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1 ed alpha(1C) and beta(2a) subunits of L-type Ca channel.
2 ical concentration of Ca ions permeating the Ca channel.
3 ration, mainly due to Ca flux through L-type Ca channels.
4 d structural studies of low-threshold T-type Ca channels.
5 selectivity and high flux that characterizes Ca channels.
6 ts in two closely related isoforms of T-type Ca channels.
7 ly with the pore-forming alpha(1)-subunit of Ca channels.
8 autoantibody-mediated disturbance of L-type Ca channels.
9 itant inhibitory influences on photoreceptor Ca channels.
10 , omega-Aga-IVA (1 microM) targeted multiple Ca channels.
11 DA and AMPA receptors but not sodium (Na) or Ca channels.
12 synaptic receptors as well as voltage-gated Ca channels.
13 inhibition of the native small conductance K(Ca) channel.
14 tant of Gbetagamma with reduced affinity for Ca-channels.
15 otein betagamma subunits (Gbetagamma) to the Ca-channels.
16 ffect is independent of the activation of BK(Ca) channels.
17 urface expression of a subset of podocyte BK(Ca) channels.
18 e-evoked outward current through podocyte BK(Ca) channels.
19 a source of Ca(2+) for the activation of BK(Ca) channels.
20 the Ca(2+)-dependent gating mechanism of BK(Ca) channels.
21 on of myocyte transient K(Ca) currents and K(Ca) channels.
22 an embryonic kidney 293T cells expressing BK(Ca) channels.
23 activation of iberiotoxin-sensitive, maxi-K(Ca) channels.
24 ) (maxi-K(Ca); K(Ca)1.1) channels, not int-K(Ca) channels.
25 negative for the entire family of SK(Ca)-IK(Ca) channels.
26 g the effective coupling of Ca2+ sparks to K(Ca) channels.
27 n, a specific blocker of small-conductance K(Ca) channels.
28 mutant abi1-1 disrupted ABA activation of I(Ca) channels.
29 assembly of hSlo1 monomers into functional K(Ca) channels.
30 ole of IbTX-sensitive large-conductance K(+)(Ca) channels.
31 eriotoxin implicating functional K(v) and BK(Ca) channels.
32 a and subsequent opening of smooth muscle BK(Ca) channels.
33 VSM in small mesenteric arteries requires BK(Ca) channels.
34 ther hyperpolarizing factor(s) activate K(+)(Ca) channels.
35 reases I(K(Ca)) due to a direct effect on K((Ca)) channels.
36 rge-conductance Ca2+-activated potassium (BK(Ca)) channels.
37 ough large-conductance Ca2+-activated K+ (BK(Ca)) channels.
38 IK1, and Slo1 calcium-activated potassium (K(Ca)) channels.
39 contribute to resting vascular tone by K(+)(Ca) channel activation and epoxyeicosatrienoic acid rele
40 nium chloride (TEA) was used to inhibit K(+)(Ca) channel activation and fluconazole was used to inhib
42 ose to Ca(2+) sensors for exocytosis and I(K(Ca)) channel activation, like the P/Q-type channels they
45 low state were examined in the presence of K(Ca) channel activators/blockers and several other vasodi
46 ast, endogenous protein kinases inhibited BK(Ca) channel activity at two functionally distinct sites.
47 of the N-terminal isoforms can fine-tune BK(Ca) channel activity in cells, highlighting a novel mech
50 bbit ventricular myocytes exposed to 1), the Ca channel agonist BayK8644 (100 nM) to increase SR Ca l
52 ng agent halothane or the ryanodine receptor Ca channels agonist 4-chloro-m-cresol was compared in bl
53 experiments were to determine whether the BK(Ca) channel agonist NS1619 is able to induce immediate p
54 sin was coadministered with the K(ATP) and K(ca) channel agonists cromakalim and NS1619 in a concentr
55 pg/ml) coadministered with the K(ATP) and K(ca) channel agonists, cromakalim and NS1619 (10(-8), 10(
56 we report the discovery of an endogenous BK(Ca) channel alpha-subunit intron-containing mRNA in the
57 ould demonstrate that changes in a unique BK(Ca) channel alpha-subunit intron-containing splice varia
58 comprises approximately 10% of the total BK(Ca) channel alpha-subunit mRNAs, is distributed in a gra
59 mulation of plasma membrane expression of BK(Ca) channels also occurs when M2 cells are transfected w
60 appeared abruptly when a voltage step opened Ca channels and disappeared or dimmed abruptly when Ca c
61 ted by calcium (Ca) signaling between L-type Ca channels and Ryanodine receptors that occurs mainly a
62 cycling incorporating stochastic openings of Ca channels and ryanodine receptors to investigate the e
64 strate that mAChR activation inhibits L-type Ca channels and thus may contribute to the suppression o
66 indings, in abi1-1, H(2)O(2) activation of I(Ca) channels and H(2)O(2)-induced stomatal closing were
67 portant repolarizing roles for both Kv and K(Ca) channels and identify distinct roles for SK channel
69 guard cells that activates plasma membrane I(Ca) channels and support a requirement for extracellular
70 d Kv2.1(-/-) islets to characterize Kv and K(Ca) channels and their respective roles in modulating th
71 sures the consequence is activation of EC IK(Ca) channels and vasodilation, reducing the myogenic ton
72 large-conductance Ca(2+)-activated K(+) (BK(Ca)) channel and subsequent smooth muscle hyperpolarizat
73 or of large-conductance Ca2+-activated K+ (K(Ca)) channels and Ca2+ spark-induced transient K(Ca) cur
74 activation of calcium-activated potassium (K(Ca)) channels and was reversed by pharmacologically incr
75 ransient dissociation of Gbetagamma from the Ca-channels and can occur during high-frequency bursts o
76 blocker with selectivity versus hERG, Na and Ca channels, and an acceptable preclinical PK profile.
77 ine receptors (Ca(2+) sparks) to activate BK(Ca) channels, and (2) endothelial-dependent mechanisms i
78 egulation of lipoxygenase/cyclooxygenase, BK(Ca) channels, and ATP receptor activation within astrocy
79 ge-conductance Ca(2+)-activated potassium (K(Ca)) channels, and decreased transient K(Ca) current fre
84 t that apamin- and iberiotoxin-insensitive K(Ca) channels are subject to diurnal modulation by the ci
85 Small- and intermediate-conductance K(+)(Ca) channels are the dominant species involved in modula
86 neuronal transcriptome using a subunit of BK(Ca) channels as bait, and the interaction was confirmed
87 evoked a robust stimulation of functional K(Ca) channels at stages before the normal appearance of t
88 mall-conductance or Slo1 large-conductance K(Ca) channels at up to 1 microM in physiologically releva
89 lar to multivesicular release (MVR) when two Ca channels/AZ open at potentials above the threshold fo
91 e high-conductance Ca(2+)-activated K(+) (BK(Ca)) channel between freshly isolated ECs and SMCs from
93 nses to the activator of large conductance K(Ca) channels (BK(Ca)), NS1619 (10(-5) M), and to the end
94 n, a specific blocker of large-conductance K(Ca) channels (BK), but not by apamin, a specific blocker
95 nel blocker -conotoxin GVIA and the P/Q-type Ca channel blocker -agatoxin IVA increased Ca(2+) signal
96 ontal cells, and showed that both the N-type Ca channel blocker -conotoxin GVIA and the P/Q-type Ca c
97 in Ca(i) were blocked by the addition of the Ca channel blocker La(3+) to the basolateral but not to
99 s increased, by either RN1734 or TRAM-34 (IK(Ca) channel blocker), but not by apamin (SK(Ca) channel
101 rs SKF525A or clotrimazole, but not by the K(Ca) channel blocker, charybdotoxin, or the cyclooxygenas
108 NMA1 encodes the pore-forming subunits of BK(Ca) channel but is expressed in a potentially very large
109 e and potent pharmacological inhibitors of K(Ca) channels but not K(V) channels reduce Ca(2+) entry i
110 e tested the hypothesis that CO activates BK(Ca) channels by binding to channel-bound heme, a BK(Ca)
111 conductance, calcium-sensitive potassium (BK(Ca)) channels by local Ca(2+) signals (Ca(2+) sparks) th
113 ecipitation and GST pull-down assays that BK(Ca) channels can associate with endogenous TRPC3 and TRP
114 transporters, including voltage-gated Na and Ca channels, cardiac ryanodine receptors, Na/Ca-exchange
115 ch-clamp electrophysiology on recombinant BK(Ca) channels cloned from mouse brain and expressed in Xe
117 Here, we show that the Slo1 subunits of BK(Ca) channels contain a novel cytoplasmic actin-binding d
118 e (Ca(V)2.2) voltage-gated calcium channels (Ca-channels) controls many cellular functions including
120 -conductance calcium-activated potassium (BK(Ca)) channels create a connection between calcium signal
121 it also reduced the composite high-threshold Ca channel current recorded in these cells (46.1 +/- 6.9
122 It similarly reduced the high-threshold Ca channel current that remains after a blockade of P-ty
123 ml(-1)) all caused a 20% increase in maxi-K(Ca) channel current that was blocked by AG-1478 or by kn
124 mic neurons 500 nm kurtoxin inhibited T-type Ca channel currents almost completely (90.2 +/- 2.5% at
128 of inactivation, and because facilitation of Ca-channel currents (I(Ca)) masks the extent and kinetic
129 te that the ATP secreted in the ASDN in a BK(Ca) channel-dependent manner is physiologically availabl
131 First, by activating TEA-inhibitable K(+)(Ca) channels, endothelium-derived hyperpolarizing factor
133 , inhibits low-threshold alpha1G and alpha1H Ca channels expressed in oocytes with relatively high po
137 sitive K (K(ATP)) and calcium sensitive K (K(ca)) channel following fluid percussion brain injury (FP
138 K(+) (K(ATP)) and calcium sensitive K(+) (K(ca)) channels following fluid percussion brain injury (F
141 ntrations maximally effective to modulate BK(Ca) channel function (100 mM), fails to gate the channel
143 ory subunit, which is required for normal BK(Ca) channel function and flow-sensitive ATP secretion in
147 so examined expression and localization of K(Ca) channel gene products in the coronary microvasculatu
149 ) Ca(2+)-activated K channels (SK(Ca) and IK(Ca) channels) generate hyperpolarization that passes to
150 ar mechanism of calcium activation of the BK(Ca) channel have focused on the large intracellular carb
151 flux is mediated by Ca(2+)-activated K(+) (K(Ca)) channels, hSKCa2 in the human leukemic T cell line
153 a channel antagonists (tetrodotoxin), L-type Ca channel (I(Ca,L)) antagonists (nifedipine, cadmium, v
154 ator of intermediate and small conductance K(Ca) channels (IK(Ca)/SK(Ca)), NS309 (10(-5) M), and to t
155 ession of Rem2 with CaV 1.2 or CaV1.3 L-type Ca + channels in a heterologous expression system comple
156 to demonstrate (1) expression of the alpha1D Ca channel in human fetal heart, (2) inhibition of alpha
157 ngly, knockout of the neuroendocrine alpha1D Ca channel in mice results in significant sinus bradycar
159 he consequence of chronic exposure of L-type Ca channels in newborn pups to maternal autoantibodies d
160 e presence of low-voltage-activated (T-type) Ca channels in nuclear neurons has fostered the inferenc
163 the endoplasmic reticulum and activation of Ca channels in the basolateral membranes of epithelial c
164 ntraction coupling, the couplon where L-type Ca channels in the sarcolemmal membrane adjoin ryanodine
165 ominant-negative suppression of the native K(Ca) channel in Jurkat T cells by overexpression of a tru
166 onsistently, expression of both K(ATP) and K(Ca) channels in 9L tumors was increased to a significant
168 oproterenol, forskolin, or dopamine opens BK(Ca) channels in coronary myocytes and that this effect i
170 , are the first to implicate AC-5 and maxi-K(Ca) channels in gene activation related to EGFR signalli
171 ad no effect on the surface expression of BK(Ca) channels in HEK293T cells or on the amplitudes of cu
172 we show that the functional expression of K(Ca) channels in LMNs developing in vitro can be stimulat
173 e strategies to assess the involvement of SK(Ca) channels in mediating the current underlying the sAH
175 ivated transient K(Ca) currents and single K(Ca) channels in myocytes that were in contact with astro
179 ical neurons and to elucidate the role of BK(Ca) channels in the initiation of immediate precondition
182 dlimb reduced the functional expression of K(Ca) channels in vivo to levels seen in LMNs deprived of
183 regulation of Ca(2+)-dependent chloride (Cl(Ca)) channels in a human pancreatoma epithelial cell lin
184 l conductance Ca(2+)-activated K(+) (SK or K(Ca)) channels in human and mouse cardiac myocytes that c
185 on of large-conductance Ca2+-activated K+ (K(Ca)) channels in lumbar motoneurons (LMNs) of the develo
186 large conductance Ca(2+)-activated K(+) (BK(Ca)) channels in smooth muscle cells downstream from the
187 d the role of calcium-activated potassium (K(Ca)) channels in this dysfunction in the human coronary
188 f the NOS/NO/sGC/cGMP/PKG pathway and the BK(Ca)-channel in mediating NO-induced reductions in SC cel
192 ptation to mean potential resulted from both Ca channel inactivation and vesicle depletion, whereas a
194 is supported by at least three subtypes of K(Ca) channels, including apamin-sensitive channels, iberi
197 ) secretion was blocked by the voltage-gated Ca channel inhibitor, nifedipine, or by hyperpolarizatio
198 toxin-sensitive, and is inhibited by the BK(Ca) channel inhibitor charybdotoxin, but not by the nitr
200 nnels by binding to channel-bound heme, a BK(Ca) channel inhibitor, and altering the interaction betw
202 large-conductance Ca(2+)-activated K(+) (BK(Ca)) channel inhibitor, iberiotoxin, produced identical
204 or without rottlerin (CP) (n=9), and the BK(Ca++) channel inhibitor paxilline 100 nmol/L was supplie
206 effects of H(2)S, as selective IK(Ca) and SK(Ca) channel inhibitors, charybdotoxin and apamin, inhibi
207 uced heme is a functional CO receptor for BK(Ca) channels, introduce a unique mechanism by which CO r
209 because we estimate that the same number of Ca channels is present at cell surface and T-tubule junc
211 rming alpha subunit of the homotetrameric BK(Ca) channel is expected to contain two intracellular RCK
213 a coupled manner with K(+) efflux through BK(Ca) channels is required for inhibitory purinergic regul
214 large-conductance Ca(2+)-activated K(+) (BK(Ca)) channel is essential for maintaining the membrane i
215 y to be due to a difference in the number of Ca channels/junction at each site because we estimate th
217 ctures (dyads) along t-tubules, where L-type Ca channels (LCCs) appose sarcoplasmic reticulum (SR) Ca
218 arge-conductance Ca(2)(+)-activated K(+) (BK(Ca)) channels, leading to ASM membrane hyperpolarization
219 f voltage-sensitive sodium (Na) and calcium (Ca) channels located on dendrites and spines in regulati
220 al for motor coordination and suggest that K(Ca) channels may constitute a potential therapeutic targ
221 s are inconsistent with the proposal that SK(Ca) channels mediate I(sAHP) in pyramidal cells and indi
222 o show that vasopressin blunted K(ATP) and K(ca) channel mediated cerebrovasodilation in a cyclooxyge
224 jects, whereas in hypercholesterolemia, K(+)(Ca) channel-mediated vasodilation compensates for the re
225 inin, but not acetylcholine, stimulates K(+)(Ca) channel-mediated vasodilation in healthy subjects, w
229 alpha(2)/delta) and T-type (I(Ba)-alpha(1H)) Ca channels, Na channels (I(Na)-hH1), and K channels (I(
231 behavior, Ca(2+) entry through voltage-gated Ca channels often supports bursting activity and mediate
232 f MOR mRNA and measured opioid inhibition of Ca channels on identified nociceptors and low-threshold
234 nst the pore-forming alpha-subunit of the BK(Ca) channel only detected its expression in the SMCs, wh
235 bited an attenuated stimulatory effect on BK(Ca) channel open probability in inside-out membrane patc
236 In the presence of intracellular calcium, BK(Ca) channels open at more negative membrane potentials.
237 t in SMCs that was absent in ECs, and the BK(Ca) channel opener NS 1619 only enhanced K(+) current in
239 rise to apparent one-to-one coupling between Ca channel opening and vesicle release, allowing presyna
240 rs explain the much lower efficacy of L-type Ca channel opening to trigger local SR Ca release at low
241 Ca(2+)-sensitive, large-conductance K(+) (BK(Ca)) channel opening as iberiotoxin (100 nM) significant
244 f PAs which was inhibited by about 60% by BK(Ca) channel or RyR blockers, in a nonadditive manner.
248 Large-conductance Ca(2+)-activated K(+) (BK(Ca)) channels play an important role in the regulation o
252 an greatly impact the distribution of the BK(Ca) channel protein to dendritic spines and intrinsic fi
253 rect interaction of positive IgG with L-type Ca channel proteins and the possible inhibition of T-typ
256 structure of the second RCK domain in the BK(Ca) channel (RCK2) is still being examined, and the pres
257 erlying the sAHP could be carried through SK(Ca) channels, recent work has uncovered anomalies that a
259 tance voltage- and Ca(2+)-activated K(+) (BK(Ca)) channels regulate important physiological processes
260 Large-conductance Ca(2+)-activated K(+) (BK(Ca)) channels regulate the physiological properties of m
261 Large-conductance Ca(2+)-activated K(+) (BK(Ca)) channels regulate the physiology of many cell types
265 intermediate-conductance K(+) (SK(Ca) and IK(Ca)) channels, respectively, and N(G)-nitro-L-arginine m
266 leak through the sarcoplasmic reticulum (SR) Ca channel (ryanodine receptor, RyR) and/or decreased ac
267 loned (cbv) cerebral artery smooth muscle BK(Ca) channels show that CO reverses BK(Ca) channel inhibi
268 channels and gap junctions or that activate Ca(++) channels significantly improve movement of NALCN-
270 inhibitory effect of Ins(3,4,5,6)P(4) on Cl(Ca) channel stimulation by CaMKII was reduced by raising
272 ovide a tentative image of the structures in Ca channels that make them exceptionally selective.
273 ns in the C terminus of alpha(1B-1) produced Ca channels that were inhibited after activation of both
274 transcript and express two novel types of K(Ca) channels that are gated by activation of a G-protein
276 inhibitor for calcium-dependent potassium (K(Ca)) channels, that are effectors in cGMP signaling.
279 s are necessary for normal trafficking of BK(Ca) channels to the plasma membrane and that the mechani
280 have previously shown that trafficking of BK(Ca) channels to the plasma membrane is associated with p
281 A is necessary for normal trafficking of BK(Ca) channels to the plasma membrane, but this effect doe
282 our molecularly defined subclasses of L-type Ca channels, two are expressed ubiquitously in the mamma
283 n/localization of Na/Ca exchanger and L-type Ca channel type 1.2 with a parallel reduction in Na/Ca e
285 ancing the inactivation of voltage-dependent Ca(++) channels (VDCCs), but not by affecting secretory
286 e uncaging, to examine how voltage-sensitive Ca channels (VSCCs) and ionotropic glutamate receptors c
287 ppocampal slices, CaV(2.3) voltage-sensitive Ca channels (VSCCs) are found selectively on spines and
288 ing and digestion were abolished when the BK(Ca) channel was blocked, revealing an essential and unex
290 e-conductance (BK-type) Ca2+-activated K+ (K(Ca)) channels was examined in developing chick lumbar mo
292 e (cGMP), protein kinase G (PKG), and the BK(Ca) channel were used to characterize their involvement
294 -conductance calcium-activated potassium (BK(Ca)) channels were studied in inside-out patches of huma
295 hus, bovine coronary SMCs densely express BK(Ca) channels whereas adjacent ECs in the same artery app
297 na, we provide evidence that the location of Ca channels with low open probability within nanometers
300 exon splicing in rSlo interact to produce BK(Ca) channels with a physiologically relevant phenotype.
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