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1 ber increased cytosolic ATP-, lumenal Ca(2+)-activated channel activities to a nearly maximum level.
2 The density of the small-conductance Ca(2+)-activated channel decreased along the apical dendrite, w
9 nel recordings show that capsaicin- and acid-activated channels have the same conductance, that the t
11 ltered the activity of either class of L-Arg-activated channels, which were blocked by micromolar con
13 oncentration dependent and the Po of the ATP-activated channel was unaffected by membrane voltage, re
14 f either beta- or gamma-ENaC block the basal-activated channel in a concentration-dependent fashion.
15 c side of the bilayer increased lumenal Ca2+-activated channel activities, suggesting that it lowered
16 indicating that calcium channels and calcium-activated channels do not participate in shaping the pre
20 inked to the control of a G-protein and cGMP-activated channels which functions to generate high syna
21 dephosphorylation of 'on' bipolar cell cGMP-activated channels, resulting in a rise in the sensitivi
23 nsistent with CaMKII phosphorylation of cGMP-activated channels leading to a voltage-dependent reduct
29 cribe the characterization of ANKTM1, a cold-activated channel with a lower activation temperature co
30 TRPC2,3,6 and 7 are widely accepted as DAG-activated channels, although TRPC3 can also be regulated
32 on 0.5 microM gamma-aminobutyric acid (GABA)-activated channels (10 +/- 1 pS) in inside-out or outsid
34 ately 70 000) did not pass through the gamma-activated channel, indicating an upper limit to the pore
38 EK293 cells exhibit increased basal and GPCR-activated channel currents, and increased Ca(2+) fluores
44 r residue conserved in all hyperpolarization-activated channels, by Ala substitution produced a depol
45 tials and distal dendritic hyperpolarization-activated channels that mediated site independence of so
47 spines through voltage-sensitive and ligand-activated channels, as well as through Ca(2+) release fr
48 ns BKCa channels primarily operate as ligand-activated channels gated by intracellular Ca(2+) and tha
50 mediated transmission, and, by using a light-activated channel to excite the network, we demonstrate
54 r potassium channels and two different light-activated channels, all of which have an effect on Vmem
59 subunit of a class of Ca(2+)-selective light-activated channels that carry the bulk of the phototrans
60 alcium influx through the TRP and TRPL light-activated channels triggers a complex regulatory hierarc
63 +) on the single N-methyl-D-aspartate (NMDA)-activated channel burst duration and frequency and on th
64 -1592, -1460 and -1754) block the open NMDA-activated channel were studied at membrane voltages (Vm)
65 provides evidence that occupancy of the NMDA-activated channel by Mgi2+ destabilizes the closed state
66 urrent, a four-state model in which the NMDA-activated channel can close while blocked by Mgi2+ is pr
68 FA reduces the mean open time of single NMDA-activated channels in a concentration-dependent manner w
69 se presynaptic terminals reveals single NMDA-activated channels, showing multiple conductance levels,
70 of both the Ca(2+)- and the Ca2+/nucleotide-activated channels, suggest a mechanism for channel open
71 ors, hyperpolarization and cyclic nucleotide-activated channels (HCNCs) and a separate target that ha
72 ls with the same property (cyclic nucleotide-activated channels) have been reported that are involved
78 Acid-sensing ion channels (ASICs) are proton-activated channels expressed in neurons of the central a
79 between 6.0 and 6.5, as expected for proton-activated channels, and current-voltage dependence did n
80 caused by RANTES, indicating that the RANTES-activated channel was the Ca2+ -activated K+ channel.
81 of membrane ionic conductances and receptor-activated channels in CNS neurons and, via these mechani
82 e identified critical functions for receptor-activated channels in the endoplasmic reticulum that all
83 els were blocked by gadolinium; the receptor-activated channels formed upon expression of higher leve
84 ), capacitative Ca2+ entry, and Ca2+ release-activated channel opening (CRAC), and often underlies th
85 tes the cooperation with the calcium release-activated channel Orai1 in directing localized cytoskele
87 ker) and gadolinium(III) chloride (a stretch-activated channel blocker) did not alter the level of ac
88 sis by adding gadolinium chloride (a stretch-activated channel blocker) to the saline (0.008 g.mL-1)
89 ure-dependent gating properties of a stretch-activated channel with a current/voltage plot indicating
96 nels may contribute to the increased stretch-activated channel activity observed in mdx myofibers.
98 describes a physiologically relevant stretch-activated channel, at both the single-channel and whole-
99 anodine receptor (RyR) and (iii) the stretch-activated channel (SAC) in both single myocytes and mult
100 ased proliferation is induced by the stretch-activated channel Piezo1 and involves calcium-triggered
101 ecome too crowded, they activate the stretch-activated channel Piezo1 to trigger extrusion of cells t
106 spider venom that is known to block stretch-activated channels in animal cells, but the spontaneous
107 We tested the hypothesis that both stretch-activated channels (SACs) and intracellular calcium ([Ca
108 lipid-mediated modifier of cationic stretch-activated channels, eliminated the voltage and divalent
109 ane, Ca2+-permeable cation channels (stretch-activated channels) opened and a global increase in [Ca2
110 block voltage-gated Ca(2+) channels, stretch-activated channels (SACs), or the Na(+)-Ca(2+) exchanger
111 th TEA, Tris or choline, eliminating stretch-activated channels but suggesting that if transmembrane
114 ation of both ERK1/2 and p38 kinase, stretch-activated channels, small GTPase proteins, and extracell
115 ed MSHA, whereas other inhibitors of stretch-activated channels (Gd(3+), ruthenium red, SKF96365) did
116 results suggest that the opening of stretch-activated channels allows ions, including Ca2+, to enter
118 s not useful in the investigation of stretch-activated channels which may underlie the myogenic respo
119 nium (III) chloride (an inhibitor of stretch-activated channels) only blocked the activation of ERK1/
120 y gadolinium (Gd3+), an inhibitor of stretch-activated channels, but is independent of extracellular
121 Consistent with the presence of stretch-activated channels, we show that Ca2+ influx is triggere
125 in creating these signal: Rho/ROCK, stretch-activated channels, and 'Molecular Strain Gauges.' We al
129 that inhibiting Ca2+ influx through stretch-activated channels using various compounds, including a
136 for the pore-forming subunit of low voltage-activated channel proteins has not been unequivocally id
137 l tissues, whereas KCNQ1 function as voltage-activated channels with very slow kinetics in cardiac ti
140 , P/Q- and R-type channels, the high voltage-activated channels most intimately associated with presy
147 d its function to maintain these low voltage-activated channels closed at resting membrane potentials
148 tion of channels did not gate as low voltage-activated channels, requiring stronger depolarizations t
150 7-P9) type I hair cells acquired low-voltage-activated channels that shortened the rise time of the r
151 chanisms (transducer adaptation, low-voltage-activated channels, nonquantal transmission, and spike t
154 c L-type voltage-gated calcium (high voltage-activated) channel with accessory proteins beta and alph
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