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Titlebook: Transient Receptor Potential Canonical Channels and Brain Diseases; Yizheng Wang Book 2017 The Editor(s) (if applicable) and The Author(s)

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书目名称Transient Receptor Potential Canonical Channels and Brain Diseases
编辑Yizheng Wang
视频video
概述Discusses the findings on the physiological and pathological functions of TRPCs in the brain.Covering the potential roles of TRPCs in brain disorders.Providing students and investigators with comprehe
丛书名称Advances in Experimental Medicine and Biology
图书封面Titlebook: Transient Receptor Potential Canonical Channels and Brain Diseases;  Yizheng Wang Book 2017 The Editor(s) (if applicable) and The Author(s)
描述.This book discusses the latest findings on the physiological and pathological functions of transient receptor potential canonical/classical (TRPC) proteins in the brain. In addition to reviewing the functions of TRPCs in brain development and neuron transmission, it mainly covers the potential roles of TRPCs in brain disorders. TRPC proteins belong to the TRP channel superfamily, which has around 30 members. Just like TRP channels, TRPCs are non-selectively permeable to cations, with a selectivity of calcium over sodium that varies among different members. The TRPC subfamily consists of six members, grouped on the basis of the similarities in gene sequence and protein structure in mammalians. What sets TRPCs apart from other subfamilies in TRPs is that their activation, stimulated by a membrane receptor-phospholipid C (PLC) cascade, contributes to the slow and sustained elevation of intracellular free calcium. Calcium ions, one of the most important types of second messengers, mediate a variety of physiological functions in the brain, including progenitor cell proliferation, dendritic formation, synaptic transmission and neuronal survival. All TRPCs except TRPC7 have been found in
出版日期Book 2017
关键词Brain tumors; Central nerve system; Neural development; Neurological disorders; TRPC proteins
版次1
doihttps://doi.org/10.1007/978-94-024-1088-4
isbn_softcover978-94-024-1486-8
isbn_ebook978-94-024-1088-4Series ISSN 0065-2598 Series E-ISSN 2214-8019
issn_series 0065-2598
copyrightThe Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature B.V. 201
The information of publication is updating

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