ライフサイエンスコーパス: mean open time

1 in long shut times and a robust increase in mean open time.

2 nel probability, while exerting no effect on mean open time.

3 ity of channel opening and increased channel mean open time.

4 L receptors had impaired gating with shorter mean open time.

5 y a single exponential, showed a decrease in mean open time.

6 nce markedly increases the small conductance mean open time.

7 longest closed time constant, so increasing mean open time.

8 e-channel conductance, reversal potential or mean open time.

9 hange in conductance, reversal potential, or mean open time.

10 , and a smaller increase in opening rate and mean open time.

11 el conductance but instead increased channel mean open time.

12 ift could be accounted for by the changes in mean open time.

13 ly lower open probability (NP(o)) and longer mean open time.

14 icant effect on unitary current amplitude or mean open time.

15 bility of the receptor with no change in the mean open time.

16 s (<6 mM) increased the open probability and mean open time.

17 osed time without significant changes in the mean open time.

18 in this range for dSlo had little effect on mean open time.

19 or 3000 microM then typically increased dSlo mean open time.

20 annel activity by increasing the duration of mean open times.

21 rease in mean closed times and a decrease in mean open times.

22 The F1304Q mutation increased mean open time (1.7 fold at -20 mV) and reduced the prob

23 % decrease in open probability by decreasing mean open time 2.5-fold and by increasing mean closed ti

24 Mean open time and burst duration were decreased in the

25 Mean open time and conductance of single channels in GIR

26 Both mean open time and desensitization were dependent primar

27 conductance was caused by decreased channel mean open time and increased channel mean closed time.

28 mine inhibited the channel by decreasing the mean open time and introducing transitions to a long clo

29 300 microM PB had similar main conductance, mean open time and mean burst duration as those activate

30 P increased reversibly the open probability, mean open time and mean burst duration of 4-AP-sensitive

31 II or protein kinase C activity, reduced the mean open time and mean open probability of 115 +/- 6 pS

32 x-2 treatment was found to increase both the mean open time and open probability of NMDA receptors.

33 DCS increased the mean open time and open probability of NR1/NR2C receptor

34 ir influence, at least in part, by enhancing mean open time and single-channel conductance.

35 Block manifested as a reduction in the mean open time and the emergence of a closed state, with

36 eased P(open) at a given voltage, increasing mean open time and the number of openings per burst.

37 lpha6(R46W)beta2delta single-channel current mean open times and burst durations were reduced.

38 were characterized by drastically elongated mean open times and distinctly slower time constants of

39 ro M Ca(2+) by decreasing channel events and mean open times and increasing mean close times.

40 ed maximal open probability, and a shortened mean open-time and prolonged mean closed-time durations.

41 markedly increased apparent desensitization, mean open time, and peak current density.

42 reducing open probability (P(o)), shortening mean open time, and prolonging mean closed time.

43 rance of the residual state, increase in the mean open time, and slowing of the transition times betw

44 The overall mean open time at +60 mV was approximately 4 ms, compare

45 state probability of hemichannel opening and mean open times at negative potentials, was observed in

46 e in Popen (39 +/- 9 %; n = 5) by decreasing mean open time, burst length and total open time per bur

47 ctly phosphorylated PC2, which increased the mean open time but not the single channel conductance of

48 es the activation threshold and shortens the mean open time but unexpectedly leads to a complete loss

49 CaM decreased mean open times but increased channel events, without si

50 dependent closings of channels after a given mean open time, but we found no correlation of terminati

51 e channel open probability by 9-fold and the mean open time by 12-fold.

52 rom dwell time histograms, but increased the mean open time by affecting the channel open probability

53 es that SP acts through reduction of channel mean open-time (cmot): GABA(A) cmot being reduced by app

54 The mean open times determined in selected mutants could be

55 The mean open time directly measured from 43 GABA-induced ch

56 robability of opening increased 4-fold while mean open time doubled.

57 of alpha1beta2 receptor channels by reducing mean open time due to a reduction in the proportion of l

58 lar to steroids, BI-2 acts by prolonging the mean open time duration through an effect on the duratio

59 and that binding of Gbetagamma prolongs its mean open time duration.

60 In global terms, PB increased the mean open time for events in clusters, without changing

61 -attached patch recordings revealed that the mean open time for single Cl- channels in response to 2

62 The mean open time for the 38 pS state (0.74 +/- 0.07 ms) wa

63 channels, 100 microM disopyramide decreased mean open time from 1.64 +/- 0.08 to 0.34 +/- 0.04 msec.

64 Epo (2 U/mL) increased both mean open time (from 4.27 +/- 0.75 to 11.15 +/- 1.80 ms)

65 ts exhibited two conductances, each with two mean open times (gamma1 = 17 pS, tau1 = 3.7 msec, and ta

66 The mean open time in the presence of 100 microM picrotoxin

67 aracterized by extremely slow kinetics, with mean open times in the range of seconds.

68 the InsP3R/Ca2+ channel open probability and mean open time increased significantly.

69 obability increased by approximately 20% and mean open times increased by approximately 4 ms, compare

70 2+) in the range of 5 to 30 microM increases mean open time, increasing Cai2+ in this range for dSlo

71 sed with transmembrane potential, making the mean open time moderately voltage dependent (tau(open) c

72 have two open-time populations with the same mean open times (MOTs).

73 t 50 mus in physiological conditions, with a mean open time of 0.5 ms.

74 h a mean chord conductance of 32 +/- 6 pS, a mean open time of 1.0 +/- 0.3 ms and a mean burst length

75 spectral density distribution gave a channel mean open time of 12.7+/-1.5 ms, range 6.37-23.42 ms.

76 mV with a reversal potential around 0 mV, a mean open time of 2.6 +/- 0.2 ms and a mean burst length

77 2+) reduces the frequency of opening and the mean open time of alpha7 nAChR channels, these data sugg

78 PNU-120596 increased the channel mean open time of alpha7 nAChRs but had no effect on ion

79 s resistance of the recording (R(A)) and the mean open time of AMPA channels.

80 10 microM PhTX-343 significantly reduced the mean open time of channel openings evoked by 1 microM AC

81 t caused only a small decrease (7.5%) in the mean open time of channel openings induced by 1 microM A

82 Moreover, RXP-E increased mean open time of Cx43 channels.

83 7.4), but not pH 7.9, ifenprodil reduces the mean open time of GluN1/GluN2B receptors, which may be r

84 aesthetics either increased or decreased the mean open time of K+-selective ion channels without alte

85 The mean open time of KirNB channels (1.1 ms) was almost the

86 The apparent mean open time of NR1/NR2C receptors was brief (0.52 +/-

87 a weak correlation between ethanol IC50 and mean open time of NR2A(Met823) mutants that was dependen

88 All three drugs reduced the mean open time of single channels and increased the prob

89 a voltage-independent manner and reduced the mean open time of single channels without affecting thei

90 el recordings revealed that NEFA reduces the mean open time of single NMDA-activated channels in a co

91 -trans-14,15-EETA (1-3 x 10(-6) m) increased mean open time of small conductance K(+) channels (13-14

92 Picrotoxinin and picrotin decreased the mean open time of the channel in a concentration-depende

93 e channel kinetic analyses revealed that the mean open time of the channel increased monotonically wi

94 The mean open time of the channel was quite long, with a ran

95 t significantly affecting the conductance or mean open time of the channel.

96 showed a clear positive correlation with the mean open time of the channel.

97 Mean open time of the dominant kinetic component decreas

98 or decrease the rate of desensitization and mean open time of the ion channel.

99 cy of LCC reopening, and a slower decline in mean open time of the LCC.

100 unitary conductance, reversal potential and mean open time of the single-channel currents were simil

101 rtant regulatory mechanism that shortens the mean open time of these otherwise long-lasting high-volt

102 nce of the two channels was similar, but the mean open time of unitary events was shorter for express

103 le-exponential open-time distributions, with mean open times of 279 +/- 58 ms (n = 4) for IRK1 and 23

104 of open-time duration and the dependence of mean open time on [Ca2+] are explained by populations of

105 dent increase in both open probabilities and mean open times on KcsA in artificial bilayers.

106 g channel opening frequency without altering mean open time or EC(50) values for glutamate or glycine

107 n kinetics of mu 1-F1304Q but did not modify mean open time or fast-inactivation kinetics.

108 ers of single channel activity (conductance, mean open time or frequency of opening).

109 e-out patches without significantly changing mean open time or single-channel conductance, suggesting

110 he Na+ single channel current amplitude, the mean open time or the mean closed time, but increased th

111 th no change in unitary conductance, channel mean open times or burst durations.

112 lved from the open period distributions with mean open times reduced 5-fold by the weakest partial ag

113 F1651A and N1662A mutants also had increased mean open times relative to WT, indicating a slowed rate

114 as calmodulin binding reduced single channel mean open time, resulting in an overall reduction in P(o

115 s, pore size, single channel conductance and mean open time suggest that the rho1 homomeric receptor

116 Mean open time (tau(o)) and mean closed time (tau(c)), o

117 tamoxifen shortens both mean closed time and mean open time; the latter is probably due to an interme

118 demonstrated that PS primarily affected the mean open time to produce its effects: positive modulati

119 pressed with CFTR exhibited decreased Po and mean open time under conditions optimal for PKA-mediated

120 channel open probability, with no change in mean open time, unitary conductance, or reversal potenti

121 ised from Xenopus oocytes, with no change in mean open time, unitary conductance, or reversal potenti

122 The mean open times varied from cell to cell, possibly owing

123 The mean open time was >11-fold longer for a channel mutagen

124 -40 mV and 68 picosiemens at +40 mV, and the mean open time was 0.9 ms at -40 mV.

125 The mean open time was 2.70 +/- 0.95 ms (range, 1.24-4.78 ms

126 Mean open time was 3.2 ms and closed times were 1.0 and

127 Single Na(+) channel mean open time was longer in ankyrin(B)(-/-) versus WT a

128 re particularly brief in WT-Y145V, where the mean open time was reduced from 102 ms at -120 mV in wil

129 In single-channel experiments, mean open time was unaltered and unitary current was onl

130 From the abbreviation of the mean open times, we estimated association rates of appro

131 At positive potentials Po and the longer mean open time were greatly increased.

132 d wild-type CFTR ion channels have identical mean open times when activated by different nucleotide l

133 ase with increased open probability (Po) and mean open time, whereas ENaC co-expressed with CFTR exhi

134 -30 mV and lengthened the longer of the two mean open times without significant effects on other kin