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World J Biol Chem. May 26, 2014; 5(2): 85-92
Published online May 26, 2014. doi: 10.4331/wjbc.v5.i2.85
Published online May 26, 2014. doi: 10.4331/wjbc.v5.i2.85
Oxidation of KCNB1 K+ channels in central nervous system and beyond
Federico Sesti, Xilong Wu, Department of Neuroscience and Cell Biology, Robert Wood Johnson Medical School, Rutgers University, Piscataway, NJ 08854, United States
Shuang Liu, Department of Neurology, Jinan Central Hospital, Jinan 50013, Shandong Province, China
Author contributions: Sesti F and Wu X collected literature; Sesti F, Wu X and Liu S discussed the manuscript; Sesti F wrote the manuscript; Liu S prepared the figure.
Supported by National Science Foundation Grant to Sesti F, No. 1026958
Correspondence to: Federico Sesti, PhD, Department of Neuroscience and Cell Biology, Robert Wood Johnson Medical School, Rutgers University, RWJMS Research Building 683, Hoes Lane West Piscataway, Piscataway, NJ 08854, United States. federico.sesti@rutgers.edu
Telephone: +1-732-2354032 Fax: +1-732-2355038
Received: November 5, 2013
Revised: January 26, 2014
Accepted: March 3, 2014
Published online: May 26, 2014
Revised: January 26, 2014
Accepted: March 3, 2014
Published online: May 26, 2014
Core Tip
Core tip: KCNB1 is a K+ channel that plays a key role in the brain, pancreas and cardiovascular system. KCNB1 is unique in that it induces apoptosis in association with oxidative stress. In this review article we discuss the diverse roles of this channel in the organs where it is expressed including recent advances in the molecular mechanisms through which KCNB1 causes cytotoxicity.