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1 ted state) and lacosamide (binds to the slow-inactivated state).
2 ions, thereby entering a tension-insensitive inactivated state.
3 presentative of a K(+) channel in the C-type inactivated state.
4 es, with innermost site S4 persisting in the inactivated state.
5 rapidly, and are slower to recover from the inactivated state.
6 nt of a mechanism ("latch") to stabilize the inactivated state.
7 rom the open-inactivated state to the closed-inactivated state.
8 el of the transition of K(V) channels to the inactivated state.
9 es not preferentially interact with the fast-inactivated state.
10 impermeable state-we hypothesize this is the inactivated state.
11 d the residency time of channels in the fast-inactivated state.
12 tions that Bay K 8644 is less favored in the inactivated state.
13 nformation which resembles the normal C-type inactivated state.
14 d IVS6, could stabilize the channel's closed/inactivated state.
15 e pore and by stabilizing the channels in an inactivated state.
16 are minimally essential for maintaining the inactivated state.
17 .5CT, consistent with destabilization of the inactivated state.
18 ther than recovery of channels from a C-type inactivated state.
19 (v)1.5, consistent with stabilization of the inactivated state.
20 ole in channel inactivation, stabilizing the inactivated state.
21 into an intermediate or a slowly developing inactivated state.
22 e proximity when the Na(+) channel is in its inactivated state.
23 s the kinetics and voltage-dependence of the inactivated state.
24 K(+)-dependent removal of channels from the inactivated state.
25 that the drug does not primarily bind to the inactivated state.
26 tion and, in the absence of fusion, to an HA-inactivated state.
27 tivation indicating a destabilization of the inactivated state.
28 ation gating from the open and from the fast inactivated state.
29 pecific ability of Cd(2+) to destabilize the inactivated state.
30 ned to assess deactivation kinetics from the inactivated state.
31 reprimed channels and -65 mV to populate the inactivated state.
32 consistent with high affinity binding to the inactivated state.
33 , indicating a slowed rate of entry into the inactivated state.
34 ational changes during the transition to the inactivated state.
35 Mg2+ to lead these channels into a prolonged inactivated state.
36 rse tubule membrane voltage sensors from the inactivated state.
37 d block through a change in affinity for the inactivated state.
38 closed and open states and destabilized the inactivated state.
39 nformation does not correspond to the C-type inactivated state.
40 cond, alternative and more slowly populated, inactivated state.
41 als as the W434F-mutant SF recovers from its inactivated state.
42 es its recruitment to DNA damage sites in an inactivated state.
43 structure of the K(v)1.2 channel in a C-type inactivated state.
44 d, upon binding, immobilizes channels in the inactivated state.
45 ctance by delaying channel recovery from the inactivated state.
46 its Navs and prolongs recovery from the fast-inactivated state.
47 d the output is the occupancy of a long-term inactivated state.
48 by increased occupancy in the closed or the inactivated state.
49 In summary, low pH stabilizes the inactivated state.
50 +), but not Mg(2+), can enhance entry to the inactivated state.
51 es to both induce and maintain the long-term inactivated state.
52 ciated channels into a fast-onset, long-term inactivated state.
53 e system could provide useful models for the inactivated state.
54 of a voltage-gated potassium channel in its inactivated state.
55 osteric inhibitor GNF-5 restores the closed, inactivated state.
56 , which was proposed to represent the C-type inactivated state.
57 the selectivity filter is in fact the C-type inactivated state.
58 fast inactivation and destabilizes the fast-inactivated state.
59 t the constricted conformation as the C-type inactivated state.
60 e constricted conformation is not the C-type inactivated state.
61 llapsed state is structurally similar to the inactivated state.
62 rectly from the proximal closed state to the inactivated state.
63 filter, leading to the non-conductive C-type inactivated state.
64 e depolarizing direction and slow entry into inactivated states.
65 their susceptibility to entering long-lived inactivated states.
66 tivation, but modulates the kinetics of slow inactivated states.
67 anges between closed resting, activated, and inactivated states.
68 ifficult for the channel to recover from the inactivated states.
69 the entry of TTX-R sodium channels into slow inactivated states.
70 .4) on deactivation gating from the open and inactivated states.
71 ering roles in channel closure from open and inactivated states.
72 ntially binding to a combination of open and inactivated states.
73 ulation of nAChRs in long-lived desensitized/inactivated states.
74 sure deactivation kinetics from open or fast inactivated states.
75 ne and phenytoin, which bind tightly to fast-inactivated states.
76 5 has both multiple open states and multiple inactivated states.
77 02) alters partitioning among fast- and slow-inactivated states.
78 sures as well as the promotion of blocked or inactivated states.
79 ally influences transitions to and from fast-inactivated states.
80 tiepileptic drugs that bind to and stabilize inactivated states.
81 ignals were obtained in the resting and slow inactivated states.
82 Nav channels, with a ~30-fold preference for inactivated states.
83 ivated states than selective binding to slow-inactivated states.
84 second prepulses, suggesting binding to fast-inactivated states.
85 de access to closed, open, and fast- or slow-inactivated states.
86 ed on apparent affinities for the respective inactivated states.
87 varying propensities to enter fast- and slow-inactivated states.
88 ct the open state and may also interact with inactivated states.
89 r binding to either fast-inactivated or slow-inactivated states.
90 .e., there is coupling between N- and C-type inactivated states.
91 on, older Xp genes are transmitted in a "pre-inactivated" state.
92 764A reduced the affinity for binding to the inactivated state 24.5-fold and 8.3-fold, respectively,
93 es in estimates between tonic and open-state/inactivated-state affinities, and they identify how diff
94 omains I-IV cause at most a 2-fold change in inactivated state affinity and have even less of an effe
96 No IS6 or IIS6 mutations studied affected inactivated-state affinity or use-dependent block by the
98 l incorporating two open states, no explicit inactivated state and a fast flicker that is different f
99 ation characterized by slower entry into the inactivated state and a hyperpolarized steady-state inac
100 rings leads to a partially conductive, leaky inactivated state and decreases the selectivity for Na(+
101 gating pore current is retained in the slow-inactivated state and is deactivated only at hyperpolari
102 inding affinity" to hH1alpha channels in the inactivated state and prolong the duration of recovery f
103 x 1 unwinds when the K(+) channel enters the inactivated state and rewinds during the transition to t
104 d the entry of sodium channels into the fast inactivated state and slowed the recovery from both fast
105 appeared to bind preferentially to open and inactivated states and caused a dose-dependent hyperpola
106 vulsants phenytoin (slowly binds to the fast-inactivated state) and lacosamide (binds to the slow-ina
107 enous Na(+) channels to transition to a slow inactivated state, and 3) a quintuplicate CRMP-2 alanine
109 equired with three closed, one open, and one inactivated state, and a voltage-independent step betwee
110 bind and unbind slowly from a channel in the inactivated state, and inactivated channels that are bou
111 The cycling of Navs through open, closed and inactivated states, and their closely choreographed rela
113 g rates of entry into and exit from the slow inactivated state are different from those controlling t
115 duced time to peak and faster entry into the inactivated state as well as extending the time to recov
116 iated with the irreversible transition to an inactivated state, as suggested by the Lumry-Eyring mode
117 occurs early in the transition from open to inactivated states, as well as the coupling between the
120 el, the W434F mutation epitomizes the C-type inactivated state because it functionally accelerates th
121 hasic block in response to pulse trains, but inactivated state block was not affected (Kd = approxima
122 % inhibitory concentrations (IC(50)) for the inactivated-state block and the resting-state block of w
126 t F1304Q mutant channels can still enter the inactivated state but do so reversibly and with altered
127 These domains appear to interact in the inactivated state but separate upon integrin activation.
128 duction in bupivacaine affinity toward their inactivated state but show only approximately twofold af
129 d accumulation of I(Na) into an intermediate inactivated state, but these effects were abolished by m
130 y of the local anesthetic etidocaine for the inactivated state by 6-fold, and mutations I409A and N41
131 lso show that external K(+) destabilizes the inactivated state by altering the conformation of the io
132 ge-gated sodium (Na(v)) channels in the slow-inactivated state by binding at or near the local anesth
133 14 knockdown biased NaV channels towards the inactivated state by decreasing channel availability, di
134 ecific manner and (2) disruption of the fast-inactivated state by PEPD mutations can be more moderate
135 3-3 adaptor proteins that hold CaMKK2 in the inactivated state by preventing dephosphorylation of pho
137 th the structures associated with the closed-inactivated state (C/I) and in the well-known closed con
138 SV-infected cells are not apoptotic, and the inactivated state can be overcome by phorbol ester stimu
140 ctures of the KcsA channel suggest that this inactivated state corresponds to a "constricted" conform
142 GDP analog that locks G proteins into their inactivated state, did not affect the dose dependence of
143 removed channels from the voltage-sensitive inactivated state, elevation of external [K(+)] up to 10
145 calcium channels transit to a nonconducting inactivated state from which they do not re-open unless
146 Preferential block of hERG1 channels in an inactivated state has been assumed because inactivation
148 evented the channel from entering the C-type inactivated state (i.e. high [K(+)](o) or the K532Y muta
149 motes the entry of the channel into a C-type inactivated state in a time- and voltage-dependent manne
152 esults suggest that lacosamide binds to fast-inactivated states in a manner similar to other antiseiz
153 e to its preferential affinity to the C-type inactivated state, in which cessation of K(+) flux stabi
155 model, in which toxin dissociation from the inactivated state is approximately 60-fold slower than f
156 ther, our data suggest that the stability of inactivated states is under tight evolutionary control,
157 IVS6 (V1589M: dissociation constant for the inactivated state (K(I)) = 44.7 microM; M1592V: K(I) = 4
160 with producing a direct stabilization of the inactivated state, mutating residues in this binding sit
162 ophysiological characteristics of the C-type inactivated state, namely, residual K(+) conductance and
163 sts that this receptor can exist in a deeply inactivated state, not responsive to ATP, and that its d
165 s of a cholesterol dimer that stabilizes the inactivated state of an inward-rectifier potassium chann
167 of a drug for binding to the open versus the inactivated state of K(v)11.1 can also be inferred from
170 affinity interaction of terfenadine with the inactivated state of L-type Ca2+ channels may play an im
171 gical experiments show that CBD binds to the inactivated state of Na(v)1.7 channels with a dissociati
172 excitability, with tight binding to the slow inactivated state of Na(v)1.8 channels contributing to e
173 ide Nav1.7 channel blocker that binds to the inactivated state of Nav1.7 channels with high affinity
175 s unusual in binding selectively to the slow-inactivated state of sodium channels, in contrast to dru
177 term exposure (up to 18 min), binding to the inactivated state of the channel to inhibit activity.
178 7 inhibitors that preferentially inhibit the inactivated state of the channel, ST-2262 is equipotent
182 the structure reported here represents a non-inactivated state of the CTNa(v), that is, the state tha
185 Our homology molecular model of the open/inactivated state of the Na(+) channel pore predicts, ba
186 ecause of preferential interactions with the inactivated state of the Na+ channel, which is occupied
188 dissociation constant), ~150 nm] to the slow inactivated state of TTX-R channels, which can be substa
189 ectrophysiological assays, CDA54 blocked the inactivated states of hNa(V)1.7 and hNa(V)1.8, two chann
190 kinetically distinct binding to the open and inactivated states of Kv11.1 that can describe the obser
191 The affinity of BPBTS for the resting and inactivated states of Na(V)1.2 was 1.2 and 0.14 microM,
192 ying compounds that bind selectively to slow inactivated states of Na(v)1.8 channels for developing e
193 uggesting particularly tight binding to slow inactivated states of Na(v)1.8 channels, which dominate
194 anges induced by TFS4 are closely related to inactivated states of RNAP in other domains of life indi
198 as isoflurane inhibit NaV by stabilizing the inactivated state or altering the inactivation kinetics.
200 he differences were caused by binding to the inactivated state rather than a different affinity of li
201 ny drugs it has been suggested that the fast inactivated state represents the high-affinity binding s
204 transition to accelerate entry into the slow inactivated state, resulting in use-dependent block.
209 ed between the pre-open closed state and the inactivated state, successfully reproduced our results f
210 bution of Nav channels in the fast- and slow-inactivated states, such as the accessory Navbeta4 chann
211 on the rates of entry into the fast or slow inactivated states, suggesting that another mechanism is
212 as channels into predominantly fast- or slow-inactivated states, suggesting that channel inhibition i
215 ependent on the availability of a particular inactivated state than the relative time that the channe
216 which also bind with higher affinity to the inactivated state than the resting state but bind at a s
217 l, more consistent with slow binding to fast-inactivated states than selective binding to slow-inacti
218 ike the Shaker Kv channel, KvAP possesses an inactivated state that is accessible from the pre-open s
220 voltage-gated sodium channels in a long-term inactivated state that recovers slowly; stronger sodium
221 ate constants entering and exiting all three inactivated states, the model accounted for the F1304Q-i
222 hERG1 K(+) channels rapidly recover from an inactivated state then slowly deactivate to a closed sta
223 may bind with high affinity to a native slow-inactivated state, thereby accelerating the development
224 to block insect sodium channels in the slow-inactivated state, thereby implying that it is also a me
225 nterface drive the channel into an hERG-like inactivated state, thereby obscuring its opening upon de
226 the likelihood that they accumulate in fast inactivated states, thereby shortening refractory period
227 slowed the recovery from both fast- and slow-inactivated states, thereby, enhancing both fast and slo
228 quinidine promotes development of the C-type inactivated state through a voltage-dependent conformati
229 bstrate binding induces a transition from an inactivated state to a pre-activated state in the dark t
230 guing possibility is that the drug causes an inactivated state to become conducting without otherwise
231 docaine (lignocaine), binds primarily to the inactivated state to block the channel was reassessed by
232 ment drug riluzole stabilises VGSCs in their inactivated state to cause the suppression of I(NaL) tha
233 del in which a bound K+ ion destabilizes the inactivated state to increase the rate of recovery of C-
234 oride channels, and that transition from the inactivated state to the closed state requires protein d
236 arization, the contributions of the open and inactivated states to flecainide binding and inhibition
237 le-exponential function, suggesting that the inactivated state transitions were no longer absorbing.
238 where a small fraction of channels are in an inactivated state under drug-free conditions, inhibition
240 itors that preferentially interacted with an inactivated state via the pore region, LTGO-33 was state
243 The transition from the resting state to the inactivated state was markedly accelerated in the presen
244 The affinity of the mutant channels in the inactivated state was similar to the wild type (WT) chan
245 e in the entry of Na+ channels into the slow-inactivated state was sufficient to account for the slow
250 To assess whether pH acts on the open or the inactivated state, we tested a double-mutant PIEZO1 that
251 nteraction networks across closed, open, and inactivated states, we identified critical residues driv
252 and direct transitions between N- and C-type inactivated states were required, i.e., there is couplin
253 -gated sodium channels assume non-conducting inactivated states which may be characterized as "fast'
254 s that effectively stabilize the channels in inactivated states, which failed to promote significant
255 ICa,L predominantly by interacting with the inactivated state with an apparent dissociation constant
256 was prolonged to 1 s, recovery from a "slow" inactivated state with intermediate kinetics (I(M)) was
257 oop modulate occupancy of a quiescent 'slow' inactivated state with intermediate kinetics (termed IM)
258 N642H) can adopt a hyper-activated and hyper-inactivated state with resistance to dephosphorylation.
259 cluded three closed states, one open and one inactivated state with transitions permitted between the
260 states (with D4S4 in the inner position) and inactivated states (with D4S4 in the outer position).