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1 ted state) and lacosamide (binds to the slow-inactivated state).
2 are minimally essential for maintaining the inactivated state.
3 rom the open-inactivated state to the closed-inactivated state.
4 es not preferentially interact with the fast-inactivated state.
5 d the residency time of channels in the fast-inactivated state.
6 nformation which resembles the normal C-type inactivated state.
7 d IVS6, could stabilize the channel's closed/inactivated state.
8 e pore and by stabilizing the channels in an inactivated state.
9 .5CT, consistent with destabilization of the inactivated state.
10 ther than recovery of channels from a C-type inactivated state.
11 (v)1.5, consistent with stabilization of the inactivated state.
12 ole in channel inactivation, stabilizing the inactivated state.
13 into an intermediate or a slowly developing inactivated state.
14 e proximity when the Na(+) channel is in its inactivated state.
15 s the kinetics and voltage-dependence of the inactivated state.
16 K(+)-dependent removal of channels from the inactivated state.
17 that the drug does not primarily bind to the inactivated state.
18 tion and, in the absence of fusion, to an HA-inactivated state.
19 tivation indicating a destabilization of the inactivated state.
20 ation gating from the open and from the fast inactivated state.
21 pecific ability of Cd(2+) to destabilize the inactivated state.
22 ned to assess deactivation kinetics from the inactivated state.
23 reprimed channels and -65 mV to populate the inactivated state.
24 consistent with high affinity binding to the inactivated state.
25 , indicating a slowed rate of entry into the inactivated state.
26 ational changes during the transition to the inactivated state.
27 Mg2+ to lead these channels into a prolonged inactivated state.
28 rse tubule membrane voltage sensors from the inactivated state.
29 d block through a change in affinity for the inactivated state.
30 closed and open states and destabilized the inactivated state.
31 by increased occupancy in the closed or the inactivated state.
32 In summary, low pH stabilizes the inactivated state.
33 +), but not Mg(2+), can enhance entry to the inactivated state.
34 es to both induce and maintain the long-term inactivated state.
35 ciated channels into a fast-onset, long-term inactivated state.
36 e system could provide useful models for the inactivated state.
37 of a voltage-gated potassium channel in its inactivated state.
38 osteric inhibitor GNF-5 restores the closed, inactivated state.
39 , which was proposed to represent the C-type inactivated state.
40 the selectivity filter is in fact the C-type inactivated state.
41 fast inactivation and destabilizes the fast-inactivated state.
42 t the constricted conformation as the C-type inactivated state.
43 e constricted conformation is not the C-type inactivated state.
44 llapsed state is structurally similar to the inactivated state.
45 rectly from the proximal closed state to the inactivated state.
46 nformation does not correspond to the C-type inactivated state.
47 filter, leading to the non-conductive C-type inactivated state.
48 ions, thereby entering a tension-insensitive inactivated state.
49 presentative of a K(+) channel in the C-type inactivated state.
50 es, with innermost site S4 persisting in the inactivated state.
51 rapidly, and are slower to recover from the inactivated state.
52 nt of a mechanism ("latch") to stabilize the inactivated state.
53 tivation, but modulates the kinetics of slow inactivated states.
54 anges between closed resting, activated, and inactivated states.
55 ifficult for the channel to recover from the inactivated states.
56 the entry of TTX-R sodium channels into slow inactivated states.
57 .4) on deactivation gating from the open and inactivated states.
58 ering roles in channel closure from open and inactivated states.
59 ivated states than selective binding to slow-inactivated states.
60 ntially binding to a combination of open and inactivated states.
61 ulation of nAChRs in long-lived desensitized/inactivated states.
62 second prepulses, suggesting binding to fast-inactivated states.
63 sure deactivation kinetics from open or fast inactivated states.
64 5 has both multiple open states and multiple inactivated states.
65 02) alters partitioning among fast- and slow-inactivated states.
66 sures as well as the promotion of blocked or inactivated states.
67 de access to closed, open, and fast- or slow-inactivated states.
68 ally influences transitions to and from fast-inactivated states.
69 ed on apparent affinities for the respective inactivated states.
70 varying propensities to enter fast- and slow-inactivated states.
71 ct the open state and may also interact with inactivated states.
72 ne and phenytoin, which bind tightly to fast-inactivated states.
73 r binding to either fast-inactivated or slow-inactivated states.
74 tiepileptic drugs that bind to and stabilize inactivated states.
75 .e., there is coupling between N- and C-type inactivated states.
76 e depolarizing direction and slow entry into inactivated states.
77 ignals were obtained in the resting and slow inactivated states.
78 their susceptibility to entering long-lived inactivated states.
79 764A reduced the affinity for binding to the inactivated state 24.5-fold and 8.3-fold, respectively,
80 es in estimates between tonic and open-state/inactivated-state affinities, and they identify how diff
81 omains I-IV cause at most a 2-fold change in inactivated state affinity and have even less of an effe
83 No IS6 or IIS6 mutations studied affected inactivated-state affinity or use-dependent block by the
85 l incorporating two open states, no explicit inactivated state and a fast flicker that is different f
86 ation characterized by slower entry into the inactivated state and a hyperpolarized steady-state inac
87 gating pore current is retained in the slow-inactivated state and is deactivated only at hyperpolari
88 inding affinity" to hH1alpha channels in the inactivated state and prolong the duration of recovery f
89 x 1 unwinds when the K(+) channel enters the inactivated state and rewinds during the transition to t
90 d the entry of sodium channels into the fast inactivated state and slowed the recovery from both fast
91 appeared to bind preferentially to open and inactivated states and caused a dose-dependent hyperpola
92 vulsants phenytoin (slowly binds to the fast-inactivated state) and lacosamide (binds to the slow-ina
93 enous Na(+) channels to transition to a slow inactivated state, and 3) a quintuplicate CRMP-2 alanine
94 equired with three closed, one open, and one inactivated state, and a voltage-independent step betwee
95 bind and unbind slowly from a channel in the inactivated state, and inactivated channels that are bou
96 The cycling of Navs through open, closed and inactivated states, and their closely choreographed rela
98 g rates of entry into and exit from the slow inactivated state are different from those controlling t
99 duced time to peak and faster entry into the inactivated state as well as extending the time to recov
100 iated with the irreversible transition to an inactivated state, as suggested by the Lumry-Eyring mode
101 occurs early in the transition from open to inactivated states, as well as the coupling between the
104 hasic block in response to pulse trains, but inactivated state block was not affected (Kd = approxima
105 % inhibitory concentrations (IC(50)) for the inactivated-state block and the resting-state block of w
108 t F1304Q mutant channels can still enter the inactivated state but do so reversibly and with altered
109 These domains appear to interact in the inactivated state but separate upon integrin activation.
110 duction in bupivacaine affinity toward their inactivated state but show only approximately twofold af
111 d accumulation of I(Na) into an intermediate inactivated state, but these effects were abolished by m
112 y of the local anesthetic etidocaine for the inactivated state by 6-fold, and mutations I409A and N41
113 ge-gated sodium (Na(v)) channels in the slow-inactivated state by binding at or near the local anesth
114 14 knockdown biased NaV channels towards the inactivated state by decreasing channel availability, di
115 ecific manner and (2) disruption of the fast-inactivated state by PEPD mutations can be more moderate
117 th the structures associated with the closed-inactivated state (C/I) and in the well-known closed con
118 SV-infected cells are not apoptotic, and the inactivated state can be overcome by phorbol ester stimu
120 ctures of the KcsA channel suggest that this inactivated state corresponds to a "constricted" conform
122 GDP analog that locks G proteins into their inactivated state, did not affect the dose dependence of
123 removed channels from the voltage-sensitive inactivated state, elevation of external [K(+)] up to 10
125 calcium channels transit to a nonconducting inactivated state from which they do not re-open unless
126 Preferential block of hERG1 channels in an inactivated state has been assumed because inactivation
128 evented the channel from entering the C-type inactivated state (i.e. high [K(+)](o) or the K532Y muta
129 motes the entry of the channel into a C-type inactivated state in a time- and voltage-dependent manne
131 esults suggest that lacosamide binds to fast-inactivated states in a manner similar to other antiseiz
132 e to its preferential affinity to the C-type inactivated state, in which cessation of K(+) flux stabi
133 model, in which toxin dissociation from the inactivated state is approximately 60-fold slower than f
134 ther, our data suggest that the stability of inactivated states is under tight evolutionary control,
135 IVS6 (V1589M: dissociation constant for the inactivated state (K(I)) = 44.7 microM; M1592V: K(I) = 4
139 sts that this receptor can exist in a deeply inactivated state, not responsive to ATP, and that its d
144 affinity interaction of terfenadine with the inactivated state of L-type Ca2+ channels may play an im
146 s unusual in binding selectively to the slow-inactivated state of sodium channels, in contrast to dru
148 term exposure (up to 18 min), binding to the inactivated state of the channel to inhibit activity.
152 the structure reported here represents a non-inactivated state of the CTNa(v), that is, the state tha
154 Our homology molecular model of the open/inactivated state of the Na(+) channel pore predicts, ba
155 ecause of preferential interactions with the inactivated state of the Na+ channel, which is occupied
157 ectrophysiological assays, CDA54 blocked the inactivated states of hNa(V)1.7 and hNa(V)1.8, two chann
158 kinetically distinct binding to the open and inactivated states of Kv11.1 that can describe the obser
159 The affinity of BPBTS for the resting and inactivated states of Na(V)1.2 was 1.2 and 0.14 microM,
163 as isoflurane inhibit NaV by stabilizing the inactivated state or altering the inactivation kinetics.
165 he differences were caused by binding to the inactivated state rather than a different affinity of li
166 ny drugs it has been suggested that the fast inactivated state represents the high-affinity binding s
169 transition to accelerate entry into the slow inactivated state, resulting in use-dependent block.
174 ed between the pre-open closed state and the inactivated state, successfully reproduced our results f
175 on the rates of entry into the fast or slow inactivated states, suggesting that another mechanism is
176 as channels into predominantly fast- or slow-inactivated states, suggesting that channel inhibition i
179 ependent on the availability of a particular inactivated state than the relative time that the channe
180 l, more consistent with slow binding to fast-inactivated states than selective binding to slow-inacti
181 ike the Shaker Kv channel, KvAP possesses an inactivated state that is accessible from the pre-open s
183 ate constants entering and exiting all three inactivated states, the model accounted for the F1304Q-i
184 hERG1 K(+) channels rapidly recover from an inactivated state then slowly deactivate to a closed sta
185 may bind with high affinity to a native slow-inactivated state, thereby accelerating the development
186 to block insect sodium channels in the slow-inactivated state, thereby implying that it is also a me
187 the likelihood that they accumulate in fast inactivated states, thereby shortening refractory period
188 slowed the recovery from both fast- and slow-inactivated states, thereby, enhancing both fast and slo
189 quinidine promotes development of the C-type inactivated state through a voltage-dependent conformati
190 guing possibility is that the drug causes an inactivated state to become conducting without otherwise
191 docaine (lignocaine), binds primarily to the inactivated state to block the channel was reassessed by
192 del in which a bound K+ ion destabilizes the inactivated state to increase the rate of recovery of C-
193 oride channels, and that transition from the inactivated state to the closed state requires protein d
195 arization, the contributions of the open and inactivated states to flecainide binding and inhibition
196 le-exponential function, suggesting that the inactivated state transitions were no longer absorbing.
199 The transition from the resting state to the inactivated state was markedly accelerated in the presen
200 The affinity of the mutant channels in the inactivated state was similar to the wild type (WT) chan
201 e in the entry of Na+ channels into the slow-inactivated state was sufficient to account for the slow
206 To assess whether pH acts on the open or the inactivated state, we tested a double-mutant PIEZO1 that
207 and direct transitions between N- and C-type inactivated states were required, i.e., there is couplin
208 -gated sodium channels assume non-conducting inactivated states which may be characterized as "fast'
209 s that effectively stabilize the channels in inactivated states, which failed to promote significant
210 ICa,L predominantly by interacting with the inactivated state with an apparent dissociation constant
211 was prolonged to 1 s, recovery from a "slow" inactivated state with intermediate kinetics (I(M)) was
212 oop modulate occupancy of a quiescent 'slow' inactivated state with intermediate kinetics (termed IM)
213 cluded three closed states, one open and one inactivated state with transitions permitted between the
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