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Mitochondrial ATP‐sensitive potassium channel activity and hypoxic preconditioning are independent of an inwardly rectifying potassium channel subunit in Caenorhabditis elegans
Author(s) -
Wojtovich Andrew P.,
DiStefano Peter,
Sherman Teresa,
Brookes Paul S.,
Nehrke Keith
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.01.021
Subject(s) - potassium channel , protein subunit , caenorhabditis elegans , atp sensitive potassium channel , potassium , chemistry , biophysics , microbiology and biotechnology , mitochondrion , inward rectifier potassium ion channel , biochemistry , biology , ion channel , endocrinology , receptor , glibenclamide , gene , diabetes mellitus , organic chemistry
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.