Ae. Alekseev et al., BURST KINETICS OF COEXPRESSED KIR6.2 SUR1 CLONES - COMPARISON OF RECOMBINANT WITH NATIVE ATP-SENSITIVE K+ CHANNEL BEHAVIOR/, The Journal of membrane biology, 159(2), 1997, pp. 161-168
Co-expression of clones encoding Kir6.2, a K+ inward rectifier, and SU
R1, a sulfonylurea receptor, reconstitutes elementary features of ATP-
sensitive K+ (K-ATP) channels. However, the precise kinetic properties
of Kir6.2/SUR1 clones remain unknown. Herein, intraburst kinetics of
Kir6.2/SUR1 channel activity, heterologously co-expressed in COS cells
, displayed mean closed times from 0.7 +/- 0.1 to 0.4 +/- 0.03 msec, a
nd from 0.4 +/- 0.1 to 2.0 +/- 0.2 msec, and mean open times from 1.9
+/- 0.4 to 4.5 +/- 0.8 msec, and from 12.1 +/- 2.4 to 5.0 +/- 0.2 msec
between -100 and -20 mV, and +20 to +80 mV, respectively. Burst durat
ion for Kir6.2/SUR1 activity was 17.9 +/- 1.8 msec with 5.6 +/- 1.5 cl
osings per burst. Burst kinetics of the Kir6.2/SUR1 activity could be
fitted by a four-state kinetic model defining transitions between one
open and three closed states with forward and backward rate constants
of 1905 +/- 77 and 322 +/- 27 sec(-1) for intraburst, 61.8 +/- 6.6 and
23.9 +/- 5.8 sec(-1) for interburst, 12.4 +/- 6.0 and 13.6 +/- 2.9 se
c(-1) for intercluster events, respectively. Intraburst kinetic proper
ties of Kir6.2/SUR1 clones were essentially indistinguishable from pan
creatic or cardiac K-ATP channel phenotypes, indicating that intraburs
t kinetics per se were insufficient to classify recombinant Kir6.2/SUR
1 amongst native K-ATP channels. Yet, burst kinetic behavior of Kir6.2
/SUR1 although similar to pancreatic, was different from that of cardi
ac K-ATP channels. Thus, expression of Kir6.2/SUR1 proteins away from
the pancreatic microenvironment, confers the burst kinetic identity of
pancreatic, but not cardiac K-ATP channels. This study reports the ki
netic properties of Kir6.2/SUR1 clones which could serve in the furthe
r characterization of novel K-ATP channel clones.