Mitochondrial ATP-sensitive potassium channel activity and hypoxic preconditioning are independent of an inwardly rectifying potassium channel subunit inCaenorhabditis elegans
| Autor: | Teresa A. Sherman, Peter V. DiStefano, Andrew P. Wojtovich, Paul S. Brookes, Keith Nehrke |
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| Rok vydání: | 2012 |
| Předmět: |
ATP-sensitive potassium channel
Protein subunit Green Fluorescent Proteins Mutant mKATP Biophysics Preconditioning Mitochondrion Biology Biochemistry Article Animals Genetically Modified KATP Channels Ischemia Stress Physiological Structural Biology Genetic model Genetics Animals Potassium Channels Inwardly Rectifying Caenorhabditis elegans Hypoxia Ischemic Preconditioning Molecular Biology Genes Helminth Wild type Cell Biology biology.organism_classification Potassium channel Kir Mitochondria Cell biology Reperfusion Irk |
| Zdroj: | FEBS Letters. 586:428-434 |
| ISSN: | 0014-5793 |
| DOI: | 10.1016/j.febslet.2012.01.021 |
| Popis: | Hypoxic preconditioning (HP) is an evolutionarily-conserved mechanism that protects an organism against stress. The mitochondrial ATP-sensitive K(+) channel (mK(ATP)) plays an essential role in the protective signaling, but remains molecularly undefined. Several lines of evidence suggest that mK(ATP) may arise from an inward rectifying K(+) channel (Kir). The genetic model organism Caenorhabditis elegans exhibits HP and displays mK(ATP) activity. Here, we investigate the tissue expression profile of the three C. elegans Kir genes and demonstrate that mutant strains where the irk genes have been deleted either individually or in combination can be protected by HP and exhibit robust mK(ATP) channel activity in purified mitochondria. These data suggest that the mK(ATP) in C. elegans does not arise from a Kir derived channel. |
| Databáze: | OpenAIRE |
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