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Progress in molecular biology and translational science. volume 133, RGS protein physiology and pathophysiology /

RGS Protein Physiology and Pathophysiology describes the current, state-of-the-art research occurring in the laboratories of leaders in the RGS protein field that utilize genetic mouse models to interrogate the function of RGS proteins in vivo. Each chapter describes the elucidated role of a specifi...

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Detalles Bibliográficos
Clasificación:Libro Electrónico
Otros Autores: Fisher, Rory A. (Editor )
Formato: Electrónico eBook
Idioma:Inglés
Publicado: Waltham, MA : Academic Press, 2015.
Edición:First edition.
Colección:Progress in molecular biology and translational science ; volume 133.
Temas:
Acceso en línea:Texto completo
Texto completo

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245 0 0 |a Progress in molecular biology and translational science.  |n volume 133,  |p RGS protein physiology and pathophysiology /  |c edited by Rory A. Fisher, Department of Pharmacology, University of Iowa. 
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490 1 |a Progress in molecular biology and translational science ;  |v volume 133 
504 |a Includes bibliographical references and index. 
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505 8 |6 880-01  |a Chapter Three: RGS Protein Regulation of Phototransduction1. Introduction; 2. From Photon to a Neural Signal: The Wonder of Phototransduction; 3. The Need for Speed: Discrepancy on G-Protein Shutoff During Phototransduction Recovery; 4. Cannot Do It Alone: The Transducin GAP Is a Protein Complex; 5. Translocation and Regulation of RGS9-1; 6. Conclusions: Emerging Functions of RGS Proteins in the Visual System; References; Chapter Four: Role of Regulators of G Protein Signaling Proteins in Bone Physiology and Pathophysiology; 1. Introduction to Bone; 2. The GPCR-G Protein-RGS Signaling Pathway. 
505 8 |a 2.1. The G Protein Complex2.2. Introduction to RGS Proteins; 3. RGS Proteins in Osteoblasts; 3.1. RGS2 in Osteoblasts; 3.2. RGS5 in Osteoblasts; 3.3. Axin in Osteoblasts; 4. RGS Proteins in Osteoclasts; 4.1. RGS10 in Osteoclasts; 4.2. RGS12 in Osteoclasts; 4.3. RGS18 in Osteoclasts; 5. GPCR-RGS Proteins Signaling in Skeletal Physiology; 5.1. RGS Proteins and PTH/PTHrP Signaling in Bone; 5.2. RGS Proteins and Wnt Signaling in Bone; 5.3. RGS Proteins and Ca2+ Oscillations; 6. GPCR/RGS Signaling in Skeletal Disorders; 6.1. PTH1R and GPCR 48 in Skeletal Development and Diseases. 
505 8 |a 6.2. CaSR in Skeletal Development and Disease6.3. The Canonical Wnt Signaling Pathway in Bone Disease; 6.3.1. Axin in Bone Development and Bone Disease; 6.3.2. Mouse Models of Wnt Signaling in Skeletal Homeostasis; 6.3.3. Bone Diseases of Defective Wnt Signaling; 6.4. RGS Proteins in Inflammatory Bone Disease; 7. Conclusion and Perspectives; Acknowledgments; References; Chapter Five: Regulator of G Protein Signaling 2: A Versatile Regulator of Vascular Function; 1. Introduction; 2. Structure and Biochemical Functions of RGS2; 3. Regulation of RGS2 Expression. 
520 |a RGS Protein Physiology and Pathophysiology describes the current, state-of-the-art research occurring in the laboratories of leaders in the RGS protein field that utilize genetic mouse models to interrogate the function of RGS proteins in vivo. Each chapter describes the elucidated role of a specific RGS protein or family of RGS proteins in normal physiology and/or disease with particular emphasis on how these discoveries inform healthcare and drug discovery. The work is a timely reference as drugs targeting G protein coupled receptors represent 40% of currently marketed therapeutics. B. 
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700 1 |a Fisher, Rory A.,  |e editor. 
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880 0 |6 505-00/(S  |a Front Cover; RGS Protein Physiology and Pathophysiology; Copyright; Contents; Contributors; Preface; Chapter One: Introduction: G Protein-coupled Receptors and RGS Proteins; 1. GPCR Physiology, Pathophysiology, and Pharmacology; 2. GPCR Signal Transduction: Heterotrimeric G Proteins; 3. G Protein Regulation; 4. RGS Proteins; References; Chapter Two: RGS-Insensitive G Proteins as In Vivo Probes of RGS Function; 1. Introduction; 2. Genetic Models of the Role of RGS in Physiology and Pathophysiology; 3. RGS Knockouts Versus RGS-Insensitive Gα Knock-In Models. 
880 8 |6 505-01/(S  |a 4. Phenotypes of Gαi2 G184S Mutant Knock-In Mice4.1. Signaling; 4.2. Heart; 4.2.1. Heart Rate; 4.2.2. Contractility; 4.2.3. Ischemia/Reperfusion Injury; 4.2.4. Heart Failure/Fibrosis; 4.2.5. Inflammation and Immunity; 4.3. Central Nervous System and Depression; 5. Observed Phenotypes with Gαo+/G184S Knock-In Mice; 5.1. General Phenotype; 5.2. Effects on Opioid Signaling; 5.3. GNAO1 in Epilepsy; 5.4. GNAO1 G184S Mutants; 5.4.1. Slice Studies; 5.4.2. In Vivo; 5.5. EIEE17: Human Mutant GNAO1 Alleles in Epilepsy; 6. Summary and Conclusions; References.