes, Kelly and Sawai, Catherine and Homminga, Irene and Meijerink, Jules and Aifantis, Iannis and Basso, Giuseppe and Cordon-Cardo, Carlos and Ai, Walden and Ferrando, Adolfo
Nature Medicine, ISSN 1078-8956, 01/2009, Volume 15, Issue 1, pp. 50 - 58
Gamma-secretase inhibitors (GSIs) block the activation of the oncogenic protein Notch homolog-1 (NOTCH1) in T cell acute lymphoblastic leukemia (T-ALL).... 
MEDICINE, RESEARCH & EXPERIMENTAL | INDUCED APOPTOSIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | RECEPTOR EXPRESSION | CYCLE ARREST | SRG3 | CELL BIOLOGY | NOTCH1 CONFERS | GOBLET CELLS | GENE | LINE | DIFFERENTIATION | PROMOTER | Glucocorticoids - administration & dosage | Glucocorticoids - therapeutic use | Cyclins - genetics | Receptors, Glucocorticoid - metabolism | Cyclin D2 | Enzyme Inhibitors - administration & dosage | Bcl-2-Like Protein 11 | Membrane Proteins - physiology | Apoptosis Regulatory Proteins - genetics | Female | Homeostasis - drug effects | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - metabolism | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - drug therapy | Dexamethasone - administration & dosage | Membrane Proteins - genetics | Mice, Inbred C57BL | Enzyme Inhibitors - pharmacology | Gene Expression Regulation, Leukemic - drug effects | Proto-Oncogene Proteins - genetics | Mice, SCID | Mice, Knockout | Dexamethasone - therapeutic use | Animals | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Models, Biological | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - genetics | Homeostasis - physiology | Proto-Oncogene Proteins - physiology | Receptors, Glucocorticoid - genetics | Apoptosis Regulatory Proteins - physiology | Mice | Amyloid Precursor Protein Secretases - antagonists & inhibitors | Receptor, Notch1 - antagonists & inhibitors | Receptor, Notch1 - genetics | Receptors, Glucocorticoid - physiology | Receptor, Notch1 - physiology | Drug Resistance, Neoplasm - drug effects | Index Medicus
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6. Full Text Novel Aspects of Glucocorticoid Actions
by Uchoa, E. T and Aguilera, G and Herman, J. P and Fiedler, J. L and Deak, T and Sousa, M. B. C
Journal of Neuroendocrinology, ISSN 0953-8194, 09/2014, Volume 26, Issue 9, pp. 557 - 572
Normal hypothalamic‐pituitary‐adrenal (HPA) axis activity leading to the rhythmic and episodic release of adrenal glucocorticoids (GCs) is essential for body... 
feedback | immune system | HPA axis | glucocorticoids | neuroplasticity | food intake | Neuroplasticity | Glucocorticoids | Feedback | Food intake | Immune system | CORTICOTROPIN-RELEASING HORMONE | RNA STABILITY | NEUROSCIENCES | HYPOTHALAMIC PARAVENTRICULAR NUCLEUS | RESPONSE ELEMENT | MESSENGER-RIBONUCLEIC-ACID | GLUCAGON-LIKE PEPTIDE-1 | STRESS-INDUCED INCREASES | ENDOCRINOLOGY & METABOLISM | RECEPTOR ANTAGONIST BLOCKS | PITUITARY-ADRENAL-AXIS | GENE-TRANSCRIPTION | Stress, Physiological - physiology | Brain - physiology | Eating - physiology | Receptors, Mineralocorticoid - physiology | Animals | Neuronal Plasticity - physiology | Models, Biological | Neurosecretory Systems - physiology | Glucocorticoids - physiology | Feedback, Physiological - physiology | Hypothalamo-Hypophyseal System - physiology | Inflammation Mediators - physiology | Receptors, Glucocorticoid - physiology | Pituitary-Adrenal System - physiology | ACTH | Corticosteroids | Steroids
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