• glucocorticoid receptor gene
• glucocorticoid resistance syndrome
• hypercortisolism

• Chronic stress
• Cortical thickness
• Hippocampal volume
• Low-grade inflammation
• Structural equation models

• Adrenal disorders
• Endocrine system
• Pituitary disorders

• Humans
• Adrenal Gland Diseases
• Adrenocorticotropic Hormone
• Cushing Syndrome/complications
• Cushing Syndrome/diagnosis
• Cushing Syndrome/genetics
• Hydrocortisone
• Mutation
• Male
• Adult

Hypertension is one of the leading causes of premature death in humans and exhibits a complex aetiology including environmental and genetic factors. Mutations within the glucocorticoid receptor (GR) can cause glucocorticoid resistance, which is characterized by several clinical features like hypercortisolism, hypokalaemia, adrenal hyperplasia and hypertension. Altered glucocorticoid receptor signalling further affects sodium and potassium homeostasis as well as blood pressure regulation and cell proliferation and differentiation that influence organ development and function. In salt-sensitive hypertension, excessive renal salt transport and sympathetic nervous system stimulation may occur simultaneously, and, thus, both the mineralocorticoid receptor (MR) and the GR-signalling may be implicated or even act interdependently. This review focuses on identified GR mutations in human primary generalized glucocorticoid resistance (PGGR) patients and their related clinical phenotype with specific emphasis on adrenal gland hyperplasia and hypertension. We compare these findings to mouse and rat mutants harbouring genetically engineered mutations to further dissect the cause and/or the consequence of clinical features which are common or different.

• Animal model
• Epithelial transport
• Glucocorticoid resistance
• Homeostasis
• Hypercortisolism
• Kidney physiology

• Depressive symptoms
• Informal cancer caregiving stress
• Negative attribution style
• Salivary cortisol

Mutations within the glucocorticoid receptor (GR) gene locus lead to glucocorticoid resistance which is characterized by several clinical symptoms such as adrenal gland hyperplasia and salt-sensitive hypertension, although the underlying mechanisms are still unknown. We studied GR haploinsufficient (GR^+/−) Sprague Dawley rats which, on a standard diet, showed significantly increased plasma aldosterone and corticosterone levels and an adrenocortex hyperplasia accompanied by a normal systolic blood pressure. Following a high salt diet, these rats developed salt-sensitive hypertension and maintained elevated enzyme-soluble epoxide hydrolase (sEH) in adrenal glands, while sEH was significantly decreased in wild-type rats. Furthermore, GR^+/− rats showed dysregulation of the equilibrated linoleic and arachidonic acid pathways, with a significant increase of less active metabolites such as 8,9-DiHETrE. In Sprague Dawley rats, GR haploinsufficiency induced steroid disturbances, which provoked hypertension only in combination with high salt intake, which was accompanied by disturbances in sEH and fatty acid metabolism. Our results suggest that sEH inhibition could be a potential target to treat hypertension in patients with GR haploinsufficiency.

• Chrousos syndrome
• adrenal gland hyperplasia
• glucocorticoid receptor
• glucocorticoid resistance
• hypertension
• soluble-epoxide hydrolase

• COVID-19
• GCR
• HPA
• critical illness

• COVID-19/metabolism
• Critical Illness
• Glucocorticoids/metabolism
• Humans
• Hypothalamo-Hypophyseal System/metabolism
• Hypothalamo-Hypophyseal System/virology
• Pituitary-Adrenal System/metabolism
• Pituitary-Adrenal System/virology
• Receptors, Glucocorticoid/metabolism
• Stress, Physiological

• NR3C1 gene mutations
• glucocorticoid hypersensitivity
• glucocorticoid receptor
• glucocorticoid resistance
• glucocorticoids

• Animals
• Drug Hypersensitivity Syndrome/etiology
• Drug Hypersensitivity Syndrome/metabolism
• Drug Hypersensitivity Syndrome/pathology
• Drug Resistance/genetics
• Glucocorticoids/pharmacology
• Humans
• Metabolism, Inborn Errors/genetics
• Metabolism, Inborn Errors/pathology
• Receptors, Glucocorticoid/deficiency
• Receptors, Glucocorticoid/genetics

• Central precocious puberty
• Long-acting GnRH analog
• Peripheral precocious puberty
• Precocious sexual maturation
• Sexual maturation

The glucocorticoid receptor (GCR) and the mineralocorticoid receptor (MR) are members of the steroid receptor superfamily of hormone-dependent transcription factors. The receptors are structurally and functionally related. They are localized in the cytosol and translocate into the nucleus after ligand binding. GCRs and MRs can be co-expressed within the same cell, and it is believed that the balance in GCR and MR expression is crucial for homeostasis and plays a key role in normal adaptation. In critical illness, the hypothalamic-pituitary-adrenal axis is activated, and as a consequence, serum cortisol concentrations are high. However, a number of patients exhibit relatively low cortisol levels for the degree of illness severity. Glucocorticoid (GC) actions are facilitated by GCR, whose dysfunction leads to GC tissue resistance. The MR is unique in this family in that it binds to both aldosterone and cortisol. Endogenous GCs play a critical role in controlling inflammatory responses in critical illness. Intracellular GC concentrations can differ greatly from blood levels due to the action of the two 11β-hydroxysteroid dehydrogenase isozymes, type 1 and type 2. 11β-hydroxysteroid dehydrogenases interconvert endogenous active cortisol and intrinsically inert cortisone. The degree of expression of the two isozymes has the potential to dramatically influence local GC availability within cells and tissues. In this review, we will explore the clinical studies that aimed to elucidate the role of MR and GCR expression in the inflammatory response seen in critical illness.

• Mineralocorticoid receptor
• Glucocorticoid receptor, Critical illness
• 11beta-hydroxysteroid dehydrogenase
• Aldosterone
• Cortisol

• Glucocorticoid receptor
• Glucocorticoid resistance
• Glucocorticoid signaling

• Animals
• Drug Resistance
• Glucocorticoids/pharmacology
• Humans
• Organ Specificity
• Promoter Regions, Genetic
• Protein Processing, Post-Translational
• RNA Splicing
• Receptors, Glucocorticoid/genetics
• Receptors, Glucocorticoid/metabolism
• Signal Transduction/drug effects

Glucocorticoids are potent anti-inflammatory drugs that are used to treat an extraordinary range of human disease, including COVID-19, underscoring the ongoing importance of understanding their molecular mechanisms. Early studies of GR signaling led to broad acceptance of models in which glucocorticoid receptor (GR) monomers tether repressively to inflammatory transcription factors, thus abrogating inflammatory gene expression. However, newer data challenge this core concept and present an exciting opportunity to reframe our understanding of GR signaling. Here, we present an alternate, two-part model for transcriptional repression by glucocorticoids. First, widespread GR-mediated induction of transcription results in rapid, primary repression of inflammatory gene transcription and associated enhancers through competition-based mechanisms. Second, a subset of GR-induced genes, including targets that are regulated in coordination with inflammatory transcription factors such as NF-κB, exerts secondary repressive effects on inflammatory gene expression. Within this framework, emerging data indicate that the gene set regulated through the cooperative convergence of GR and NF-κB signaling is central to the broad clinical effectiveness of glucocorticoids in terminating inflammation and promoting tissue repair.

• glucocorticoid receptor
• inflammation
• negative feedback
• repression
• transcriptional enhancer

• Cortisol
• Critical illness
• Glucocorticoid receptors
• Interleukins
• Stress response

• Adrenal Cortex/metabolism
• Adrenocorticotropic Hormone/metabolism
• Critical Illness
• Cytokines/metabolism
• Female
• Glucocorticoids/metabolism
• Humans
• Hydrocortisone/metabolism
• Hypothalamo-Hypophyseal System
• Longitudinal Studies
• Male
• Metabolism, Inborn Errors/metabolism
• Middle Aged
• Pituitary-Adrenal System/metabolism
• Prospective Studies
• Protein Isoforms/metabolism
• Receptors, Glucocorticoid/deficiency
• Receptors, Glucocorticoid/metabolism
• Signal Transduction/physiology
• Steroids/metabolism

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that has important health and economic impacts in the elderly. Despite a better understanding of the molecular mechanisms leading to the appearance of major pathological hallmarks (senile plaques and neurofibrillary tangles), effective treatments are still lacking. Sporadic AD forms (98% of all cases) are multifactorial, and a panoply of risk factors have been identified. While the major risk factor is aging, growing evidence suggests that chronic stress or stress-related disorders increase the probability to develop AD. An early dysregulation of the hypothalamic-pituitary-adrenal axis (HPA axis or stress axis) has been observed in patients. The direct consequence of such perturbation is an oversecretion of glucocorticoids (GC) associated with an impairment of its receptors (glucocorticoid receptors, GR). These steroids hormones easily penetrate the brain and act in synergy with excitatory amino acids. An overexposure could be highly toxic in limbic structures (prefrontal cortex and hippocampus) and contribute in the cognitive decline occurring in AD. GC and GR dysregulations seem to be involved in lots of functions disturbed in AD and a vicious cycle appears, where AD induces HPA axis dysregulation, which in turn potentiates the pathology. This review article presents some preclinical and clinical studies focusing on the HPA axis hormones and their receptors to fight AD. Due to its primordial role in the maintenance of homeostasis, the HPA axis appears as a key-actor in the etiology of AD and a prime target to tackle AD by offering multiple angles of action.

• 11β hydroxysteroid dehydrogenase
• AVP (arginine vasopressin)
• Alzheimer’s disease
• CRH (corticotropin-releasing hormone)
• HPA axis (hypothalamus-pituitary-adrenal)
• glucococorticoids
• stress-related disorder

• early-life stress
• epigenetics
• individuality
• low birth weight
• mitochondria
• predisposition
• stress

• Adult attachment avoidance
• adult attachment anxiety
• asthma severity
• cortisol
• maternal warmth

Dexamethasone is a widely used glucocorticoid, which has been prescribed increasingly in recent years. The effects of Dexamethasone on the ovary and uterus was investigated in present study.

Twenty (20) adult female Wistar rats, weighing 130-170 g were assigned to four (4) groups of five (5) animals each. The rats in the control group received saline, while the rats in the experimental group was subjected to oral treatment of dexamethasone of 12 mg/kg, 10 mg/kg, and 7 mg/kg doses daily for a period of 10 days, respectively. The rats were slaughtered after 24 hours of the last administration, and the uterus and ovaries were harvested following abdominal incision. Histological and biochemical investigations were carried out and the results were analyzed using ANOVA with the Graph-Pad prism software package 6.

There was a significant decrease in the activities of the carbohydrate metabolic enzymes of the uterus in the dexamethasone-treated groups compared to the control group (p<0.05). Vacuolation, atrophy, thick epithelium, enlarged cells, inactive interstitial glands and follicular cyst, characterized the histological observation in the dexamethasone-treated groups in a dose-dependent manner.

This present study revealed that high-dose dexamethasone causes multiple changes in the histological features of the ovary and uterus, exerting type I and type II anti-oestrogenic effects on the female reproductive compartment.

• anti-oestrogenic
• dexamethasone
• endocrine disruptors and stress
• ovary
• uterus

Environmental factors such as chemicals, stress and pathogens are now widely believed to play important roles in the onset of some brain diseases, as they are associated with neuronal impairment and acute or chronic inflammation. Alzheimer’s disease (AD) is characterized by progressive synaptic dysfunction and neurodegeneration that ultimately lead to dementia. Neuroinflammation also plays a prominent role in AD and possible links to viruses have been proposed. In particular, the human immunodeficiency virus (HIV) can pass the blood-brain barrier and cause neuronal dysfunction leading to cognitive dysfunctions called HIV-associated neurocognitive disorders (HAND). Similarities between HAND and HIV exist as numerous factors involved in AD such as members of the amyloid and Tau pathways, as well as stress-related pathways or blood brain barrier (BBB) regulators, seem to be modulated by HIV brain infection, leading to the accumulation of amyloid plaques or neurofibrillary tangles (NFT) in some patients. Here, we summarize findings regarding how HIV and some of its proteins such as Tat and gp120 modulate signaling and cellular pathways also impaired in AD, suggesting similarities and convergences of these two pathologies.

• Alzheimer’s disease
• HIV-associated neurocognitive disorders
• hypothalamo-pituitary-adrenal axis
• neuroinflammation
• viral neuroinfection

• ACEs
• Behavioral health
• Cost
• High utilizer
• Social determinants of health

• GR signaling
• Glucocorticoid receptor
• Glucocorticoid resistance
• Mutations
• NR3C1
• Récepteur aux glucocorticoïdes
• Résistance aux glucocorticoïdes
• Signalisation glucocorticoïde

• Cushing Syndrome/genetics
• Genetic Predisposition to Disease
• Glucocorticoids/metabolism
• Humans
• Hypothalamo-Hypophyseal System/physiology
• Metabolism, Inborn Errors/genetics
• Metabolism, Inborn Errors/metabolism
• Mutation
• Pituitary-Adrenal System/physiology
• Polymorphism, Genetic
• Receptors, Glucocorticoid/deficiency
• Receptors, Glucocorticoid/genetics
• Receptors, Glucocorticoid/metabolism
• Signal Transduction/genetics

Glucocorticoid resistance is a rare, sporadic or familial condition caused by mutation of the gene encoding the glucocorticoid receptor (GR). Clinically it is characterized by symptoms developed due to local, tissue-specific, or generalized partial insensitivity to glucocorticoids.

A 31-year-old woman was evaluated because of infertility at the Endocrine Unit of the 2nd Department of Medicine, Semmelweis University. During her laboratory investigations, elevated serum and salivary cortisol were observed which failed to be suppressed after administration of 1 mg dexamethasone. 24 h urinary cortisol was increased, but a normal midnight serum cortisol was detected suggesting a maintained circadian rhythm. Plasma dehydroepiandrosterone-sulfate and androstendione levels were also elevated. Repeated plasma ACTH measurements indicated slightly elevated or normal values. Bone mineral density was normal. All laboratory results confirmed the diagnosis of glucocorticoid resistance. Genetic counseling followed by Sanger sequencing of the coding region of the gene encoding human glucocorticoid receptor was performed and a missense mutation (Arg714Gln, R714Q) in a heterozygous form was detected. Following family screening, the same mutation was found in her clinically-healthy 35-year-old sister who had no fertility problems.This variant was not detected in more than 60 patients and controls tested either for glucocorticoid resistance or Cushing’s syndrome in our Laboratory and it was absent in Exome Variant Server, HumanGene Mutation Database and ExAC databases.

Our case fulfils the diagnostic criteria of glucocorticoid resistance, also named Chrousos syndrome. The glucocorticoid receptor gene mutation detected in our patient has been already reported in a 2-year-old child with hypoglycaemia, hypokalaemia, hypertension and premature puberty. These distinct phenotypes may suggest that other factors may modify the functional consequences of the R714Q variant of GR.

• Glucocorticoid receptor
• Glucocorticoid resistance
• Mutation

• Anti-inflammatory
• Biotherapeutics
• Colorectal cancer
• Inflammation
• Inflammatory bowel disease
• Phytochemicals
• Probiotics
• Small drug molecules

• biomechanics
• bone–brain–nervous system interactions
• endocrine pathways
• exercise
• osteoporosis

The brain evolved cellular mechanisms for adapting synaptic function to energy supply. This is particularly evident when homeostasis is challenged by stress. Signaling loops between the mitochondria and synapses scale neuronal connectivity with bioenergetics capacity. A biphasic “inverted U shape” response to the stress hormone glucocorticoids is demonstrated in mitochondria and at synapses, modulating neural plasticity and physiological responses. Low dose enhances neurotransmission, synaptic growth, mitochondrial functions, learning, and memory whereas chronic, higher doses produce inhibition of these functions. The range of physiological effects by stress and glucocorticoid depends on the dose, duration, and context at exposure. These criteria are met by neuronal activity and the circadian, stress-sensitive and ultradian, stress-insensitive modes of glucocorticoid secretion. A major hallmark of stress-related neuropsychiatric disorders is the disrupted glucocorticoid rhythms and tissue resistance to signaling with the glucocorticoid receptor (GR). GR resistance could result from the loss of context-dependent glucocorticoid signaling mediated by the downregulation of the activity-dependent neurotrophin BDNF. The coincidence of BDNF and GR signaling changes glucocorticoid signaling output with consequences on mitochondrial respiration efficiency, synaptic plasticity, and adaptive trajectories.

• Glucocorticoid receptor
• NR3C1 mutations
• glucocorticoid resistance
• glucocorticoid signalling
• glucocorticoids

Dexamethasone is a type of steroidal medications that is prescribed in many cases. In this study, a new reaction system using kinetic spectrophotometric method for quantitative determination of dexamethasone is proposed. The method is based on the catalytic effect of dexamethasone on the oxidation of Orange G by bromate in acidic media. The change in absorbance as a criterion of the oxidation reaction progress was followed spectrophotometrically. To obtain the maximum sensitivity, the effective reaction variables were optimized. Under optimized experimental conditions, calibration graph was linear over the range 0.2–54.0 mg L⁻¹. The calculated detection limit (3s_b/m) was 0.14 mg L⁻¹ for six replicate determinations of blank signal. The interfering effect of various species was also investigated. The present method was successfully applied for the determination of dexamethasone in pharmaceutical and biological samples satisfactorily.

Cushing's disease, also known as adrenocorticotropic hormone (ACTH)-secreting pituitary adenomas (PAs) that cause excess cortisol production, accounts for up to 85% of corticotrophin-dependent Cushing's syndrome cases. However, the genetic alterations in this disease are unclear. Here, we performed whole-exome sequencing of DNA derived from 12 ACTH-secreting PAs and matched blood samples, which revealed three types of somatic mutations in a candidate gene, USP8 (encoding ubiquitin-specific protease 8), exclusively in exon 14 in 8 of 12 ACTH-secreting PAs. We further evaluated somatic USP8 mutations in additional 258 PAs by Sanger sequencing. Targeted sequencing further identified a total of 17 types of USP8 variants in 67 of 108 ACTH-secreting PAs (62.04%). However, none of these mutations was detected in other types of PAs (n = 150). These mutations aggregate within the 14-3-3 binding motif of USP8 and disrupt the interaction between USP8 and 14-3-3 protein, resulting in an elevated capacity to protect EGFR from lysosomal degradation. Accordingly, PAs with mutated USP8 display a higher incidence of EGFR expression, elevated EGFR protein abundance and mRNA expression levels of POMC, which encodes the precursor of ACTH. PAs with mutated USP8 are significantly smaller in size and have higher ACTH production than wild-type PAs. In surgically resected primary USP8-mutated tumor cells, USP8 knockdown or blocking EGFR effectively attenuates ACTH secretion. Taken together, somatic gain-of-function USP8 mutations are common and contribute to ACTH overproduction in Cushing's disease. Inhibition of USP8 or EGFR is promising for treating USP8-mutated corticotrophin adenoma. Our study highlights the potentially functional mutated gene in Cushing's disease and provides insights into the therapeutics of this disease.

• Adult
• Aged
• Binding Sites/genetics
• Female
• Humans
• Hypothalamo-Hypophyseal System/metabolism
• Male
• Metabolism, Inborn Errors/genetics
• Metabolism, Inborn Errors/metabolism
• Middle Aged
• Pituitary-Adrenal System/metabolism
• Point Mutation
• Receptors, Glucocorticoid/deficiency
• Receptors, Glucocorticoid/genetics
• Receptors, Glucocorticoid/metabolism

• dendritic spine
• plasticity
• hpa axis
• rhythms
• glucocorticoid resistance
• transcription
• fkbp5
• mkp-1

• Animals
• Brain/metabolism
• Brain-Derived Neurotrophic Factor/metabolism
• Glucocorticoids/metabolism
• Humans
• Neuronal Plasticity/physiology
• Neurons/metabolism
• Signal Transduction/physiology

• MH086651 NIMH NIH HHS
• NS21072 NINDS NIH HHS
• R01 NS021072 NINDS NIH HHS
• R01 AG025970 NIA NIH HHS
• R01 MH086651 NIMH NIH HHS
• R56 NS021072 NINDS NIH HHS

• Animals
• COS Cells
• Cells, Cultured
• Chlorocebus aethiops
• Cricetinae
• DNA/metabolism
• HCT116 Cells
• HeLa Cells
• Humans
• Hydrophobic and Hydrophilic Interactions
• Metabolism, Inborn Errors/genetics
• Point Mutation/physiology
• Protein Binding/genetics
• Protein Interaction Domains and Motifs/genetics
• Protein Interaction Domains and Motifs/physiology
• Receptors, Glucocorticoid/chemistry
• Receptors, Glucocorticoid/deficiency
• Receptors, Glucocorticoid/genetics
• Structure-Activity Relationship

• Intramural NIH HHS

• Adrenocorticotropic Hormone/metabolism
• Drug Resistance/genetics
• Glucocorticoids/metabolism
• Glucocorticoids/pharmacology
• Humans
• Hypothalamo-Hypophyseal System/metabolism
• Hypothalamo-Hypophyseal System/physiology
• Metabolism, Inborn Errors/diagnosis
• Metabolism, Inborn Errors/genetics
• Metabolism, Inborn Errors/metabolism
• Metabolism, Inborn Errors/physiopathology
• Models, Biological
• Mutation/physiology
• Pituitary-Adrenal System/metabolism
• Pituitary-Adrenal System/physiology
• Receptors, Glucocorticoid/deficiency
• Receptors, Glucocorticoid/genetics
• Receptors, Glucocorticoid/metabolism
• Signal Transduction/genetics
• Syndrome

• ZIA HD008732-12 Intramural NIH HHS

• hpa axis
• peromyscus californicus
• stress
• corticosterone
• fecal glucocorticoid metabolites
• diurnal rhythm

• Animals
• Circadian Rhythm/drug effects
• Corticosterone/blood
• Dexamethasone/pharmacology
• Female
• Glucocorticoids/metabolism
• Hypothalamo-Hypophyseal System/drug effects
• Hypothalamo-Hypophyseal System/metabolism
• Male
• Mice
• Pituitary-Adrenal System/drug effects
• Pituitary-Adrenal System/metabolism

• R21 MH087806 NIMH NIH HHS
• 1R21MH087806 NIMH NIH HHS

• HPA axis
• aging
• inflammation
• inflammatory disease
• older adults
• stress

• Aged
• Aged, 80 and over
• Aging
• Cytokines/blood
• Humans
• Hypothalamo-Hypophyseal System/physiology
• Immunity
• Immunomodulation
• Inflammation/immunology
• Neurosecretory Systems/physiology
• Pituitary-Adrenal System/physiology
• Stress, Psychological/immunology

• R24 AG031089 NIA NIH HHS
• R24 AG031089-01 NIA NIH HHS

• Cardiovascular Risk Factors
• Insulin Resistance
• Metabolic Syndrome
• Thyroid Function

• Adult
• Asian People
• Blood Glucose/analysis
• Blood Pressure
• Cholesterol, HDL/blood
• Cholesterol, LDL/blood
• Female
• Follow-Up Studies
• Humans
• Logistic Models
• Male
• Metabolic Syndrome/physiopathology
• Middle Aged
• Predictive Value of Tests
• Republic of Korea
• Risk Factors
• Thyroid Gland/physiopathology
• Thyrotropin/blood
• Thyroxine/blood
• Triglycerides/blood
• Waist Circumference

• glucocorticoid receptor
• primary generalized glucocorticoid resistance
• glucocorticoid signal transduction

• Animals
• Glucocorticoids/genetics
• Glucocorticoids/metabolism
• Humans
• Mutation
• Receptors, Glucocorticoid/genetics
• Receptors, Glucocorticoid/metabolism
• Signal Transduction/genetics

• Intramural NIH HHS

• human glucocorticoid receptor (hgr)
• generalized glucocorticoid resistance
• mutations in the hgr gene
• polymorphisms of the hgr gene

• Drug Resistance/genetics
• Gene Expression Regulation
• Glucocorticoids/metabolism
• Glucocorticoids/pharmacology
• Humans
• Mutation
• Protein Processing, Post-Translational
• Protein Structure, Tertiary
• Receptors, Glucocorticoid/chemistry
• Receptors, Glucocorticoid/genetics
• Receptors, Glucocorticoid/metabolism
• Response Elements/genetics

• ZIA HD008732-08 Intramural NIH HHS

• Anemia, Hemolytic, Autoimmune/chemically induced
• Anemia, Hemolytic, Autoimmune/etiology
• Anemia, Hemolytic, Autoimmune/therapy
• Antineoplastic Agents/adverse effects
• Antineoplastic Agents/therapeutic use
• Humans
• Leukemia, Lymphocytic, Chronic, B-Cell/complications
• Leukemia, Lymphocytic, Chronic, B-Cell/etiology
• Leukemia, Lymphocytic, Chronic, B-Cell/therapy
• Models, Biological
• Vidarabine/adverse effects
• Vidarabine/analogs & derivatives
• Vidarabine/therapeutic use

• Amino Acid Sequence
• Drug Resistance/genetics
• Glucocorticoids/pharmacology
• Humans
• Molecular Sequence Data
• Mutation
• Receptors, Glucocorticoid/chemistry
• Receptors, Glucocorticoid/genetics
• Response Elements/physiology
• Signal Transduction

• Intramural NIH HHS

• Active Transport, Cell Nucleus/physiology
• Animals
• Binding Sites
• COS Cells
• Child
• Chlorocebus aethiops
• Endocrine System Diseases/genetics
• Endocrine System Diseases/metabolism
• Glucocorticoids/metabolism
• Humans
• Ligands
• Male
• Nuclear Receptor Coactivator 2/metabolism
• Point Mutation
• Protein Structure, Secondary
• Receptors, Glucocorticoid/chemistry
• Receptors, Glucocorticoid/genetics
• Receptors, Glucocorticoid/metabolism
• Signal Transduction/physiology
• Transfection

• Intramural NIH HHS