Oxidation of KCNB1 K^+ channels in central nervous system and beyond
Oxidation of KCNB1 K^+ channels in central nervous system and beyond作者机构：Department of Neuroscience and Cell Biology Obert Wood Johnson Medical School Rutgers University Piscataway NJ 08854 United States Department of Neurology Jinan Central Hospital
出 版 物：《World Journal of Biological Chemistry》 (世界生物化学杂志（英文版）（电子版）)
年 卷 期：2014年第5卷第2期
页 面：85-92页
学科分类：1002[医学-临床医学] 100203[医学-老年医学] 10[医学]
基 金：Supported by National Science Foundation Grant to Sesti F No.1026958
主 题：Apoptosis Kv2.1 Aging Reactive oxygen species Alzheimer’ s disease
摘 要：KCNB1, a voltage-gated potassium(K+) channel that conducts a major delayed rectifier current in the brain, pancreas and cardiovascular system is a key player in apoptotic programs associated with oxidative stress. As a result, this protein represents a bona fide drug target for limiting the toxic effects of oxygen radicals. Until recently the consensus view was that reactive oxygen species trigger a pro-apoptotic surge in KCNB1 current via phosphorylation and SNARE-dependent incorpora-tion of KCNB1 channels into the plasma membrane. However, new evidence shows that KCNB1 can be modified by oxidants and that oxidized KCNB1 channels can directly activate pro-apoptotic signaling pathways. Hence, a more articulated picture of the pro-apoptotic role of KCNB1 is emerging in which the protein induces cell s death through distinct molecular mechanisms and activation of multiple pathways. In this review article we discuss the diverse functional, toxic and protective roles that KCNB1 channels play in the major organs where they are expressed.
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