Journal article
Evidence for redox sensing by a human cardiac calcium channel
Scientific Reports, Vol.6, Article number: 19067
2016
Abstract
Ion channels are critical to life and respond rapidly to stimuli to evoke physiological responses. Calcium influx into heart muscle occurs through the ion conducting α1C subunit (Cav1.2) of the L-type Ca2+ channel. Glutathionylation of Cav1.2 results in increased calcium influx and is evident in ischemic human heart. However controversy exists as to whether direct modification of Cav1.2 is responsible for altered function. We directly assessed the function of purified human Cav1.2 in proteoliposomes. Truncation of the C terminus and mutation of cysteines in the N terminal region and cytoplasmic loop III-IV linker did not alter the effects of thiol modifying agents on open probability of the channel. However mutation of cysteines in cytoplasmic loop I-II linker altered open probability and protein folding assessed by thermal shift assay. We find that C543 confers sensitivity of Cav1.2 to oxidative stress and is sufficient to modify channel function and posttranslational folding. Our data provide direct evidence for the calcium channel as a redox sensor that facilitates rapid physiological responses.
Details
- Title
- Evidence for redox sensing by a human cardiac calcium channel
- Authors/Creators
- P. Muralidharan (Author/Creator) - School of Anatomy, Physiology and Human BiologyH. Cserne Szappanos (Author/Creator)E. Ingley (Author/Creator) - UWA Centre for Medical ResearchL. Hool (Author/Creator) - School of Anatomy, Physiology and Human Biology
- Publication Details
- Scientific Reports, Vol.6, Article number: 19067
- Publisher
- Nature Publishing Group
- Identifiers
- 991005544211407891
- Murdoch Affiliation
- Murdoch University
- Language
- English
- Resource Type
- Journal article
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