Limiting oxidation in potassium channel kv2.1 using cysteine-alanine mutation

TL;DRAbstract

The Kv2.1 (KCNB1) channel is expressed in the cortex and hippocampus. Interaction between cysteine residues of the kv2.1 channel plays a role in the formation of disulfide bonds. Disulfide bond formation following oxidative stress suggests that cysteine interaction in voltage-gated K+ channel kv2.1 plays a key role in the oxidation of kv2.1. Previous research has shown that oxidation of potassium (K+) channels by reactive oxygen species (ROS) is a major factor in the loss of neuronal function [6]. The purpose of this study was to use cysteine-alanine mutations to prevent oxidation of K+ channel kv2.1. In this thesis, the anti-oxidant properties of the double mutant C73AC29A were investigated. The affects were observed using site-directed mutagenesis and the polymerase chain reaction (PCR). PCR was utilized to form a double mutant between C73A and C29A. SDS-Page and Western Blot analysis were used to analyze whether there was more or less oxidation in the double mutant C73AC29A compared

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