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【电子书分享】急性氧敏感中的信号通路:诺华基金会专题讨论会2

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发表于 2020-6-12 08:03:46 | 显示全部楼层 |阅读模式
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/ O$ S3 y5 ?' v+ o标题(title):Signalling Pathways in Acute Oxygen Sensing: Novartis Foundation Symposium 272& e6 e2 B+ [6 O' C. ~+ D
急性氧敏感中的信号通路:诺华基金会专题讨论会2724 B- f8 V0 ~" S

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作者(author):Novartis Foundation(eds.)7 S% d% O% f7 p6 L$ I
出版社(publisher):
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格式(extension):pdf
( ~& w6 ^: H" h% v; F4 g注意:如果文件下载解压完成后为无法打开的格式,请修改后缀名为格式对应后缀% d7 F$ F* r( }4 V# c6 f
氧传感是许多组织的一项关键生理功能,但传感器的身份、传感器与效应器之间的信号传导途径以及终点效应器机制都是争论的话题。这本书评估了已经提出的各种介质,包括线粒体,NAD(P)H氧化酶,细胞色素p450酶,以及对酶和离子通道的直接影响。人们重新对线粒体的作用感兴趣,部分是基于线粒体抑制剂模拟缺氧的能力,但在机制上几乎没有共识。一些人赞成这样的观点,即主要的信号事件是由于电子传输链(ETC)的普遍抑制而导致的细胞氧化还原状态和活性氧物种(ROS)的减少;另一些人则支持ETC的复合物III的关键作用和ROS生成的增加,而另一些人则怀疑这两种成分中的任何一种是关键的中介。书中讨论了所有这些假设,以及线粒体对生理性缺氧反应能力的概念问题。
  f  V( Q  v! a  M' y6 y! H! k书中涉及的另一个争议领域是端点效应器的身份。一些作者赞成K+通道抑制,随后是去极化和通过L型通道进入Ca2+,而另一些人则认为,从细胞内存储释放Ca2+,或电容性Ca2+进入和其他电压无关的途径可能更为重要。这本书还描述了内皮依赖性钙致敏途径涉及Rho和其他激酶的证据。; S5 N3 l5 T: c+ o9 q1 m  f5 N
虽然其中一些差异可归因于组织间的差异,但许多差异必须与解释或方法上的差异有关。在这本书中,在不同组织中工作的急性氧感应领域的专家讨论了这些争论及其可能的起源,并讨论了解决这些争论的可能途径。4 j, F+ H0 l$ r3 a. q; r
这本书将引起所有在氧气感应领域工作的人们的极大兴趣,特别是癌症和伤口愈合,以及药物发现和生物技术.内容:
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1 e, t9 b8 D5 i: u/ f* ~Oxygen sensing is a key physiological function of many tissues, but the identity of the sensor, the signalling pathways linking the sensor to the effector, and the endpoint effector mechanisms are all subjects of controversy. This book evaluates the various mediators that have been proposed, including the mitochondria, NAD(P)H oxidases, cytochrome p450 enzymes, and direct effects on enzymes and ion channels. There has been a resurgence of interest in the role of mitochondria, based partly on the ability of mitochondrial inhibitors to mimic hypoxia, but there is little consensus concerning mechanisms. Some favour the view that the primary signalling event is a reduction in cell redox state and reactive oxygen species (ROS) due to general inhibition of the electron transport chain (ETC); others support a key role for complex III of the ETC and an increase in ROS generation, while others doubt either of these components is the key intermediary. All these hypotheses are discussed in the book, together with conceptual problems concerning the ability of mitochondria to respond to physiological hypoxia.
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The other area of controversy covered in the book is the identity of the endpoint effector(s). Some authors favour K+ channel inhibition, followed by depolarization and Ca2+ entry via L-type channels, while others propose that release of Ca2+ from intracellular stores, or capacitative Ca2+ entry and other voltage-independent pathways may be more important. The book also describes evidence for an endothelium-dependent Ca2+-sensitizing pathway involving Rho and possibly other kinases.
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) T7 J9 u. ]* A. \ While some of these differences can be attributed to variation between tissues, many must be related to differences in interpretation or methodology. In this book, experts in the field of acute oxygen sensing working in different tissues address these controversies and their possible origins, and discuss possible approaches whereby these controversies might be resolved.
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: K" C, T' o2 \- z4 |! M The book will be of great interest to all those working in fields where oxygen sensing is important, particularly cancer and wound healing, as well as researchers in drug discovery and biotechnology.Content:
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