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1 neurons is dominated by another unidentified delayed rectifier.
2 In most cells, the dominant Kv current was a delayed rectifier.
3 he SLO-2 current is a major component of the delayed rectifier.
4 eptors target only the fast component of the delayed rectifier.
5 uppress pro-arrhythmic events than the rapid delayed rectifier.
6 hannels (R- and T-type calcium, fast sodium, delayed rectifier, A-type, and small-conductance calcium
10 nnels comprising both N-type and non-N-type (delayed rectifier) alpha-subunits depends upon the numbe
14 lective loss of circadian modulation of fast delayed-rectifier and A-type K+ currents was observed.
15 currents: the sodium current and the M-type, delayed rectifier, and calcium-dependent potassium curre
18 ls, and had smaller outward currents through delayed rectifier channels (I(KV)) and noninactivating c
21 channel can be distinguished from most other delayed rectifier channels by its very high threshold of
22 bundance, knowledge of the function of these delayed rectifier channels has been limited by the lack
27 ing channel conductance to generate the slow delayed rectifier current ( I Ks) that is critical for t
28 ns that specifically affect channels for the delayed rectifier current (I(K)) has made their genetic
30 ed by coronary microembolizations, the rapid delayed rectifier current (I(Kr)) density was increased.
32 (+) ) currents such as the slowly activating delayed rectifier current (IKs ) and the small conductan
33 e electrophysiological recording of the slow delayed rectifier current (IKs) and investigation of pha
34 larization is determined in part by the slow delayed rectifier current (IKs), through the tetrameric
36 of genes encoding the slow component of the delayed rectifier current (LQT1, LQT5), the rapid compon
37 ent (LQT1, LQT5), the rapid component of the delayed rectifier current (LQT2, LQT6), or the Na(+) cur
38 ociated with an increase in the amplitude of delayed rectifier current and a shift of activation towa
39 vations identity the channels that carry the delayed rectifier current and provide an in vivo physiol
40 el subtype might contribute to the beta-cell delayed rectifier current and that this current could be
43 75X mutant failed to generate the ultrarapid delayed rectifier current I(Kur) vital for atrial repola
47 for the gating of the slow component of the delayed rectifier current is formulated and validated ag
49 parallel with increases in I(Kv) and produce delayed rectifier current when heterologously expressed,
51 ient outward current, rapid component of the delayed rectifier current, and the L-type calcium curren
53 gated potassium channels responsible for the delayed rectifier current, including Kv2.1, are usually
55 (Ks), the slowly activating component of the delayed rectifier current, plays a major role in repolar
56 increased the rapid component, I(Kr), of the delayed rectifier current, thereby accelerating repolari
57 beta-subunit KCNE1 to generate IKs, the slow delayed rectifier current, which plays a critical role i
63 the voltage-dependent activation of neuronal delayed rectifier currents (IK), leading to enhanced IK
65 ssion of which modulates function of cardiac delayed rectifier currents (IKr and IKs), and mutations
66 operties commensurate with a contribution to delayed rectifier currents and are expressed in neurones
69 rapid decay and reduced peak conductance of delayed rectifier currents from INS-1 cells and from pri
70 -gated potassium (Kv) channel that generates delayed rectifier currents in mammalian heart and brain.
71 les the magnitude and kinetics of endogenous delayed rectifier currents in PC12 cells and hippocampal
76 A-type K(+) current did not increase but the delayed rectifier doubled in adults compared with nymphs
77 with Kv3.1 or Kv3.2 subunits underlie fast, delayed-rectifier (DR) currents that endow neurons with
78 matic nucleus (SCN) neurons express the fast delayed rectifier (FDR) potassium current and raise ques
79 paration, we show that the magnitude of fast delayed rectifier (FDR) potassium currents has a diurnal
80 functions as a beta subunit for the cardiac delayed rectifier I(Kr), these results suggest that this
82 K(+) current, possibly the slowly activating delayed rectifier I(Ks), may account in part for this fo
84 activated more than 10-fold faster than the delayed rectifier I(Kv) over the physiological voltage r
85 on the density of the inward (I(K1)) and the delayed rectifier (I(K)) currents are more contradictory
86 of the two molecular components of the rapid delayed rectifier (I(K,r)), HERG and KCNE2, have been li
87 ve suggested that the rapid component of the delayed rectifier (I(Kr)) may contribute importantly to
88 ients created by heterogeneities of the slow-delayed rectifier (I(Ks)) and transient outward (I(to))
90 K subunit underlie slowly activating cardiac delayed rectifier (I(Ks)) in the heart, whereas two othe
92 taneous betaAS-mediated increase in the slow delayed rectifier, I(Ks), limits betaAS sensitivity.
93 KCNE1 increased the slow component of the delayed rectifier, I(Ks), without clear phenotypic seque
97 assium channels) and that block of the rapid delayed rectifier (IKr ) is the primary mechanism whereb
98 ong-QT syndrome by direct block of the rapid delayed rectifier (IKr) also seem to inhibit PI3K signal
99 KCNQ1 and KCNE1 assemble to form the slow delayed rectifier (IKs) channel critical for shortening
102 lization was positively correlated with slow delayed rectifier (IKs) current density; 3) KCNQ1 and ca
103 on gating of the transient outward (Ito) and delayed rectifier (IKslow) components of K(+) current wi
104 ts of the cloned channel sqKv1A compose the "delayed rectifier" in the squid giant axon system, but d
105 clinically relevant prediction that the slow delayed rectifier is better able to stabilize the action
106 a repolarization reserve when IKr, the rapid delayed rectifier, is reduced by disease or drug and can
109 ming alpha-subunit of the rapidly activating delayed rectifier K(+) channel in the heart, which plays
111 rom HEK293 cells stably transfected with the delayed rectifier K(+) channel Kv2.1, long depolarizatio
113 demonstrate that Kv1-family (Shaker-related) delayed rectifier K(+) channels in the central medial th
118 factors governing this activity, we studied delayed rectifier K(+) conductances in acutely isolated
119 d the inward rectifier K(+) current (I(K1)), delayed rectifier K(+) current (I(K)), and transient out
121 tions of PD-307243 on the rapid component of delayed rectifier K(+) current (I(Kr)) in rabbit ventric
124 gating kinetics of the slow component of the delayed rectifier K(+) current (I(Ks)) contribute to pos
127 e (by 90%) of the atrial-specific ultrarapid delayed rectifier K(+) current (I(Kur)), or the transien
129 nhanced rabbit ventricular slowly activating delayed rectifier K(+) current (IKs ) by negatively shif
132 ucleated patches showed that GTx inhibited a delayed rectifier K(+) current activating beyond -30 mV
133 sistently predicted an increase in the rapid delayed rectifier K(+) current and a drastic decrease in
134 H NPY neurons have a large, leptin-sensitive delayed rectifier K(+) current and that leptin sensitivi
135 in HERG (LQT2), the gene encoding the rapid delayed rectifier K(+) current I(Kr), account for a sign
136 tant HERG protein is a mechanism for reduced delayed rectifier K(+) current in LQT2, and high-affinit
139 ) current and a drastic decrease in the slow delayed rectifier K(+) current, and this prediction was
140 K and KvLQT1 channel subunits induces a slow delayed rectifier K(+) current, I(Ks), characterized by
141 to calibrate INaL and the rapidly activating delayed rectifier K(+) current, IKr, in the Faber-Rudy c
144 ammonium (TEA) is frequently used to inhibit delayed rectifier K(+) currents (I(DR)) during electroph
146 cts of left ventricular hypertrophy (LVH) on delayed rectifier K(+) currents and their contribution t
149 n can be detected as a marked enhancement of delayed rectifier K(+) currents in voltage clamp measure
150 lowly (I(Ks)) and rapidly (I(Kr)) activating delayed rectifier K(+) currents were recorded by the who
152 ded L- (I(Ca.L)) and T- (I(Ca.T)) type Ca2+, delayed rectifier K+ (I(K)), hyperpolarization-activated
153 oltage-gated K+ channel Kv2.1 is an abundant delayed rectifier K+ (IK) channel expressed at high leve
155 e editing of mRNAs that encode the classical delayed rectifier K+ channel (SqK(v)1.1A) in the squid g
156 -cAMP (300 microM), which increased the slow delayed rectifier K+ channel current (IK,s) density to a
157 tion of mRNA identified transcripts encoding delayed rectifier K+ channel subunits Kv1.6, Kv4.1, Kv4.
158 (human ether-a-go-go-related gene) encodes a delayed rectifier K+ channel vital to normal repolarizat
166 nt resembling the rapidly activating cardiac delayed rectifier K+ current (Ikr) in its time and volta
168 e (HERG) give rise to the rapidly activating delayed rectifier K+ current (IKr), the perturbation of
169 units to form channels that conduct the slow delayed rectifier K+ current (IKs) important for repolar
170 sitive (IC50 = 9 mM), iberiotoxin-resistant, delayed rectifier K+ current and a Na+ current inhibited
172 nK assembles with KvLQT1 to produce the slow delayed rectifier K+ current IKs and may assemble with H
173 ntral neurons, is a major contributor to the delayed rectifier K+ current in hippocampal neurons and
181 oltage clamp of isolated myocytes identified delayed rectifier K+ currents that activated rapidly (ti
182 ulted in the activation of a time-dependent, delayed rectifier K+current (IK) in the endothelial cell
186 n rat brain slices showed that GTx inhibited delayed-rectifier K(+) current but not transient A-type
188 contains an L-type Ca(2+) current, a "rapid" delayed-rectifier K(+) current, a small slowly-activated
189 2+) current, assessment of the role of rapid delayed-rectifier K(+) current, and Ca(2+)-activated K(+
190 mitant inhibition of the rapid or ultrarapid delayed-rectifier K(+) currents (IKr and IKur, respectiv
191 rval prolongation or inhibition of the rapid delayed-rectifier K(+)-current (IKr) encoded by the huma
192 and the reasons for this, the density of the delayed-rectifier K+ current and its two components, i(K
195 dependent Kv2.1 K(+) channels, which mediate delayed rectifier Kv currents (I(K)), are expressed in l
197 ne at subsurgical concentrations potentiated delayed rectifier Kv1 channels at low depolarizing poten
198 ngs demonstrate the exquisite sensitivity of delayed rectifier Kv1 channels to modulation by volatile
199 ric channels, but selectively associate with delayed rectifier Kv2 subunits to form heteromeric chann
200 etry of heteromeric channels composed of the delayed rectifier Kv2.1 subunit and the modulatory Kv9.3
203 alteration in the function or expression of delayed, rectifier (Kv2.1) potassium channels on heterot
205 to the two hMSC models expressing functional delayed rectifier-like human ether a-go-go K+ channel 1
210 nels and we categorized them as belonging to delayed-rectifier, M-, D-, or A-type K(+) channels previ
212 inactivating potassium current known as the delayed rectifier plays a major role in membrane repolar
213 ents are modulated by A-like K+ channels and delayed rectifiers (possibly K(V)1.2) but not by Ca(2+)-
214 characterize the properties of variant slow delayed rectifier potassium (I(Ks)) channels identified
217 r taurine in the regulation of voltage-gated delayed rectifier potassium (K(V)) channels in retinal n
219 d gene (hERG) encodes the rapidly activating delayed rectifier potassium channel (I(Kr)) which plays
220 re-forming subunit of the rapidly activating delayed rectifier potassium channel (IKr), which is impo
226 tions in the gene encoding the voltage-gated delayed rectifier potassium channel Kv1.1 as underlying
228 achea correae, inhibits Kv1.3, a Shaker-type delayed rectifier potassium channel present in human T l
229 The Kv2.1 gene encodes a highly conserved delayed rectifier potassium channel that is widely expre
231 al features of inactivation of the rat Kv2.1 delayed rectifier potassium channel, expressed in Xenopu
235 assium 2.1 (Kv2.1) channels are the dominant delayed rectifier potassium channels responsible for act
236 ongation of the action potential by block of delayed rectifier potassium channels would be expected t
237 currents (primarily through rapid and slowed delayed rectifier potassium channels) and that block of
240 cement of L-type Ca(2+) current (I(CaL)) and delayed rectifier potassium current (I(K)) in guinea pig
241 m current (I(Ca)) and rapid component of the delayed rectifier potassium current (I(Kr)) by verapamil
245 evelopmental regulation of voltage-dependent delayed rectifier potassium current (I(Kv)) of Xenopus p
251 ng the beta subunit of the slowly activating delayed rectifier potassium current (IKs) channel protei
255 tuated in the presence of rapidly activating delayed rectifier potassium current blockers (E-4031 and
259 e of the rapidly activating component of the delayed rectifier potassium current) or block multiple i
260 A modulation of I(KS) (slow component of the delayed rectifier potassium current) remained intact.
261 nt, an A-type transient potassium current, a delayed rectifier potassium current, and a muscarinic po
263 s (transient potassium current, I(K(A)), and delayed rectifier potassium current, I(K(V))) were recor
267 the more slowly activating component of the delayed rectifier potassium current, IKs, and using whol
268 In cardiomyocytes, the slowly activating delayed rectifier potassium current, or IKs, is believed
271 tetraethylammonium (TEA) characteristic of a delayed rectifier potassium current; and 3) remaining ou
273 l cord astrocytes and have demonstrated that delayed rectifier potassium currents (I(Kd)), in particu
274 annels, such as Kv2.1 and SK, which underlie delayed rectifier potassium currents and afterhyperpolar
275 ng in mammalian neurons requires ultra-rapid delayed rectifier potassium currents generated by homome
276 ides a mechanism for influence over multiple delayed rectifier potassium currents in mammalian CNS vi
277 eased the TRPV1 currents, depressed the slow delayed rectifier potassium currents, and increased the
278 type 1b) expression in rat neurons depresses delayed rectifier potassium currents, limits the magnitu
279 intrinsic conductances, the sodium (gNa) and delayed-rectifier potassium (gK(DR)) channels were found
282 d neurotransmitter/neuromodulator receptors, delayed-rectifier potassium channels, calcium-dependent
283 cocaine in the heart is a suppression of the delayed-rectifier potassium current (I(K)) that is impor
284 interpretation that, at the cellular level, delayed-rectifier potassium current is a main contributo
285 ier potassium current, the slowly activating delayed-rectifier potassium current, the inward rectifie
286 n currents, including the rapidly activating delayed-rectifier potassium current, the slowly activati
292 suggest that the four point mutations impair delayed-rectifier type potassium currents by different m
296 function of Kv2.1, the major somatodendritic delayed rectifier voltage-dependent K+ channel in centra
298 The Shaw-like potassium channel Kv3.1, a delayed rectifier with a high threshold of activation, i
300 ta1.3 subunit converts K(v)1.5 channels from delayed rectifiers with a modest degree of slow inactiva
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