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Titlebook: G Proteins, Receptors, and Disease; Allen M. Spiegel (Chief, Metabolic Diseases Branch Book 1998 Springer Science+Business Media New York

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发表于 2025-3-21 18:00:03 | 显示全部楼层 |阅读模式
书目名称G Proteins, Receptors, and Disease
编辑Allen M. Spiegel (Chief, Metabolic Diseases Branch
视频video
丛书名称Contemporary Endocrinology
图书封面Titlebook: G Proteins, Receptors, and Disease;  Allen M. Spiegel (Chief, Metabolic Diseases Branch Book 1998 Springer Science+Business Media New York
描述More than a collection of review articles, G Proteins, Receptors, and Disease summarizes in depth the state of our knowledge today concerning not only how cells communicate via G-protein-coupled signal transduction processes, but also how defects in these proteins and their receptors can cause serious human disease involving many different organ systems. Written by leading investigators, each chapter describes in detail the structure and function of a particular G protein or receptor, outlines possible mutations, and discusses fully the molecular pathogenesis of associated diseases. Diagnostic and therapeutic implications are also discussed when relevant...In its unique blend of cutting-edge basic science and clinical medicine, G Proteins, Receptors, and Disease offers deep insights into the physiological significance of this key signal transduction pathway, as well as into the molecular basis of diseases ranging from obesity to malignancy. The basic understanding of the complex signal transduction process achieved here provides a firm foundation for future efforts to prevent and cure these diseases.
出版日期Book 1998
关键词ACTH; Diabetes; Diabetes mellitus; G proteins; Gonadotropin; insulin; insulin resistance; signal transducti
版次1
doihttps://doi.org/10.1007/978-1-4612-1802-9
isbn_softcover978-1-4612-7290-8
isbn_ebook978-1-4612-1802-9Series ISSN 2523-3785 Series E-ISSN 2523-3793
issn_series 2523-3785
copyrightSpringer Science+Business Media New York 1998
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Albright Hereditary Osteodystrophy, Pseudohypoparathyroidism, and Gs Deficiency, characterized by hypocalcemia, hyperphosphatemia, and elevation of serum PTH in the setting of normal renal function, is the major clinical feature. In the original report by Fuller Albright, PHP patients showed reduced calcemic and phosphaturic responses to injected bovine parathyroid extract comp
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,Gαs-Activating Mutations,ot only in all vertebrates, but also in invertebrates, such as . and .. G. couples receptors for numerous peptide hormones and monoamines to stimulation of adenylyl cyclase. Although it is now clear that G-protein βγ-subunits can independently modulate adenylyl cyclase (positively or negatively depe
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,Gα12- and Gα13-Subunits of Heterotrimeric G-Proteins A Novel Family of Oncogenes,receptors in normal and aberrant cell growth. As such, a number of oncogenes have been found to code for altered forms of these receptors ., their ligands (.), or for molecules thought to participate in their growth-promoting pathways .. Another family of structurally related cell-surface receptors
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Hypo- and Hyperthyroidism Caused by Mutations of the TSH Receptor,imarily through a positive control exerted by the pituitary hormone thyroid stimulating hormone (TSH) and a negative control exerted by iodine. In most physiological circumstances the maintenance of eumetabolism requires steady concentrations of circulating thyroid hormones. This is achieved by a cl
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Inactivating and Activating Mutations of the FSH Receptor Gene,that participate in the regulation of reproductive functions, and those of the gonadotropin receptors (R) have received considerable attention. Since the discovery of the first luteinizing hormone receptor (LHR) mutations in 1993 ., more than 15 mutations have been so far reported in this gene (. Ch
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Nephrogenic Diabetes Insipidus and Vasopressin Receptor Mutations,g tubules contain selective cells known as principal cells, responsive to the neurohypophyseal antidiuretic hormone arginine-vasopressin (AVP). The major action of AVP is to facilitate urinary concentration by allowing water to be transported passively down an osmotic gradient between the tubular fl
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