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

1 itivity to endogenous protons, and decreased channel open probability.

2 pholipid products corresponded to changes in channel open probability.

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

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

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

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

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

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

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

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

11 hat blocked ENaC palmitoylation also reduced channel open probability.

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

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

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

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

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

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

18 he plasma membrane, response time course and channel open probability.

19 ld, likely because of an increase in average channel open probability.

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

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

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

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

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

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

26 that FLNAC substantially reduces ENaC single channel open probability.

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

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

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

30 to promote dimerization and thereby increase channel open probability.

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

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

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

34 tion of Ca(V)1.2, observed as an increase in channel open probability.

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

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

37 sulfhydryl reduction had limited effects on channel open probability.

38 unteracted by interventions that reduce RyR2 channel open probability.

39 The peptide inhibits ENaC by reducing channel open probability.

40 the opposite effect of increasing intrinsic channel open probability.

41 ly correlating with previous measurements of channel open probability.

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

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

44 s more slowly, without appreciable change of channel opening probability.

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

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

47 ), binds to the InsP3R and thereby increases channel open probability, an event associated with chemo

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

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

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

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

52 1a/GluN2D receptors are characterized by low channel open probability and prolonged deactivation time

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

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

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

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

57 ed bilayers and is used here to estimate ion channel open probability and to examine the diffusion be

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

59 surrounding regions markedly affect both the channel-open probability and the activation of the chann

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

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

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

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

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

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

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

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

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

69 respectively, without appreciable change of channel-opening probability, as compared with GluA4 chan

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 Namely, 10 uM dantrolene reduced RyR channel open probability by ~50% in the presence of 3 mM

86 ed Kv1.1 current amplitudes by enhancing the channel open probability, causing a hyperpolarizing shif

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

88 Channel open probability decreased significantly in the

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

90 Channel open probability did not appreciably change over

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

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

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

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

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

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

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

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

99 V)B binding to a(1C) stabilizes an increased channel open probability gating mode by a mechanism that

100 binding to alpha(1C) stabilizes an increased channel open probability gating mode by a mechanism that

101 ot alpha-actinin-1 binding, decreased single-channel open probability, gating charge movement, and it

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

103 ave high efficacy and produce maximum single-channel open probabilities greater than 0.9.

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

105 = 10-20 mmHg) markedly inhibited this BK(Ca) channel open probability in a voltage-dependent manner i

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

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

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

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

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

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

112 nditions, but have impaired ENaC activation (channel open probability) in the kidney during salt rest

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

114 Single-channel open probability increased in response to negati

115 Channel open probability increased with intracellular [H

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

117 TRAAK channel open probability increases as [Formula: see text

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

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

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

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

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

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

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

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

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

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

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

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

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

131 tion profoundly decreased the maximum single-channel open probability of homomeric GlyRs (to 0.16; cf

132 2+)-releasing activity as well as the single channel open probability of InsP(3)R2 was enhanced by AT

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

134 onditions (pH 6.4) reduce the maximum single channel open probability of recombinant homomeric GlyRs

135 onditions (pH 6.4) reduce the maximum single channel open probability of recombinant homomeric GlyRs

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

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

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

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

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

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

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

143 t the agonist-induced Ca(2+) release, single-channel open probability (P(0)), and Ca(2+) sensitivitie

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

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

146 Single-channel open probability (P(o)) of neuronal SLO-2 is ~50

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

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

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

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

151 inhibitory effect of high [Ca(2+)] on single-channel open probability (P(o)) was reduced in mutant ch

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

171 .1 to 10 microM caused a gradual increase in channel open probability (Po).

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

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

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

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

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

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

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

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

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

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

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

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

184 Estimates of the channel opening probability through variance analysis an

185 vation to increase Ca(2+) influx but reduces channel open probability to decrease Ca(2+) influx was r

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

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

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

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

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

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

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

193 129 pS in the presence of 2-mM spermine and channel open probability was significantly reduced in a

194 Single channel open probability was voltage dependent and decre

195 The mutation-induced increase in channel opening probability was insensitive to manipulat

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

197 ne-receptor channel type-2), and RyR2 single-channel open-probability were significantly increased in

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

199 subunit is expressed alone but increases the channel open probability when the BKalpha is coexpressed

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

201 CLR robustly reduced channel open probability while barely decreasing unitary

202 y enhanced agonist potency, and/or increased channel open probability, while the GluN2D(Ser573Phe), (

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

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

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

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

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

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

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

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

211 mainly attributable to an increase in single-channel open probability, without changes in membrane ab