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- W2387200215 abstract "Objectives To study the effects of site-directed mutation R371H and P266T on characters of ATP sensitive potassium channel (KATP) in order to reveal the arrhythmogenic mechanism of the two sites mutation. Methods Wild-type (wt) , R371H or P266T mutant of Kir6. 2 cDNA plus SUR2A were expressed in human embryonic kidney cells. Standard patch-clamp technique was used to study the allosteric modulation of ATP sensitive by intracellular pH. Results Inward rectifier potassium currents were recorded in wt, R371H, P266T successfully. While exposed in different pH, half current inhibition of ATP concentration (IC50) of wt in pH6. 8 was significant higher than that in pH7. 4(70 vs 22μmol/L, P 0. 05) , and the ATP-current curve was shifted to higher ATP concentration. The IC50 of both R371H and P266T in pH 6. 8 and pH 7. 4 had no significant difference. Conclusion The loss of allosteric modulation of ATP sensitive by intracellular pH maybe an important arrhythmogenic mechanism of R371H and P266T mutation." @default.
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- W2387200215 date "2006-01-01" @default.
- W2387200215 modified "2023-09-23" @default.
- W2387200215 title "The effects of site-directed mutation on characters of ATP sensitive potassium channel" @default.
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