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TABLE OF CONTENTS

  • INTRODUCTION
  • EVOLUTION OF THE GLUCOCORTICOID RECEPTOR
  • STRUCTURE OF THE HUMAN GR GENE AND PROTEIN
  • TRANSCRIPTIONAL AND TRANSLATIONAL REGULATION OF GR ISOFORMS
  • ACTION OF GR
  • 1. Nucleocytoplasmic Shuttling of GRα
  • 2. Mechanisms of Transcriptional Activation by GRα 
  • 3. Interaction of GR with Other Transcription Factors
  • A. Nuclear Factor-kB (NF-kB)
  • B. Activator Protein-1 (AP-1)
  • C. cAMP-Responsive Element-Binding Protein (CREB)
  • D. Transforming Growth Factor (TGF) ß Downstream Smad6
  • E. CAAT/Enhancer-binding Protein (C/EBP)
  • F. Other Transcription Factors
  • FACTORS THAT MODULATE GR ACTION
  • 1. New Ligands with Selective Activities
  • 2. Epigenetic modulation of the GR
  • a. Acetylation and CLOCK-mediated counter regulation of target tissue glucocorticoid action against diurnally fluctuating circulating glucocorticoids
  • b. Phosphorylation
  • c. Ubiquitination
  • d. SUMOylation
  • 3. 11 ß-Hydroxysteroid Dehydrogenases (11ß-HSDs)
  • 4. Chaperones and Cochaperones
  • 6. Chemicals and Other Compounds
  • 7. Non-coding RNA Growth Arrest-specific 5 (Gas5)
  • THE SPLICING VARIANT GRß ISOFORM
  • PATHOLOGIC MODULATION OF GR ACTIVITY
  • 1. Natural Pathologic GR Mutations that Cause Familial/Sporadic Generalized Glucocorticoid Resistance or Chrousos Syndrome
  • 2. GR Mutation-mediated  Hypersensitivity Syndrome
  • 3. GR Polymorphisms
  • 3. Viral Infection
  • A. Human Immunodeficiency Virus Type-1
  • B. Adenovirus
  • ACKNOWLEDGEMENTS