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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
7                                          The delayed rectifier activated at potentials above -20 mV a
8                              Extra-subfamily delayed rectifier alpha-subunits, regardless of their ca
9 e N-type alpha-subunits with intra-subfamily delayed rectifier alpha-subunits.
10 nnels comprising both N-type and non-N-type (delayed rectifier) alpha-subunits depends upon the numbe
11 ing enteric neurotransmission or by blocking delayed rectifier and ATP-sensitive K(+) currents.
12 ABA(A) and glycine), ion channels (potassium delayed rectifier and I(h)) and gap junctions.
13                                  Blockade of delayed rectifiers and A-like K+ channels, by tityustoxi
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
16 ron with stochastic ion channels exclude the delayed rectifier as a possible noise source.
17 l activity of the pancreatic islet beta-cell-delayed rectifier channel, Kv2.1.
18 ls, and had smaller outward currents through delayed rectifier channels (I(KV)) and noninactivating c
19  more negative than the activation range for delayed rectifier channels (Kv).
20                                          Kv2 delayed rectifier channels are, however, unique exceptio
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
23 probability, through increased activation of delayed rectifier channels.
24 re capable of forming functional heteromeric delayed rectifier channels.
25 dicate that Kv2 subunits function as classic delayed-rectifier channels in vertebrate neurons.
26 -subunits, versus their slowly inactivating (delayed rectifier) counterparts.
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
29 D) by interacting with Q1 and augmenting the delayed rectifier current (I(K)).
30 ed by coronary microembolizations, the rapid delayed rectifier current (I(Kr)) density was increased.
31                                  The rapidly delayed rectifier current (I(Kr)) has been described in
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
35        Kv1.5 channels conduct the ultrarapid delayed rectifier current (IKur) that contributes to act
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
41                    Blockade of the potassium delayed rectifier current by tetraethylammonium (5 mM) o
42             The major subunit of the cardiac delayed rectifier current I(Kr) is encoded by the human
43 75X mutant failed to generate the ultrarapid delayed rectifier current I(Kur) vital for atrial repola
44 channel that conducts the rapidly activating delayed rectifier current in the heart.
45 malian brain and is a major component of the delayed rectifier current in the hippocampus.
46  in murine portal vein and contribute to the delayed rectifier current in these myocytes.
47  for the gating of the slow component of the delayed rectifier current is formulated and validated ag
48                           The changes in the delayed rectifier current may participate in the Ca2+-de
49 parallel with increases in I(Kv) and produce delayed rectifier current when heterologously expressed,
50                  Both cell types expressed a delayed rectifier current with similar voltage dependenc
51 ient outward current, rapid component of the delayed rectifier current, and the L-type calcium curren
52  modulation of the cardiac slowly activating delayed rectifier current, I(Ks).
53 gated potassium channels responsible for the delayed rectifier current, including Kv2.1, are usually
54          Namely I(ks), the slowly activating delayed rectifier current, is produced by KvLQT1/KCNE1,
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
58 ifen, ethylbromide tamoxifen did not inhibit delayed rectifier current.
59 s responsible for the rapid component of the delayed rectifier current.
60 s because of reduced activation of the rapid delayed-rectifier current IKr.
61        We also determined that the remaining delayed-rectifier current in cultured myocytes was carri
62 nstituting approximately 60-80% of the total delayed-rectifier current.
63 the voltage-dependent activation of neuronal delayed rectifier currents (IK), leading to enhanced IK
64  neuronal M-currents (IK,M) and cardiac slow delayed rectifier currents (IK,s), respectively.
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
67                   Kcna1(-/-) mice lack Kv1.1-delayed rectifier currents and exhibit severe spontaneou
68                   We find that TEA-sensitive delayed rectifier currents are important determinants of
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
72                                              Delayed rectifier currents sensitive to 4-AP are importa
73                                              Delayed rectifier currents were not affected by oestroge
74                 Our results suggest that the delayed rectifier currents, which regulate action potent
75  an increase in the inactivation rate of the delayed rectifier currents.
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
81                                          The delayed rectifier I(Ks) potassium channel, formed by coa
82 K(+) current, possibly the slowly activating delayed rectifier I(Ks), may account in part for this fo
83  minK (KCNE1) produces the slowly activating delayed rectifier I(ks).
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))
89                                     The slow delayed rectifier (I(KS)) channel is composed of KCNQ1 (
90 K subunit underlie slowly activating cardiac delayed rectifier (I(Ks)) in the heart, whereas two othe
91 the T wave through their effect on the rapid-delayed rectifier, I(Kr).
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
94 n (the BK-type current IK,f in IHCs, and the delayed rectifier IK,n in both cell types).
95 hearing to form the major part of the mature delayed rectifier, IK,s.
96 may assemble with HERG to modulate the rapid delayed rectifier IKr.
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
100                                 Cardiac slow delayed rectifier (IKs) channel is composed of KCNQ1 (po
101                                     The slow delayed rectifier (IKs) channel is composed of the KCNQ1
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
107 CNA5) underlies the human atrial ultra-rapid delayed rectifier K current (I(Kur)).
108                       The rapidly activating delayed rectifier K(+) channel (IKr) is encoded by the h
109 ming alpha-subunit of the rapidly activating delayed rectifier K(+) channel in the heart, which plays
110 roduct forms the pore-forming subunit of the delayed rectifier K(+) channel in the heart.
111 rom HEK293 cells stably transfected with the delayed rectifier K(+) channel Kv2.1, long depolarizatio
112 nel gene, we show that this gene encodes the delayed rectifier K(+) channels in Drosophila.
113 demonstrate that Kv1-family (Shaker-related) delayed rectifier K(+) channels in the central medial th
114 apidly (I(Kr)) and slowly (I(Ks)) activating delayed rectifier K(+) channels in the heart.
115                                              Delayed rectifier K(+) channels may mediate the PYK2 act
116                                          For delayed rectifier K(+) channels, consideration of the me
117          Sustained-regular cells show mainly delayed rectifier K(+) channels.
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
120 ody wall muscles showed a specific effect on delayed rectifier K(+) current (I(K)).
121 tions of PD-307243 on the rapid component of delayed rectifier K(+) current (I(Kr)) in rabbit ventric
122 annel responsible for the rapidly activating delayed rectifier K(+) current (I(Kr)).
123                Addition of slowly activating delayed rectifier K(+) current (I(Ks)) blockade led to f
124 gating kinetics of the slow component of the delayed rectifier K(+) current (I(Ks)) contribute to pos
125                                     The slow delayed rectifier K(+) current (I(Ks)) is a major determ
126                                  The cardiac-delayed rectifier K(+) current (I(KS)) is carried by a c
127 e (by 90%) of the atrial-specific ultrarapid delayed rectifier K(+) current (I(Kur)), or the transien
128        Rabbit ventricular rapidly activating delayed rectifier K(+) current (IKr ) amplitude and volt
129 nhanced rabbit ventricular slowly activating delayed rectifier K(+) current (IKs ) by negatively shif
130              ABSTRACT: The slowly activating delayed rectifier K(+) current (IKs ) contributes to rep
131               The atrial-specific ultrarapid delayed rectifier K(+) current (IKur) inactivates slowly
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
137 that form the pore of the rapidly activating delayed rectifier K(+) current in the heart.
138 nnels are responsible for the high threshold delayed rectifier K(+) current typical of Kv2.1.
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
142 channel conducting the slow component of the delayed rectifier K(+) current, IKs.
143 a-go-go-related gene (HERG), which encodes a delayed rectifier K(+) current.
144 ammonium (TEA) is frequently used to inhibit delayed rectifier K(+) currents (I(DR)) during electroph
145 +) current (I(to)), but not the fast or slow delayed rectifier K(+) currents (I(Kr)/I(Ks)).
146 cts of left ventricular hypertrophy (LVH) on delayed rectifier K(+) currents and their contribution t
147                                              Delayed rectifier K(+) currents are critical to action p
148 dentifying ICC and in studies of the role of delayed rectifier K(+) currents in ICC functions.
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
151                                          Two delayed rectifier K(+) currents with distinct electrophy
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
154                                              Delayed rectifier K+ (IKs) channels formed by heteromult
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
159  (human ether-a-go-go-related gene), a human delayed rectifier K+ channel, in Xenopus oocytes.
160 2+ channel and is not accessible to the slow delayed rectifier K+ channel.
161 assium channels, which typically behave like delayed rectifier K+ channels in other species.
162               The sensitivity of murine slow delayed rectifier K+ channels to cAMP was tested by both
163              In contrast, we found that slow delayed rectifier K+ channels were not changed significa
164 on of Ca2+- and voltage-gated K+ channels or delayed rectifier K+ channels.
165 istinct localization of L-type Ca2+ and slow delayed rectifier K+ channels.
166 nt resembling the rapidly activating cardiac delayed rectifier K+ current (Ikr) in its time and volta
167 11.1 alpha-subunit of the rapidly activating delayed rectifier K+ current (IKr) in the heart.
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
171                                VIP increased delayed rectifier K+ current and L-type calcium current
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
174              The kinetics of inactivation of delayed rectifier K+ current in murine colonic myocytes
175 h KCNE1 to form channels that conduct a slow delayed rectifier K+ current, IKs.
176 -function of the atrial specific ultra-rapid delayed rectifier K+ current, IKur.
177                    The role of IKs, the slow delayed rectifier K+ current, in cardiac ventricular rep
178             KCNQ1 channels underlie the slow delayed rectifier K+ current, mediate repolarization of
179                                              Delayed rectifier K+ currents are involved in the contro
180            We conclude that CaMKII regulates delayed rectifier K+ currents in murine colonic myocytes
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
183 ion was selectively sensitive to blockers of delayed-rectifier K channels (K(DR)).
184 lpha and PTPepsilon modulate the activity of delayed-rectifier K(+) channels (I(K)).
185 otentially arrhythmogenic reductions in slow delayed-rectifier K(+) current (IKs).
186 n rat brain slices showed that GTx inhibited delayed-rectifier K(+) current but not transient A-type
187                Whereas the activation of the delayed-rectifier K(+) current causes bandpass behavior
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
193                                              Delayed-rectifier K+ currents (I(DR)) in pancreatic beta
194                                 By contrast, delayed rectifier Kv channels (e.g., Kv1.1) and Nav chan
195 dependent Kv2.1 K(+) channels, which mediate delayed rectifier Kv currents (I(K)), are expressed in l
196  voltage-dependent activation of Kv2.1-based delayed-rectifier Kv currents (I(DR)).
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
201                                              Delayed-rectifier Kv2.1 potassium channels regulate soma
202                       The drug inhibited the delayed rectifier (Kv2) potassium channels from Drosophi
203  alteration in the function or expression of delayed, rectifier (Kv2.1) potassium channels on heterot
204            A similar effect of PIP(2) on the delayed rectifiers Kv7.1 and Kv11.1, two voltage-gated K
205 to the two hMSC models expressing functional delayed rectifier-like human ether a-go-go K+ channel 1
206 s suggest that the modulated currents may be delayed rectifier-like IK.
207 ones results, in part, from an inhibition of delayed rectifier-like IK.
208 dium current (TTX-R I(Na)) and to suppress a delayed rectifier-like potassium current (I(K)).
209  I(h) was caused by its interaction with the delayed-rectifier M-type K(+) current.
210 nels and we categorized them as belonging to delayed-rectifier, M-, D-, or A-type K(+) channels previ
211 fundus ICC, DTX-K blocked a component of the delayed rectifier outward current.
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
215  is the pore-forming subunit of cardiac slow-delayed rectifier potassium (IKs) channels.
216                                          The delayed rectifier potassium (K(+)) channel KCNB1 (Kv2.1)
217 r taurine in the regulation of voltage-gated delayed rectifier potassium (K(V)) channels in retinal n
218                    The regulation of cardiac delayed rectifier potassium (Kv) currents by cAMP-depend
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
221 re-forming subunit of the rapidly activating delayed rectifier potassium channel (IKr).
222  the alpha subunit of the rapidly activating delayed rectifier potassium channel (IKr).
223                             The cardiac slow delayed rectifier potassium channel (IKs), comprised of
224 ferentiation and the accompanying changes in delayed rectifier potassium channel activity.
225 el, Isk-related family, member 1 (KCNE1) the delayed rectifier potassium channel I(Ks).
226 tions in the gene encoding the voltage-gated delayed rectifier potassium channel Kv1.1 as underlying
227 ate and thereby suppress the activity of the delayed rectifier potassium channel Kv1.2.
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
230               HERG encodes the cardiac rapid delayed rectifier potassium channel that mediates repola
231 al features of inactivation of the rat Kv2.1 delayed rectifier potassium channel, expressed in Xenopu
232 e (HERG) that encodes the rapidly activating delayed rectifier potassium channel.
233 re-forming subunit of the rapidly activating delayed rectifier potassium channel.
234                             Gene transfer of delayed rectifier potassium channels represents a novel
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
238                                   We found a delayed rectifier potassium conductance that appeared as
239 ed a proportionally larger activation of the delayed rectifier potassium conductance.
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
242 yellowfin tunas, through the blocking of the delayed rectifier potassium current (I(Kr)).
243 ibrillation produces an increase of the slow delayed rectifier potassium current (I(Ks)).
244                  A developmental increase in delayed rectifier potassium current (I(Kv)) in embryonic
245 evelopmental regulation of voltage-dependent delayed rectifier potassium current (I(Kv)) of Xenopus p
246 ptor subtype and involving inhibition of the delayed rectifier potassium current (I(Kv)).
247                  The rapid components of the delayed rectifier potassium current (IKr) and the inward
248                       Drugs are screened for delayed rectifier potassium current (IKr) blockade to pr
249  ascribed to inhibition of the cardiac rapid delayed rectifier potassium current (IKr).
250                          Effects on the slow delayed rectifier potassium current (IKs) are less recog
251 ng the beta subunit of the slowly activating delayed rectifier potassium current (IKs) channel protei
252                                     The slow delayed rectifier potassium current (IKs) is a key repol
253 -of-function' mutation, which increases slow-delayed rectifier potassium current (IKs).
254  of LV in the presence of rapidly activating delayed rectifier potassium current blockade.
255 tuated in the presence of rapidly activating delayed rectifier potassium current blockers (E-4031 and
256                                              Delayed rectifier potassium current diversity and regula
257                                  The cardiac delayed rectifier potassium current mediates repolarizat
258                                          The delayed rectifier potassium current plays a critical rol
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
262               IKs, the slow component of the delayed rectifier potassium current, figures prominently
263 s (transient potassium current, I(K(A)), and delayed rectifier potassium current, I(K(V))) were recor
264                                    the rapid delayed rectifier potassium current, I(Kr), which flows
265                      The 2 components of the delayed rectifier potassium current, IKr (rapid) and IKs
266                       The rapidly activating delayed rectifier potassium current, IKr, was studied in
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
269 iled model of the cardiac rapidly activating delayed rectifier potassium current.
270  by indirect, rate-dependent changes in slow delayed rectifier potassium current.
271 tetraethylammonium (TEA) characteristic of a delayed rectifier potassium current; and 3) remaining ou
272                            The amplitudes of delayed rectifier potassium currents (I(Kd)) in CA1 neur
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
280 ions in the function and localization of the delayed-rectifier potassium channel, Kv2.1.
281                    This also depends on slow delayed-rectifier potassium channels, and preferred thet
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
287                        Kv2 channels underlie delayed-rectifier potassium currents in various neurons,
288            KEY POINTS: Kv2 channels underlie delayed-rectifier potassium currents in various neurons,
289                                  Kv2 family "delayed-rectifier" potassium channels are widely express
290 with reduction in the rapid component of the delayed rectifier repolarizing current (I(Kr)).
291                       Mutational analysis on delayed rectifier type K(+) channels demonstrate increas
292 suggest that the four point mutations impair delayed-rectifier type potassium currents by different m
293  A-type Kv4 current to a slowly inactivating delayed rectifier-type potassium current.
294                                              Delayed-rectifier-type K(+) channels had a single-channe
295 -sensitive currents indicates that they were delayed rectifier types of I(K).
296 function of Kv2.1, the major somatodendritic delayed rectifier voltage-dependent K+ channel in centra
297                                            A delayed rectifier voltage-gated K(+) channel (Kv) repres
298     The Shaw-like potassium channel Kv3.1, a delayed rectifier with a high threshold of activation, i
299         The current had characteristics of a delayed rectifier with activation positive to -50 mV and
300 ta1.3 subunit converts K(v)1.5 channels from delayed rectifiers with a modest degree of slow inactiva

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