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

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 regulat...

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Detalles Bibliográficos
Clasificación:Libro Electrónico
Otros Autores: Tao, Ya-Xiong (Editor )
Formato: Electrónico eBook
Idioma:Inglés
Publicado: Amsterdam ; Boston : Elsevier/Academic Press, [2009]
Colección:Progress in molecular biology and translational science ; v. 89.
Temas:
G proteins > Receptors.
G proteins > Health aspects.
Cellular signal transduction.
Signal Transduction
Prot�eines G > R�ecepteurs.
Transduction du signal cellulaire.
Cellular signal transduction
G proteins > Receptors
Acceso en línea:Texto completo
Texto completo
Tabla de Contenidos:
  • Front Cover; Progress in Molecular Biology and Translational Science G Protein-Coupled Receptors in Health and Disease, Part B; Copyright; Contents; Contributors; Preface; Chapter 1: 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; Acknowledgments; References; Chapter 2: 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 CompartmentsIV. Nonpeptide 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; Chapter 3: 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 ModifiersVII. 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
  • AcknowledgmentsReferences; Chapter 4: Diseases Associated with Mutations of the Human Lutropin Receptor; I. Introduction; II. The LHCGR and Human Physiology; III. The LHCGR Protein and the LHCGR Gene; IV. Activating Mutations of the LHCGR; V. Inactivating Mutations of the LHCGR; Acknowledgments; Note Added in Proof; References; Chapter 5: 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 SyndromeV. Structure-Function Insights from Studies of Constitutively Active FSHR Mutants; VI. Conclusions; Acknowledgments; References; Chapter 6: 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; Color Plate

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