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1 Ca diffusion, SERCA uptake activity, and RyR open probability.
2 s and rates inversely correlate with channel-open probability.
3 of sIPSCs and potentiation of single-channel open probability.
4 e significant changes in ATP sensitivity and open probability.
5 rotein kinase A results in increased channel open probability.
6 s with different single-channel kinetics and open probability.
7 70N, respectively), while increasing channel open probability.
8 than the GluN2A subunit, which has a higher open probability.
9 nce of ?160 pS and high, voltage-independent open probability.
10 RGS7(-/-)/RGS11(-/-) rod BCs have a very low open probability.
11 nse time course and increases single-channel open probability.
12 hannel environment, which change the channel open probability.
13 ed Na(+) self-inhibition and reduced channel open probability.
14 Ca(V)1.2, observed as an increase in channel open probability.
15 AC substantially reduces ENaC single channel open probability.
16 i, voltage and cAMP, exclusively control the open probability.
17 activated ENaC by increasing single-channel open probability.
18 s mediated by an allosteric reduction of the open probability.
19 y via its own receptor affecting the channel open probability.
20 it, likely reflecting an increase in channel open probability.
21 ed an ohmic behavior and a voltage-dependent open probability.
22 te dimerization and thereby increase channel open probability.
23 s open as well as an increase in the maximum open probability.
24 lyoxal increased and then decreased the RyR2 open probability.
25 nced calcium influx due to increased channel open probability.
26 and ryanodine receptor type 2 (RyR2) channel open probability.
27 KII and results in a decrease in the channel open probability.
28 drophilic pore of large conductance and high open probability.
29 ed TRPV3 single-channel conductance, but not open probability.
30 eceptors, and estimate the subunit-dependent open probability.
31 cts on single-channel conductance as well as open probability.
32 to endogenous protons, and decreased channel open probability.
33 nsferase increased InsP(3)R-3 single channel open probability.
34 e in the plasma membrane, and single-channel open probability.
35 ion at the selectivity filter and overall PD open probability.
36 observed Ca(2+) dependence of the channel's open probability.
37 n closed time, and thereby enhancing overall open probability.
38 sistent with an effect of bile acids on ENaC open probability.
39 ipid composition strongly increased the KcsA open probability.
40 ked ENaC palmitoylation also reduced channel open probability.
41 lowly, without appreciable change of channel opening probability.
42 g NMDA receptors also have a two-fold higher open probability (0.037) than exon 5-lacking receptors (
43 Ca(2)(+) channels in IHCs showed a low mean open probability (0.21 at -20 mV), but this increased si
44 ow that the receptor has a high constitutive open probability (~0.1), but is only weakly activated by
45 ficient mdx muscle: (1) increased MS channel open probability, (2) a shift of MS channel gating to la
46 emble alpha1 receptors in their high maximum open probability (99.1% cf. 98% for alpha1), but differ
47 at a decreased TRPV5 pore size and a reduced open probability accompany the plasmin-mediated reductio
48 pendence in the opposite direction, reducing open probability; acidification also reduced the number
49 -RyR) have increased calcium sensitivity and open probability, amplifying calcium transient at a cost
50 to the InsP3R and thereby increases channel open probability, an event associated with chemotherapy-
51 to three conductance levels with comparable open probabilities and displays modal behavior similar t
52 ver, these mutant channels have higher basal open probabilities and limited responses to the agonist
53 in induces a dose-dependent increase in both open probabilities and mean open times on KcsA in artifi
54 truncated form of TREK1 with a much reduced open probability and a proposed increased permeability t
56 ce had abolished vasopressin-stimulated ENaC open probability and apical membrane channel number.
57 nt mutation, D569N, that reduces the resting open probability and Ca(2+) permeability of the transduc
59 ) -channels from Tric-a KO mice have a lower open probability and gate more frequently in subconducti
61 tage-dependent changes in the single-channel open probability and is not species- or subunit-dependen
64 D receptors are characterized by low channel open probability and prolonged deactivation time course
65 It also decreased TRPV1 current density and open probability and reduced the proportion of pancreati
66 ls causes adaptation, rapidly reducing their open probability and resetting their operating range.
67 CPVT-CaMs caused greater RyR2 single-channel open probability and showed enhanced binding affinity to
68 mal development, but exhibit reduced resting open probability and slowed onset of MET currents, consi
70 ing regions markedly affect both the channel-open probability and the activation of the channel by an
71 dogenous AA-dependent inhibition, increasing open probability and the fraction of functional channels
72 1/2B/2D receptors because agonist potencies, open probability and the glutamate deactivation time cou
76 mino acid substitutions in ENaC that depress open probability and was precluded by proteolytic cleava
77 TP block, dramatically increased the channel open probability, and affected the interaction of Kir6.2
79 l domains of GluN2A subunits reduces channel open probability, and low-affinity voltage-dependent bin
81 t an H620Q mutant, shown to increase channel open probability, and the dual corrector/potentiator CFF
82 s revealed that FMRP loss reduced BK channel open probability, and this defect was compensated in dKO
84 ility approaching 1.0 and maximum functional open probability approaching 0.7 imply that, within the
85 ignificant "window current" at that voltage (open probability, approximately 1%), Ca(V)3.1 channels r
86 ignificant "window current" at that voltage (open probability, approximately 1%), which makes them a
87 ively, without appreciable change of channel-opening probability, as compared with GluA4 channel alon
88 in the range of 15 to 250 pS, with a larger open probability at 0 mV as compared with Cx43, which su
90 ted by calmodulin (CaM), which decreases its open probability at diastolic and systolic Ca(2+) concen
91 0C channels exhibited a significantly higher open probability at diastolic Ca(2+) concentrations, ass
92 itutively open mutant BK channels, with high open probability at negative voltages, as well as a loss
93 1 pS (n = 17; symmetrical 150 mm K(+) ) with open probability being both voltage- and Ca(2+) -depende
94 he channel, nor is there a difference in the open probability between high and low [K(+)] as determin
95 ock-insensitive channels had lower intrinsic open probabilities but retained high sensitivity to zinc
96 ith end-stage heart failure, increased basal open probability but did not attenuate stimulatory respo
97 creases both alpha and alphabeta4 BK channel open probability, but only alpha BK develops acute toler
98 glycine potency by 2-fold, increases channel open probability by 6-fold, and reduces receptor sensiti
99 found that 4 mM NPA caused a 62% decrease in open probability by decreasing mean open time 2.5-fold a
100 increase in ryanodine receptor type 2 (RyR2) open probability by direct oxidation of the RyR2 protein
101 Rp29 may promote ENaC cleavage and increased open probability by directing ENaC to the Golgi via coat
102 enprodil decreased NMDA receptor equilibrium open probability by raising an energetic barrier to acti
103 Namely, 10 uM dantrolene reduced RyR channel open probability by ~50% in the presence of 3 mM free Mg
104 tching and subsequent ROS production on RyR2 open probability, Ca2+ sparks, and the myoplasmic calciu
105 egnenolone sulfate closely matched predicted open probability calculated assuming energetic additivit
107 2-MARCKS complex, which is necessary for the open probability conformation of the channel and preserv
108 luded by proteolytic cleavage that increases open probability, consistent with an effect of bile acid
109 rameters, a reflection of ryanodine receptor open probability, consistent with the effect of IP3 sign
110 receptors activate in long episodes of high open probability, consisting of groups of openings in qu
111 to produce frequent firings, decreasing RyR open probability counter-intuitively promotes long-lasti
113 channels are constitutively active and their open probability depends on the lipidic composition of t
114 eraction domain helix markedly reduced basal open probability despite intact binding of Ca(V)beta to
115 ctivation, reflecting an increase in channel open probability due to a loss of the inhibitory effect
116 .1 in giant liposomes, resulting in a higher open probability due to more frequent opening bursts.
117 In the context of channels that have a low open probability due to retention of an inhibitory tract
118 In the context of channels that have a low open probability due to retention of an inhibitory tract
119 showed that the mutant channels have higher open probability, due to a modification of gating, and n
125 of caveolin-1 significantly reduced channel open probability (from 0.05 +/- 0.01 to 0.005 +/- 0.001;
127 to alpha(1C) stabilizes an increased channel open probability gating mode by a mechanism that require
128 arresting surface Ca(V)1.2 channels in a low open probability gating mode, rather than by interfering
130 recombinant receptors suggests that the high-open-probability gating mode of AMPA receptors containin
131 -actinin-1 binding, decreased single-channel open probability, gating charge movement, and its coupli
132 low open probability GluN2C- than the higher open probability GluN2A-subunit-containing receptors.
133 , being more effective in the inherently low open probability GluN2C- than the higher open probabilit
134 F mutation was highly active (single-channel open probability >0.3) in the absence of ATP and protein
135 or BAPTA caused smaller increases in resting open probability in Bth mutant OHCs than in wild-type co
136 ituted into lipid bilayers revealed enhanced open probability in cAF samples, providing a molecular b
137 spontaneous Ca(2+) release events, and RyR2 open probability in cAF, whereas protein kinase A inhibi
138 centrations of bupivacaine decreased channel open probability in GluN2 subunit- and pH-independent ma
142 icit in Q1412X-CFTR suggest that the reduced open probability in Q1412X-CFTR is the result of a disru
144 annel analysis showed that PKA decreased the open probability in wild-type but not S334A mutant chann
145 sly showed that PIP(2) increases the channel open probability, in this work we find that activation b
146 (2+)] = 25 muM, tauac = 0.082 ms, the IP(3)R open probability increased by approximately 20% and mean
147 found that after carbohydrate stimulus, ENaC open probability increased in split-open isolated collec
148 e activity in as little as 0.01% PIP(2), and open probability increases to approximately 0.4 at 1% PI
151 C456S) mutant channels have a higher channel open probability, induce more calcium influx, and enhanc
152 mics simulations show that the difference in open probability is caused by one long closed state in K
154 hannels are unique among VGICs because their open probability is increased by membrane hyperpolarizat
155 essed by extracellular [Au(CN)2](-) when the open probability is markedly reduced by introducing a se
156 98% for alpha1), but differ in that maximum open probability is reached when all five binding sites
157 he GluN2B subunit, which has a lower channel open probability, is on average more closed than the Glu
158 muM Ca(2+), Ln(3+) potently inhibited RyR's open probability (Kd Eu(3+) = 167 +/- 5 nM and Kd Sm(3+)
159 +) currents as a consequence of their higher open probabilities, leading to increased firing rates in
166 ividual transport rates to quantify absolute open probabilities of EAAT2 anion channels from ratios o
170 steroid alfaxalone had an estimated maximal open probability of 0.6 in oocytes and 0.01 in HEK cells
171 wild type) and reached a maximum one-channel open probability of about 45% at 100 mm glycine (compare
172 ate ENaC-mediated currents by increasing the open probability of active channels without recruiting a
173 pression of Ca(2+) release in ICC limits the open probability of Ano1 channels, reducing the excitabi
174 s were activated to similar extents (maximum open probability of approximately 0.8 at 0 mV) by 0.1-30
176 t activated alpha2M (alpha2M*) increased the open probability of BKCain an oscillatory pattern in hMS
177 f theophylline was due to an increase in the open probability of calcium-activated potassium channels
178 showed that mechanical stimulation increased open probability of carboxyfluorescein-permeable membran
180 pharmacologic strategies for modulating the open probability of channels obeying equilibrium versus
181 owed that PKC activation lowered the overall open probability of ClC-1 in the voltage range relevant
182 state is low (~1%), consistent with the low open probability of CLC-2 observed experimentally in the
184 bability on VG; 2), the voltage at which the open probability of each gate equals 0.5; 3), the gating
185 d A6 collecting duct cells revealed that the open probability of ENaC was sensitive to the sgk1 inhib
186 foundly decreased the maximum single-channel open probability of homomeric GlyRs (to 0.16; cf. 0.99 f
187 used to continuously monitor the number and open probability of InsP3R channels in the same excised
188 tagamma subunits (2-250 ng /mL) enhanced the open probability of Kv7.4 channels without changing unit
190 id (10 mum), a channel opener, increased the open probability of methionine-inhibited unitary current
191 tein phosphatase 2a inhibition increased the open probability of mitoK(ATP) channels through GSK3beta
192 ollowed by quiescence, leading to an overall open probability of only approximately 0.15 after 4 s un
193 2814 phosphorylation in CREM mice normalized open probability of RyR2 channels and SR Ca(2+) release,
194 Ser2814 (S2814D(+/+) mice) exhibit a higher open probability of RyR2, higher sarcoplasmic reticulum
195 timulation of cardiac myocytes increases the open probability of sarcolemmal voltage-sensitive Ca2+ c
196 east in part, by upregulating the levels and open probability of Shaker (Sh) potassium channels to su
197 ) spark frequency in atrial myocytes and the open probability of single RyR2 channels from JPH2 knock
198 important role in determining the intrinsic open probability of SK channels in the absence of Ca(2+)
201 odel indicates that the maximal steady-state open probability of the alpha4beta2delta receptor is ~0.
202 atically affects CaM's ability to reduce the open probability of the cardiac ryanodine receptor (RyR2
203 this difference is related to changes in the open probability of the CFTR channel during exercise, re
205 ng to shorter mean close-time and hence high open probability of the channel in comparison to IP3R in
206 d that the GORK S722E mutation increases the open probability of the channel in the absence, but not
208 -alpha that is crucial for activation of the open probability of the channel, but not membrane expres
209 Oxidation of RyR2s was found to increase the open probability of the channel, whereas CaMKII can be a
212 face thiol disulfide formation increases the open probability of the heme pocket and allows nitrite b
213 lation; and 3) phosphorylation increases the open probability of the heme pocket, which increases lig
215 esent in the immature cochlea, the increased open probability of the mechanotransducer channels cause
216 Depolarization did not increase the resting open probability of the MET current of Tmc1(Bth/Bth) OHC
218 t-exposure test response correlates with the open probability of the preceding desensitizing response
219 ved shut conformations, thereby reducing the open probability of the receptor with no change in the m
220 to a total absence of one and increased the open probability of the remaining two thermoresponsive C
221 drophobic barrier within the pore, and a low open probability of the selectivity filter (SF) gate.
223 dition, protonation conditions determine the open probability of TMEM16A without changing its calcium
224 optical fluctuation analysis to estimate the opening probability of individual voltage-gated calcium
225 capsaicin (CAP) responses, thus reducing the opening probability of the channel by stabilizing its cl
227 e mean channel conductance, but not the peak open probability, of recombinant GluA2-containing AMPARs
228 racterizing 1), the steepness of each gate's open probability on VG; 2), the voltage at which the ope
229 ned by comparing steady-state single-channel open probability or macroscopic peak responses elicited
230 deactivation, an increase in single channel open probability, or a reduction in C-type inactivation.
235 Additionally, mitoBK(Ca) displays a high open probability (P(o) ) and voltage half-activation (V(
238 ation, H(2)O(2) significantly increased ENaC open probability (P(o)) and single-channel current ampli
239 Another mutation, K1250A, known to increase open probability (P(o)) of DeltaF508 CFTR channels, exac
241 ed [(3)H]ryanodine binding and increased the open probability (P(o)) of single RyR2 channels reconsti
243 revealed InsP(3)-independent gating and high open probability (P(o)) under optimal cytoplasmic Ca(2+)
246 a(2+)]i, suggesting Ca(2+) regulation of MCU open probability (P(O)); (iii) in the heart, two feature
249 ly activated by GABA that has a maximal peak open probability (P(Open,peak)) of 0.4, taurine (maximal
251 t activation, Ca(2+)-dependent inactivation, open probability), permeation (ion selectivity, affinity
253 ctance (g) and a approximately 13-fold lower open probability (Po ), were found with the R117H mutati
255 ulin on the channel, thus increasing channel open probability (PO) and Ca(2+)-dependent inactivation.
256 ngle channel conductance, maximal achievable open probability (Po) and the [Ca2+] required for activa
259 hannels were incorporated into bilayers, the open probability (Po) of channels from Tric-a KO mice wa
261 hyl)-2'-deoxy-ATP (P-dATP), can increase the open probability (Po) to approximately 0.7, implying tha
263 due less hydrophobic (L596A/G/W/Q/K) reduces open probability [Po; loss-of-function (LOF)], likely du
265 ticulum (SR) Ca load is high, increasing RyR open probability promotes long-lasting sparks by potenti
267 urface regions and simultaneously boosts its open probability so that Ca(V) 1.2 is mostly active when
268 e structure affects both zinc inhibition and open probability, supporting the general model in which
270 ure of the dynamic changes in single-channel open probability that account for changes in macroscopic
271 and made careful measurements of the maximum open probability the channel can attain at different tem
272 ree models of RyR gating that have identical open probabilities: the commonly used two-state Markov g
273 of the tetramer or allosteric regulation of open probability through voltage-dependent subunit activ
278 ctivator of TRPM8 channels, because absolute open probability values measured with fully activated vo
279 Kbeta4 subunit alleviated reduced BK channel open probability via increasing BK channel open frequenc
282 -native crest of the sarcolemma, where their open probability was dramatically increased (0.034+/-0.0
284 ductance calcium-activated K(+) (BK) channel open probability was reduced by loss of fragile X mental
287 yH-101-sensitive CFTR conductances, and CFTR open probabilities were reduced by 80% in GFP-positive c
290 tor channel type-2), and RyR2 single-channel open-probability were significantly increased in POAF.
291 ted in RyR2 channels that had relatively low open probability, whereas the fast block was unaffected
292 nnels occasionally switched from low to high open probability, which perhaps reflects occasional bind
293 ed agonist potency, and/or increased channel open probability, while the GluN2D(Ser573Phe), (Ser1271P
294 id sequence identity, they exhibit different open probabilities with ca. 90% in KcvNTS and 40% in Kcv
295 om WT mice, multiple channels gate with high open probability with a more than six-fold increase in a
297 ce that the location of Ca channels with low open probability within nanometers of the release sites
298 4C mutation dramatically reduced the maximum open probability without altering channel conductance.
299 e cell currents by decreasing single channel open probability without loss of surface receptors.
300 that protons regulate TMEM16A by tuning its open probability without modifying the single channel cu