G Protein-Coupled Receptors in Health and Disease. Part B /

G Protein-Coupled Receptors in Health and Disease. Part B /

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Bibliographic Details
Imprint:Amsterdam ; Boston : Elsevier/Academic Press, 2009.
Description:1 online resource (xii, 173 pages, 4 unnumbered pages of plates) : illustrations (some color).
Language:English
Series:Progress in molecular biology and translational science, 1877-1173 ; v. 89
Progress in molecular biology and translational science ; v. 89.
Subject:
G proteins -- Receptors.
G proteins -- Health aspects.
Cellular signal transduction.
Cellular signal transduction.
G proteins -- Receptors.
Electronic books.
Format: E-Resource Book
URL for this record:http://pi.lib.uchicago.edu/1001/cat/bib/12616311
Hidden Bibliographic Details
Other authors / contributors:Tao, Ya-Xiong, editor.
ISBN:9780123747563
0123747562
1283608588
9781283608589
9786613921031
6613921033
0080911943
9780080911946
Notes:Includes bibliographical references and index.
Text in English.
Summary:G protein-coupled receptors (GPCRs) transduce signals from a diverse array of endogenous ligands, including ions, amino acids, nucleotides, lipids, peptides, and large glycoprotein hormones. They are also responsible for our sensing of exogenous stimuli, including photons and odorants. GPCRs regulate almost every aspect of our physiological functions. It is estimated that 40% to 50% of currently used therapeutic drugs target GPCRs directly or indirectly. Because the current drugs target only a small portion of the GPCRs, opportunities for targeting the remaining GPCRs is enormous. This volume reviews the latest developments in this rapidly advancing field. * This series provides a forum for discussion of new discoveries, approaches, and ideas * Contributions from leading scholars and industry experts * Reference guide for researchers involved in molecular biology and related fields.
Other form:0-12-374756-2
Table of Contents:
  • Contributors
  • Preface
  • GPR56 and Its Related Diseases
  • I. GPR56
  • II. GPR56 and Brain Malformation
  • III. The Role of GPR56 in Brain Development
  • IV. GPR56 and Cancer
  • V. GPR56 Signaling
  • VI. Concluding Remarks
  • References
  • V2R Mutations and Nephrogenic Diabetes Insipidus
  • I. Cellular Actions of Vasopressin
  • II. Rareness and Diversity of AVPR2 Mutations
  • III. Most Mutant V2 Receptors Are Not Transported to the Cell Membrane and Are Retained in the Intracellular Compartments
  • IV. NonpeptLde Vasopressin Receptor Antagonists Act as Pharmacological Chaperones to Functionally Rescue Misfolded Mutant V2 Receptors Responsible for X-Linked NDI
  • V. Gain of Function of the Vasopressin V2 Receptor: Nephrogenic Syndrome of Inappropriate Antidiuresis
  • References
  • Calcium-Sensing Receptor and Associated Diseases
  • I. Calcium Homeostasis
  • II. CASR and Diseases
  • III. CASR is a Family C GPCR
  • IV. Human CASR
  • V. Orthosteric Agonists
  • VI. Allosteric Modifiers
  • VII. Structure and Function
  • VIII. Receptor Downregulation and Protein Kinase C
  • IX. Receptor-Activity-Modifying Proteins and CASR Trafficking
  • X. Ubiquitination and Conformational Checkpoint in CASR Processing
  • XI. CASR and Overview of Signaling Pathways
  • XII. CASR and the Parathyroid
  • XIII. CASR and the Renal Tubule
  • XIV. Disorders Associated with CASR (Table I)
  • XV. CASR Mutation Repertoire
  • XVI. Autoantibodies and the CASR
  • XVII. CASR Polymorphisms
  • XVIII. Altered Expression of CASR and Disease
  • XIX. CASR Allosteric Modifiers in the Clinic
  • XX. Summary
  • References
  • Diseases Associated with Mutations of the Human Lutropin Receptor
  • I. Introduction
  • II. The LHCGR and Human Physiology
  • III. The LHCGR Protein and tire LHCGR Gene
  • IV. Activating Mutations of the LHCGR
  • V. Inactivating Mutations of die LHCGR
  • References
  • Follicle Stimulating Hormone Receptor Mutations and Reproductive Disorders
  • I. Introduction
  • II. Follicle Stimulating Hormone Receptor
  • III. Inactivating FSHR Mutations and Hypergonadotropic Hypogonadism
  • IV. Gain-of-Function FSHR Mutations and Spontaneous Ovarian Hyperstimulation Syndrome
  • V. Structure-Function Insights from Studies of Constitutively Active FSHR Mutants
  • VI. Conclusions
  • References
  • The Human Prostacyclin Receptor: From Structure Function to Disease
  • I. History
  • II. Molecular and Structural Biology
  • III. Pathophysiology
  • IV. Therapeutics
  • V. Genetic Variants
  • References
  • Index

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