ライフサイエンスコーパス: channel open probability

1 linositol bisphosphate) that increase K(ATP) channel open probability.

2 into a dose-dependent decrease in the single-channel open probability.

3 e plasma membrane evoked a rapid decrease in channel open probability.

4 course of sIPSCs and potentiation of single-channel open probability.

5 g the impact of a given Ca2+ transient on SK channel open probability.

6 TSET was associated with a large increase in channel open probability.

7 r activation and may result from a change in channel open probability.

8 on along with a dramatic reduction in single channel open probability.

9 f channel run-down, and decreases the single-channel open probability.

10 D2) by protein kinase A results in increased channel open probability.

11 ing to NR1 causes a 4-fold reduction in NMDA channel open probability.

12 re further evident during analysis of single-channel open probability.

13 mechanism that involves a decrease in single channel open probability.

14 L and K170N, respectively), while increasing channel open probability.

15 ude without a marked reduction in the single-channel open probability.

16 ic response time course and increases single-channel open probability.

17 ediate channel environment, which change the channel open probability.

18 t enhanced Na(+) self-inhibition and reduced channel open probability.

19 hat blocked ENaC palmitoylation also reduced channel open probability.

20 that FLNAC substantially reduces ENaC single channel open probability.

21 AKPWYD)] activated ENaC by increasing single-channel open probability.

22 activity via its own receptor affecting the channel open probability.

23 ha subunit, likely reflecting an increase in channel open probability.

24 to promote dimerization and thereby increase channel open probability.

25 in enhanced calcium influx due to increased channel open probability.

26 ontent, and ryanodine receptor type 2 (RyR2) channel open probability.

27 d by CaMKII and results in a decrease in the channel open probability.

28 minyltransferase increased InsP(3)R-3 single channel open probability.

29 ence time in the plasma membrane, and single-channel open probability.

30 sulfhydryl reduction had limited effects on channel open probability.

31 unteracted by interventions that reduce RyR2 channel open probability.

32 The peptide inhibits ENaC by reducing channel open probability.

33 the opposite effect of increasing intrinsic channel open probability.

34 ly correlating with previous measurements of channel open probability.

35 ross the membrane electric field, modulating channel open probability.

36 pholipid products corresponded to changes in channel open probability.

37 EtOH increased somatic but not dendritic BK channel open probability.

38 micromol/L) and significantly lowered single channel open probability.

39 s extents and rates inversely correlate with channel-open probability.

40 free [Ca(2+)] to <10 nm increased WT single channel open probability 10-fold, but not that of GF BNa

41 ophin-deficient mdx muscle: (1) increased MS channel open probability, (2) a shift of MS channel gati

42 ion of the hKv7.4a channel by decreasing the channel open probability and altering activation kinetic

43 lains this effect in terms of changes in the channel open probability and in the transduction between

44 e of voltage-dependent changes in the single-channel open probability and is not species- or subunit-

45 nomers or CGA/CGB heteromers the InsP3R/Ca2+ channel open probability and mean open time increased si

46 1a/GluN2D receptors are characterized by low channel open probability and prolonged deactivation time

47 pe CaM, CPVT-CaMs caused greater RyR2 single-channel open probability and showed enhanced binding aff

48 exhibited reduced Ca(2+) sensitivity, single-channel open probability and tamoxifen sensitivity.

49 channel analyses showed that both CFTR Cl(-) channel open probability and the number of CFTR Cl(-) ch

50 association rate even though protons reduce channel open probability and thus MK-801 access to its b

51 that H(2)O(2) significantly increased TRPC6 channel open probability and whole-cell currents.

52 They allow one to determine not only the channel-opening probability and rates of receptor desens

53 uction channels, this deflection changes the channels' open probability and elicits an electrical res

54 ive to ATP block, dramatically increased the channel open probability, and affected the interaction o

55 -terminal domains of GluN2A subunits reduces channel open probability, and low-affinity voltage-depen

56 cate that an H620Q mutant, shown to increase channel open probability, and the dual corrector/potenti

57 annel properties-single-channel conductance, channel open probability, and the number of functional c

58 wever, mutations at Glu-92 could also change channel open probability, and these changes correlated w

59 analyses revealed that FMRP loss reduced BK channel open probability, and this defect was compensate

60 conductance, whereas external protons affect channel open probability as well as single-channel condu

61 -Deazaadenosine also blocked the increase in channel open probability associated with addition of ald

62 CaM reduced channel open probability at <10 micro M Ca(2+) by decrea

63 fragment, stabilized by NS309, increases the channel open probability at a given Ca(2+) concentration

64 on of the channel, resulting in a diminished channel open probability at voltages near the resting me

65 ect of N-terminal deletions of Kir6.2 on the channel open probability, ATP sensitivity and sulphonylu

66 binding of two glutamate molecules, with the channel-opening probability being 0.93 +/- 0.10.

67 At-RA significantly reduced single-channel open probability but did not change unitary cond

68 ne the effects of inhibitors not only on the channel-opening probability but also on the opening and

69 cohol increases both alpha and alphabeta4 BK channel open probability, but only alpha BK develops acu

70 esults show that PAS (0.1 mM) reduces single-channel open probability by 50% solely by increasing app

71 ate and glycine potency by 2-fold, increases channel open probability by 6-fold, and reduces receptor

72 e activity of the InsP(3)R by increasing the channel open probability by 9-fold and the mean open tim

73 inhibition, an allosteric down-regulation of channel open probability by extracellular Na(+).

74 ed by brief GABA pulses, THDOC increased the channel open probability by further increasing the numbe

75 Single-channel data showed that SNP reduced channel open probability by reducing channel open freque

76 hes, the PKC-dependent enhancement of cation channel open probability could be prevented by the src h

77 Channel open probability decreased significantly in the

78 es the mean single-channel open duration and channel open probability determined in excised outside-o

79 Channel open probability did not appreciably change over

80 FTR exhibited a two-fold reduction in single channel open probability due primarily to shortened open

81 hannel activation, reflecting an increase in channel open probability due to a loss of the inhibitory

82 The overall channel open probability during a burst was high (mean,

83 ved between agonist concentration and single-channel open probability during the first minute followi

84 Channel open probabilities for PC-2 and S812A show a bel

85 imal recording conditions the maximal single-channel open probability for all three mammalian InsP3R

86 pontaneous KACh activity, 5 mM TEA increased channel open probability fourfold in the absence of adde

87 presence of caveolin-1 significantly reduced channel open probability (from 0.05 +/- 0.01 to 0.005 +/

88 In some recordings from mdx myotubes, MS channel open probability gradually increased to levels a

89 solic GOF mutation was highly active (single-channel open probability >0.3) in the absence of ATP and

90 = 10-20 mmHg) markedly inhibited this BK(Ca) channel open probability in a voltage-dependent manner i

91 sing concentrations of bupivacaine decreased channel open probability in GluN2 subunit- and pH-indepe

92 d an attenuated stimulatory effect on BK(Ca) channel open probability in inside-out membrane patches.

93 of coordinated variation in ATP:ADP and KATP channel open probability in intact cells.

94 se channel/ryanodine receptors and decreases channel open probability in planar lipid bilayers.

95 tability is manifested as an increase in the channel open probability in the absence of ATP (Po(zero)

96 h-affinity binding site and directly enhance channel-open probability in bilayer lipid membrane in a

97 previously showed that PIP(2) increases the channel open probability, in this work we find that acti

98 Single-channel open probability increased in response to negati

99 Channel open probability increased with intracellular [H

100 The agonist-induced channel opening probability increased with bilayer chole

101 hCaV3.2(C456S) mutant channels have a higher channel open probability, induce more calcium influx, an

102 Both models support the notion that channel open probability is modulated by calcium that en

103 ipid bilayers revealed that InsP(3)-mediated channel open probability is significantly reduced ( appr

104 On the basis of these rate constants, the channel opening probability is calculated to be 0.95 +/-

105 ain of the GluN2B subunit, which has a lower channel open probability, is on average more closed than

106 Ethanol also increased BK channel open probability measured in single-channel reco

107 but with 10-250 nM [Ca2+]i the total single channel open probability (NP(o)) increased with depolari

108 opener diazoxide (200-500 microM) increased channel opening probability (NP(o)) by 486 +/- 120% wher

109 patches, sodium nitroprusside increased the channel open probability (NPo) of cslo-alpha channels 3.

110 here was approximately a 10-fold increase in channel open probability (NPo).

111 mal for wild type) and reached a maximum one-channel open probability of about 45% at 100 mm glycine

112 Blocking MAPKs also increased channel open probability of BK in IC and thereby it may

113 In contrast, the single channel open probability of CFTR was strongly reduced in

114 2+)-releasing activity as well as the single channel open probability of InsP(3)R2 was enhanced by AT

115 ased Ca(2+) signals and augmented the single channel open probability of InsP(3)R2.

116 ide sensitivity, activation rate, and single-channel open probability of SLO-2.

117 Similarly, ATP increased the single channel open probability of the mutated InsP3R1 to the s

118 cal channel-closing rate constant and thus a channel-opening probability of 0.85 vs 0.96 for rGluK2.

119 binding of two glutamate molecules with the channel-opening probability of 0.96.

120 determined by comparing steady-state single-channel open probability or macroscopic peak responses e

121 no alterations in the glutamate sensitivity, channel open probability or the single channel conductan

122 owing of deactivation, an increase in single channel open probability, or a reduction in C-type inact

123 -ROMK1 interaction not only decreases single-channel open probability (P(o)) but gives rise to a ROMK

124 In recombinant cells VX-770 increased CFTR channel open probability (P(o)) in both the F508del proc

125 n-dependent endocytosis, (2) a diminution of channel open probability (P(o)) that occurs without impa

126 with wild type alpha and gamma increased the channel open probability (P(o)) to approximately 1.

127 ed with cardiac LTCC complexes and increases channel open probability (P(O)) to dynamically increase

128 ce of 100 microM cytoplasmic ATP, the K(ATP) channel open probability (P(o)) was increased by 240 +/-

129 rial KCa channels due to a major decrease in channel open probability (P(o)), a mechanism different f

130 el gating, resulting in divergent effects on channel open probability (P(o)).

131 apical sodium channel activity by decreasing channel open probability (P(o)).

132 sults in a dramatic decrease in the receptor-channel open probability (P(o)).

133 tactin decreases ENaC activity via affecting channel open probability (P(o)).

134 mplexes to the plasma membrane and enhancing channel open probability (P(o)).

135 channel studies, E4032A exhibits infrequent (channel-open probability, P(o) < 0.005) and brief (<250

136 The channel open probability (Po = 0.84 +/- 0.03, n = 5) at

137 ed the F60Y mutation increases the intrinsic channel open probability (Po(0)), thereby indirectly pro

138 f calmodulin on the channel, thus increasing channel open probability (PO) and Ca(2+)-dependent inact

139 The relationship between channel open probability (Po) and Vj was well described

140 As channel open probability (Po) approached zero, a small r

141 microM) decreased unitary L- and N-type Ca2+ channel open probability (Po) in cell-attached patches t

142 The mutations do not change the channel open probability (Po) in the absence of ATP, sup

143 yers resulted in a 2-fold increase in single channel open probability (Po) of ORCC but not of CFTR.

144 The single channel open probability (Po) of rENaC was decreased by

145 es stimulated with cAMP agonists, the single-channel open probability (Po) of the phenylalanine 508-d

146 Upper and lower limits for mean channel open probability (Po), calculated from fluctuati

147 RyR2 dissociates FKBP12.6 and regulates the channel open probability (Po).

148 .1 to 10 microM caused a gradual increase in channel open probability (Po).

149 ggest that this is due to an increase in Na+ channel open probability (Po).

150 ude of the whole-cell current and the single-channel open probability (Po).

151 , calstabin1, and displayed increased single channel open probability (Po).

152 nds that non-additively increase L-type Ca2+ channel opening probability (Po) by inducing mode 2 gati

153 racellular membrane surface reduced the KATP channel open probability (Popen) in a dose-dependent man

154 lfonate (MTSET)) reagents markedly inhibited channel open probability primarily by reducing the rate

155 otentiation correlates with increased single channel opening probability, reflected in increased freq

156 In other recordings, MS channel open probability remained low after seal formati

157 At nanomolar concentrations, it increased channel open probability severalfold without inducing a

158 EtOH concentration (50 mm) that increased BK channel open probability strongly decreased the duration

159 ble capture of the dynamic changes in single-channel open probability that account for changes in mac

160 s inhibition is the result of a reduction in channel open probability that is not accompanied by a ch

161 Estimates of the channel opening probability through variance analysis an

162 Instead, the anaesthetic reduced channel open probability to the same extent as observed

163 al side of the channel caused an increase in channel open probability under control conditions as wel

164 Our modelling also suggests that channel open probability varies with the number of serot

165 of the BKbeta4 subunit alleviated reduced BK channel open probability via increasing BK channel open

166 the chloride channel activity by increasing channel open probability (via an increased channel open

167 ic Ca(2+) (200 nM), the voltage at which the channel open probability was half-maximal (V(1/2)) was s

168 arge-conductance calcium-activated K(+) (BK) channel open probability was reduced by loss of fragile

169 129 pS in the presence of 2-mM spermine and channel open probability was significantly reduced in a

170 Single channel open probability was voltage dependent and decre

171 eas ryanodine receptor expression and single-channel open probability were increased.

172 c dissociation constant of glutamate and the channel-opening probability were found to be 450 +/- 200

173 n the C-terminus also markedly increased the channel open probability, which may account for the decr

174 on was produced by selective decrease in the channel open probability with a modest drop in the singl

175 nt voltage-dependent gating, which increases channel open probability with depolarization.

176 uced (1) an increase in channel number times channel open probability, with no change in mean open ti

177 roximately 33%; and (4) increases the single-channel open probability without affecting the unitary c

178 glutathione and DTT increased single BK(Ca) channel open probability without affecting unitary condu

179 ncreased the mean open time by affecting the channel open probability without increasing the number o

180 ced whole cell currents by decreasing single channel open probability without loss of surface recepto

181 el recordings indicated that FFA reduced the channel-open probability without modifying the current a