Transcriptional and physiological responses to chronic ACTH treatment by the mouse kidney

Keyphrases

• Physiological Response 100%
• Mouse Kidney 100%
• Transcriptional Response 100%
• Mineralocorticoid 100%
• ACTH Therapy 100%
• Glucocorticoid Excess 66%
• Gene Expression 33%
• Vitamin D 33%
• Oxidative Stress 33%
• Enzyme System 33%
• Weight Gain 33%
• Kidney 33%
• Metabolism 33%
• Thymus 33%
• Renal Function 33%
• Involution 33%
• Adverse Effects 33%
• Corticosteroids 33%
• Organic Anions 33%
• Major Change 33%
• Plasma Renin Activity 33%
• Xenobiotic Metabolism 33%
• Hematocrit 33%
• Physiological Significance 33%
• Deoxycorticosterone 33%
• Induced Hypertension 33%
• Antinatriuresis 33%
• CYP24A1 33%
• CYP27B1 33%
• Aldosterone 33%
• NR3C1 33%
• Electrolyte Homeostasis 33%
• Kaliuresis 33%
• Hypertonicity 33%
• Fluid Homeostasis 33%
• Urine Electrolytes 33%
• Electrolyte Excretion 33%
• HSD11B1 33%
• FKBP5 33%
• TRPV5 33%
• Volume Contraction 33%
• Water Turnover 33%
• Calciuria 33%
• Calb1 33%
• Phosphaturia 33%
• Gene Encoding 33%
• Metabolic Pathways 33%
• Urinary Steroids 33%

Biochemistry, Genetics and Molecular Biology

• Adrenocorticotropic Hormone 100%
• Glucocorticoid 66%
• Mineralocorticoid 33%
• Metabolic Pathway 22%
• Corticosteroid 11%
• Plasma Renin Activity 11%
• Organic Anion 11%
• Enzyme 11%
• Gene Expression 11%
• Oxidative Stress 11%
• Homeostasis 11%
• Vitamin D 11%
• Xenobiotic Metabolism 11%
• Hematocrit 11%
• Kidney Function 11%
• Kaliuresis 11%
• Involution 11%
• Calcium Urine Level 11%
• Hypertonic Solution 11%
• Steroid Urine Level 11%
• Electrolyte Urine Level 11%
• Aldosterone 11%
• 11-Deoxycorticosterone 11%