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1 e presence of agonist (i.e., to nAChR in the desensitized state).
2 presence of agonist (i.e., for nAChR in the desensitized state).
3 st for 50 ms (open state) or at equilibrium (desensitized state).
4 maMet-291) that was reduced by 50-80% in the desensitized state.
5 g, Ser) residues inhibited transition to the desensitized state.
6 5 was not accessible for modification in the desensitized state.
7 wal alleviation by maintaining nAChRs in the desensitized state.
8 on of the resting channel and stabilizes the desensitized state.
9 te overlaps the PCP locus in the resting and desensitized state.
10 ing locus at a nonluminal domain in the AChR desensitized state.
11 ubtype of glutamate receptor subunits to the desensitized state.
12 ed incorporation in the alpha-subunit in the desensitized state.
13 d of alpha M2, labeled preferentially in the desensitized state.
14 and-gated ion channels enter a nonconducting desensitized state.
15 l recovery by reducing the entry into a deep desensitized state.
16 indistinguishable from the equilibrium slow desensitized state.
17 al to the apparent nicotine affinity for the desensitized state.
18 ecomes energetically more favorable than the desensitized state.
19 appears to contribute to the affinity of the desensitized state.
20 on reactions during the lifetime of the late desensitized state.
21 on, indicating that it probably stabilizes a desensitized state.
22 at the base of the pore, representative of a desensitized state.
23 onist dissociation and the transition to the desensitized state.
24 ssed channels, enhances the stability of the desensitized state.
25 l structure of GLIC does not correspond to a desensitized state.
26 trinsically occurring closed conformation or desensitized state.
27 ndent gating transitions from the resting to desensitized state.
28 sting state, whereas propofol stabilized the desensitized state.
29 reflects rapid recovery of mast cells from a desensitized state.
30 th respect to the barrier for entry into the desensitized state.
31 that the crystal structures may represent a desensitized state.
32 ow of cations and subsequently enters into a desensitized state.
33 nstead caused the channel to enter a closed, desensitized state.
34 the decoupling of the dimer interface in the desensitized state.
35 actory state is distinct from the well-known desensitized state.
36 3EAM) correspond to the to the (well-known) desensitized state.
37 hat delays transition from the closed to the desensitized state.
38 reasing only with the transition to the slow desensitized state.
39 sting state with that in the carbamylcholine-desensitized state.
40 that memantine stabilizes a Ca(2+)-dependent desensitized state.
41 rapped in a conformation that represents the desensitized state.
42 e closed state selectively over the inactive desensitized state.
43 t differ in structure between the closed and desensitized states.
44 channel opening and dissociate from open and desensitized states.
45 e receptors, are the resting, activated, and desensitized states.
46 onformational change from the resting to the desensitized states.
47 e closed state to glutamate-bound active and desensitized states.
48 tional transitions between closed, open, and desensitized states.
49 ment of affinities for binding to closed and desensitized states.
50 ree energy difference between the active and desensitized states.
51 hat recovery is slower from the longer-lived desensitized states.
52 s convert primarily to fast but also to slow desensitized states.
53 s, conducting open states, and nonconducting desensitized states.
54 ated two agonist binding steps, and open and desensitized states.
55 , and gate rapidly between closed, open, and desensitized states.
56 ing receptor desensitization and stabilizing desensitized states.
57 ry into reduced receptor forms and also into desensitized states.
58 to involve the entry of GABAA receptors into desensitized states.
59 o undergo the transition between resting and desensitized states.
60 but reduced affinity of the open channel and desensitized states.
61 lix at similar efficiency in the resting and desensitized states.
62 interface conformation in the closed and the desensitized states.
63 nformation is nearly identical in closed and desensitized states.
64 ave similar conformations in the resting and desensitized states.
65 distinct from the resting and longest-lived desensitized states.
66 nate potency and diminishing the ensemble of desensitized states.
67 ternary conformation between the resting and desensitized states.
68 n antagonist-bound resting and agonist-bound desensitized states.
69 in addition to naive and sensitized states, desensitized states.
70 s that favor the closed and the ligand-bound desensitized states.
71 t least in part, with the destabilization of desensitized states.
72 he auxiliary subunit GSG1L in the closed and desensitized states.
73 eceptor responses is dominated by entry into desensitized states.
74 s different conformations in the resting and desensitized states.
75 rives the receptors into a nonfunctional, or desensitized, state.
77 edo nAChRs with higher affinity in the nAChR desensitized state ([(3)H]phencyclidine; IC50 = 4 muM) t
78 boration of the structural properties of the desensitized state, a state that is by definition inacti
80 nit helix bundle, photolabeling in the nAChR desensitized state (+agonist) deltaM2-18' and two residu
81 nds in the ion channel preferentially in the desensitized state and binds with lower affinity to a si
82 es in alphaM2 and the alphaM1-M2 loop in the desensitized state and compared these rates to rates pre
84 information on the relationship between the desensitized states and the phases of macroscopic desens
85 free energy of binding (in this case to the desensitized state) and on the electrostatic potential a
86 ed state), or > or =1 h (equilibrium or slow desensitized state) and then rapidly frozen (<1 ms) and
87 n (with photolabeling reduced by >90% in the desensitized state); and (iii) at the gamma-alpha interf
88 ding protein template is in the activated or desensitized state, and the absence of a bound agonist i
89 efined extracellular sites, stabilization of desensitized states, and association with annular or bou
90 Rs have at least two non-equivalent paths to desensitized states, and that choline dissociates faster
91 ting state to the higher affinity active and desensitized states, and the greater effects of the muta
92 he closed/resting, open/activated and closed/desensitized states, and the mechanism by which conforma
93 hrough activated (sensitized) and inhibited (desensitized) states, and, while many of the molecular c
94 onformations of the nonconducting closed and desensitized states are different at the level of the M3
95 consistent desensitization, suggesting that desensitized states are required for the neurosteroid to
96 he structural transition from the resting to desensitized state as monitored by the extent of decreas
97 ts suggest stabilization of Ca(2+)-dependent desensitized states as a new strategy for pharmaceutical
98 f a functional acid-sensing ion channel in a desensitized state at 3 A resolution, the location and c
99 so photolabeled in nAChRs in the equilibrium desensitized state at approximately half the efficiency.
100 and are highly likely to enter and remain in desensitized states at rates determined by the structure
101 e have located the closed gate in the stable desensitized state between alphaG240 and alphaL251.
102 easurable effect on the rate of entry into a desensitized state, but it greatly accelerated the recov
103 of the kainate receptor GluK2 subtype in its desensitized state by cryo-electron microscopy (cryo-EM)
105 e been localized in the Torpedo nAChR in the desensitized state by use of a photoactivatible derivati
106 ptor alpha1 subunit in the open, closed, and desensitized states by using electrophysiology-coordinat
107 r of the open channel, and recovery from the desensitized state can be controlled independently.
108 h occupancy or access increased in the nAChR desensitized state compared to the closed channel state.
109 d] higher affinity when the AChRs are in the desensitized states compared to the resting states.
111 ptors can accumulate in slowly equilibrating desensitized states during repetitive receptor activatio
112 eases occupancy of GluN1/2A and native NMDAR desensitized states entered after accumulation of intrac
113 in the closed state (absence of agonist) and desensitized state (equilibrated with agonist) revealed
114 Human lung mast cells readily recover from a desensitized state following removal of desensitizing an
116 t all open states, as well as all closed and desensitized states from which channel opening can occur
117 t, alpha4beta2 nAChRs accumulate in a "deep" desensitized state, from which recovery is very slow.
118 flux desensitization, implying that the fast desensitized state has an agonist dissociation rate that
120 proximately 250 s), showing that one or more desensitized states have fluorescence like that of the r
121 Dl) = 229 s, while in chicken ASIC1a the two desensitized states have similar values tau(D) 4.5 s.
123 ith 10-fold higher affinity to nAChRs in the desensitized state (IC(50) = 70 microm) than in the clos
125 hances the agonist-induced transition to the desensitized state in the prokaryotic channel GLIC.
126 ing activation, these receptors enter into a desensitized state in which the ion channel shuts even t
127 tion, many ligand-gated ion channels enter a desensitized state in which the neurotransmitter remains
129 C transitions between the resting, open, and desensitized states in response to extracellular acidifi
130 block receptor desensitization by making the desensitized state inaccessible but rather by stabilizin
132 Ch) receptors have shown that entry into the desensitized state is accelerated by protein kinase A-de
136 quilibrated with agonist) revealed selective desensitized state labeling in the delta subunit of delt
138 now have probed the structure in the stable desensitized state obtained after many minutes of exposu
139 el, identified by photolabeling in the nAChR desensitized state of amino acids within the M2 helices
145 phencyclidine locus in either the resting or desensitized state of the nicotinic acetylcholine recept
146 allosteric interaction that destabilizes the desensitized state of the receptor and that potentiation
147 NR2A subunits within a dimer measured in the desensitized state of the receptor are longer than the d
148 em from the capacity of agonists to form the desensitized state of the receptor, carbamylcholine bind
153 t of cleft closure between the activated and desensitized states of the glutamate bound form of the r
155 dings point to the existence of two distinct desensitized states: one requiring several seconds for f
157 1.5 and 10 ms (activated states), 1 s (fast desensitized state), or > or =1 h (equilibrium or slow d
158 is sequential mixing method of measuring the desensitized state population at each agonist site can b
162 ifts the population of AMPA receptors into a desensitized state, rather than simply being insufficien
163 ases the duration of bursts and destabilizes desensitized states, resulting in a rapid component of r
164 hat only the inhibition of quinacrine in the desensitized state seems to be mediated by a mutually ex
165 from desensitization of hASIC1a revealed two desensitized states: short- and long-lasting with time c
166 es of the receptor, including a model of the desensitized state, showed that barbiturates preferentia
167 tween agonist affinity, gating efficacy, and desensitized state stability in shaping macroscopic dese
168 d bilayer while the receptor is in a closed, desensitized state, suggesting that at least one open-ch
169 th higher affinity in the ion channel in the desensitized state than in the closed channel state and
170 tates, there is a more obvious cutoff in the desensitized state than in the resting state, suggesting
171 r GluN2B subunit enter into a nonconducting, desensitized state that can impact synaptic responses an
172 and then transition to an ATP-bound closed, desensitized state that requires an agonist-free washout
173 consisting of nonconducting, conducting, and desensitized states that are starting to become well cha
174 the large difference in stability of the two desensitized states that makes hASIC1a desensitization m
175 , and alpha2betaepsilon2) reveal that in the desensitized state, the alphadelta interface forms the l
176 tamate when the receptor is primarily in the desensitized state, the dimer interface is decoupled, co
177 t persists during the transition to the fast desensitized state, the extent of photoincorporation dec
179 entiating propofol-bound, and two conducting-desensitized states, the activating propofol-bound and G
181 el 1 resembles a resting state and model 2 a desensitized state, thus providing snapshots of gating t
182 tate and in the previously determined low-pH desensitized state, TM2 is a discontinuous alpha helix i
183 mma2L subunit (Y235, F236) were critical for desensitized states to prolong deactivation after remova
185 during the resting to open and open to fast desensitized state transitions, implying that the local
186 lteration of kinetics of entry and exit from desensitized states underlies the allosteric modificatio
187 P2X2 receptors were forced into a prolonged desensitized state upon activation by ATP through a mech
189 that for wild-type alpha7 nAChR, the 3-furan desensitized state was relatively stabilized compared wi
190 The occupancy of an AChR for each of the desensitized states was calculated as a function of time
191 and LBD domains into the density map of the desensitized state we have derived a structural model fo
192 (125)I]TID binding sites in the nAChR in the desensitized state, we examined the effect of phencyclid
193 t one electrically intermediate off state, a desensitized state, when ligands remain bound at the lig
195 naive receptors favored a slow transition to desensitized states, whereas occupancy of the third bind
196 ssembly regulates the rate of entry into the desensitized state, which occurs when the dimer interfac
197 Torpedo nAChR ion channel in the resting and desensitized states with IC(50) values of 2.5 and 0.7 mm
198 usion system shows that human ASIC1a has two desensitized states with markedly different stabilities.
199 ference in structure between the resting and desensitized states within the M2 ion channel domain was
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