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1  involve the voltage-dependent release of an open channel blocker.
2 n-channel noise, as expected for a fast-type open channel blocker.
3  tail of the beta4 subunit acts as a classic open-channel blocker.
4 onate (TBPS) are GABA(A) receptor (GABA(A)R) open channel blockers.
5 les are known to inhibit the PD by acting as open channel blockers.
6  has been generally assumed that they act as open-channel blockers.
7 ine, and philanthotoxin are weakly permeable open-channel blockers.
8 out a prepulse was completely blocked by the open channel blocker, (+)-5-methyl-10,11-dihydro-5H-dibe
9 ore, and this is also the site at which many open channel blockers affect Kv channels.
10                                        Using open channel blockers as tool compounds and a combinatio
11 that polyamines do not only act as classical open channel blockers as was previously thought.
12                  Both Kvbeta subunits act as open channel blockers at physiological membrane potentia
13  suggested that quinidine acts as a cationic open-channel blocker at a site in the internal mouth of
14  these data suggest that amiloride and other open channel blockers bind to sites revealed during the
15 ridine derivative quinacrine act directly as open channel blockers, but can act indirectly as well.
16                                           An open-channel blocker can protect several of these cystei
17                               We studied the open-channel blockers disopyramide and flecainide, and t
18             Chlorisondamine, an irreversible open channel blocker for nnAChRs, caused a time-dependen
19 he activation gate in the VSD is unknown and open channel blockers for VSDs have not yet been identif
20 several D1 ligands act as voltage-dependent, open-channel blockers for NMDA receptors, regardless of
21 nto the future design of kinetically tunable open-channel blockers for the AChR.
22 ive magnitude of the dissociation rate of an open-channel blocker from the open but blocked channel (
23 -dependent phosphorylation, inhibited by the open-channel blocker glibenclamide.
24           However, quinacrine, a fluorescent open-channel blocker, has been recently shown to bind to
25     Our results suggest that PhTX acts as an open channel blocker; however, provided that the toxin r
26 receptors exhibits the characteristics of an open-channel blocker: (i) no competition with agonists,
27 using MK-801, an N-methyl-D-aspartate (NMDA) open channel blocker, implicates glutamate receptors in
28                             Experiments with open channel blockers indicate that the potentiation inv
29         Modelling Mg2+ as an impermeant fast open channel blocker indicated that external Mg2+ blocke
30         Modelling Ni2+ as an impermeant slow open channel blocker indicated that Ni2+ blocked the por
31     Moving the positive charge also restored open-channel blocker interactions that are lost in K95Q.
32 e tolbutamide because weak (i.e., fast-type) open channel blockers introduce brief events into multic
33                                   Other NMDA open channel blockers ketamine and memantine showed a si
34 nsitized state, suggesting that at least one open-channel blocker might act allosterically outside th
35 y synaptic activation in the presence of the open channel blocker MK-801 did not impair the AP5-sensi
36 rge transfer in the presence of NMDA and the open channel blocker MK-801, indicating an increased num
37 uring block of NMDA-elicited currents by the open channel blocker MK-801, indicating increased number
38 g the rate of block of NMDA receptors by the open channel blocker MK-801, we confirmed that the initi
39 anced charge transfer in the presence of the open channel blocker MK-801.
40 ns using fast-application techniques and the open channel blocker MK-801.
41 rs on cultured hippocampal neurons using the open-channel blockers (+)-MK-801 and ketamine to tag syn
42 cts as a relatively non-discriminatory rapid open channel blocker of all types of high voltage-activa
43  Dofetilide acts as a slow-onset/slow-offset open channel blocker of this current at nanomolar concen
44       This suggests that glibenclamide is an open-channel blocker of CFTR.
45 Argiope lobata, is a potent but nonselective open-channel blocker of ionotropic glutamate (iGlu) rece
46         KV beta subunits also function as an open-channel blocker of KV channels.
47              The effects of the irreversible open-channel blocker of N-methyl-D-aspartate receptors,
48  We conclude that PhTX-343 mainly acts as an open-channel blocker of nAChRs with strong subtype selec
49 ine toxins from spiders and wasps are potent open-channel blockers of ionotropic glutamate (iGlu) rec
50 CMS include cholinergic agonists, long-lived open-channel blockers of the acetylcholine receptor ion
51                                              Open-channel blockers of the nicotinic acetylcholine rec
52 sis approaches, we identified citrate as an "open channel blocker" of AtALMT9 and used this tool to e
53 ribe a class of small molecules which act as open channel blockers on the Hv1 VSD and find that a hig
54 d to exhibit differential sensitivity to the open channel blockers phencyclidine and dizolcipine (MK-
55 ogenous neurotransmitter L-glutamate and the open-channel blocker picrotoxin.
56  a partial agonist, but can be blocked by an open channel blocker, picrotoxin.
57            Thus, beta4 may be the endogenous open-channel blocker responsible for resurgent kinetics.
58  channels are dilating, and as a consequence open channel blockers such as amiloride are allowed deep
59 ibition; this effect was largely occluded by open-channel blockers, suggesting that lidocaine binding
60  are clinically useful NMDA receptor (NMDAR) open channel blockers that inhibit NMDARs with similar p
61  by MK801 (dizocilpine hydrogen maleate), an open channel blocker, this potentiation was attributable
62                 Treatment with quinidine, an open-channel blocker used to treat the human disorder, r
63 ubstituted cysteine accessibility method and open channel blockers, we found that the M3 segment form
64           Because alcohols apparently act as open-channel blockers, we infer from our results that mo
65 petitive NMDA antagonists, more specifically open channel blockers, which may be alternatives to high
66 interpreted as deoxycholic acid acting as an open-channel blocker, which may relate to deoxycholic ac
67 potential and/or Memantine, an NMDA receptor open channel blocker, would reduce noise-induced loss of

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