ライフサイエンスコーパス: inactivated channel

1 conducting states with high affinity for the inactivated channel.

2 terminate without additional recruitment of inactivated channels.

3 the drug does not directly bind to closed or inactivated channels.

4 interfere with MTSET modification of C449 in inactivated channels.

5 gating, with a preference for activated over inactivated channels.

6 myotubes, we found a novel class of stretch-inactivated channels.

7 e-dependent manner, with higher affinity for inactivated channels.

8 d voltages suggestive of an interaction with inactivated channels.

9 hannels, but has little affect on resting or inactivated channels.

10 that cocaine preferentially binds to open or inactivated channels.

11 ot affect the cocaine affinity of resting or inactivated channels.

12 ide, another blocker thought to bind to slow-inactivated channels.

13 and has a much lower affinity for closed and inactivated channels.

14 ymphocytes show that Ko+ can bind to open or inactivated channels.

15 d even more tightly (K(d) = 0.2 muM) to slow-inactivated channels.

16 g of extracellular tetraethylammonium to the inactivated channel, although the tetraethylammonium doe

17 intramembrane charge movement from unblocked inactivated channels and determine the effect of Ca2+ in

18 anesthetics, reduced high-affinity block of inactivated channels and frequency-dependent block of op

19 We found that drugs that target inactivated channels are AF-selective, whereas drugs tha

20 mV was the same, and high affinity block of inactivated channels at -70 mV was the same.

21 resulting in an increase in the fraction of inactivated channels at negative resting voltages.

22 o steady state fast inactivation yet reduced inactivated channel block by cocaine by up to 27-fold an

23 recovered more rapidly than WT channels from inactivated channel block.

24 r demonstrated that TEA bound well to C-type inactivated channels, but did not interfere with MTSET m

25 The role of inactivated channel conformation and use dependence for

26 e and benzocaine bind in the closed and open/inactivated channel conformation is proposed.

27 Consistent with a high affinity for the inactivated channel conformation, lidocaine produced mor

28 4-hydroxybenzoate interact with the open and inactivated channels during repetitive pulses, but durin

29 Affinities of both resting and inactivated channels for R-mexiletine block were approxi

30 subunits dramatically reduce the affinity of inactivated channels for the local anesthetic etidocaine

31 putative cytosolic interface of the S6 helix inactivated channel function and could be candidates for

32 etaflumizone interacts with resting and fast-inactivated channels in a manner that is distinct from o

33 local [Ca(2+)] when the average fraction of inactivated channels is significant.

34 hannels (K(d) = 170 muM) but tightly to fast-inactivated channels (K(d) = 5 muM) and even more tightl

35 nding mechanism, which has high affinity for inactivated channels (KI = 17 microM) and low affinity f

36 gh-affinity, voltage-dependent block of open/inactivated channels linked to stabilization of the S4s

37 We propose that in inactivated channels, residue mu1-N434 interacts directl

38 Rat Vr1, stretch-inactivated channel (SIC), and vanilloid receptor 5' spl

39 , again suggesting a preferential binding to inactivated channel state(s).

40 .8), suggesting that the drug stabilizes the inactivated channel state.

41 eflect preferential drug binding to open and inactivated channel states.

42 from a channel in the inactivated state, and inactivated channels that are bound by K+ will recover w

43 release sites with a substantial fraction of inactivated channels that exhibit puffs and sparks that

44 In inactivated channels, the potency of bupivacaine was inc

45 The current may reflect recovery of inactivated channels through open states, because in Pur

46 ination is facilitated by the recruitment of inactivated channels throughout the duration of the puff

47 for estimating local anaesthetic affinity of inactivated channels was developed to reduce errors due

48 current was minimal and charge movement from inactivated channels was maximal after conditioning to a

49 Mexiletine affinity for inactivated channels was reduced by mutations in IVS6 (V

50 ion, the voltage-dependent gating of stretch-inactivated channels was similar to that of stretch-acti

51 th mexiletine, the dissociation constant for inactivated channels was ~600 times lower (~11 nM), conf

52 of this idea, stretch-activated and stretch-inactivated channels were not detected in the same membr

53 rug block by slowing R-mexiletine binding to inactivated channels, whereas rhF1762A reduced block by

54 slow, concentration-dependent inhibition of inactivated channels, which had an apparent K(D) of 3.4