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Titlebook: G Protein-Coupled Receptor Kinases; Vsevolod V. Gurevich,Eugenia V. Gurevich,John J.G. Book 2016 Springer Science+Business Media New York

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書目名稱G Protein-Coupled Receptor Kinases
編輯Vsevolod V. Gurevich,Eugenia V. Gurevich,John J.G.
視頻videohttp://file.papertrans.cn/381/380005/380005.mp4
概述Features detailed examinations of known GRK-dependent mechanisms, both associated with GPCR functions and receptor-independent.Covers a wide range of studies from invertebrates to humans.Provides prac
叢書名稱Methods in Pharmacology and Toxicology
圖書封面Titlebook: G Protein-Coupled Receptor Kinases;  Vsevolod V. Gurevich,Eugenia V. Gurevich,John J.G. Book 2016 Springer Science+Business Media New York
描述This collection explores up-to-date descriptions of known G protein-coupled receptor kinase (GRK)-dependent mechanisms, both associated with G protein-coupled receptor (GPCR) functions and the receptor-independent. The chapters cover a wide range of studies from invertebrates to humans, with sections of the volume covering GRK structure, mechanisms of activation, and interaction with GPCRs, GRKs in cell signaling, as well as physiological and pathophysiological mechanisms regulated by GRKs.? Written for the .Methods in Pharmacology and Toxicology. series, this book features the kind of practical detail necessary for success in the laboratory.?Authoritative and timely, .G Protein-Coupled Receptor Kinases. features the kind of comprehensive mechanistic elucidation of GRK functions and their regulation in cells necessary for a better understanding of cell biology as well as for devising novel research approaches and therapeutic strategies..
出版日期Book 2016
關(guān)鍵詞G protein-coupled receptors (GPCRs); Cell signaling; Pathophysiological regulation; GPCR signaling; GRK
版次1
doihttps://doi.org/10.1007/978-1-4939-3798-1
isbn_softcover978-1-4939-8142-7
isbn_ebook978-1-4939-3798-1Series ISSN 1557-2153 Series E-ISSN 1940-6053
issn_series 1557-2153
copyrightSpringer Science+Business Media New York 2016
The information of publication is updating

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Rainer-Peter Meyer,Fabrizio Moro,Fritz Heftihis chapter summarizes the current state of knowledge, discusses the relationship between GRK1 and GRK7 in the context of . disease, and pinpoints fruitful future directions for advancement of the vision research field.
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https://doi.org/10.1007/3-540-33316-9 cAMP signaling to Epac/PKCε/ERK- mediated pathway. Via mechanisms that remain to be elucidated, low monocyte GRK2 leads to IL-10 deficiency and prolonged inflammatory pain. The clinical relevance of these findings is discussed in the light of the observed decrease of GRK2 in nociceptors, glia and l
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100 Keywords Wirtschaftsprüfung, contractility, and blood pressure, in response to catecholamines and other neurohormones. For these reasons, GPCRs are dynamically regulated to prevent overstimulation that could lead to cardiac diseases like heart failure (HF). This dampening process, known as desensitization, is initiated throug
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