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1 ation (-33.1 +/- 2.6 mV, n = 4, by 10 microM retigabine).
2  stability of 23a and 24a in comparison with retigabine.
3 erent activity that were nearly abolished by retigabine.
4 ange, well within the therapeutic window for retigabine.
5 reby influences the unique gating effects of retigabine.
6 r by local infusion of the M-channel opener, retigabine.
7 mes more potent and also more selective than retigabine.
8 lly restored by the neuronal K(v)7 activator retigabine.
9 nted by incubation with the M-channel opener retigabine.
10 uction of deactivation distinct from that of retigabine.
11 ) and absence (7.6 +/- 0.01 pS) of 10 microM retigabine.
12 ng that KCNQ2 may be the molecular target of retigabine.
13                                              Retigabine (0.1 to 10 microM) also slowed the rate of ch
14                                              Retigabine (0.1 to 10 microM) induced a potassium curren
15                             When compared to retigabine (0.93 +/- 0.43 muM), the EC(50)s for Kv7.2 cu
16                      The M-current enhancers Retigabine (10 and 30muM) and Flupirtine (30muM) had a d
17                         The K(V) 7 activator retigabine (10 muM) had no effect on voltage-dependent K
18 ain slices, whereas KCNQ channel activation (retigabine, 2-40 mum) silenced these neurons.
19                     In addition, compared to retigabine, 23a and 24a showed also higher potency in ac
20 re, it can be rescued by bath perfusion with retigabine, a KCNQ channel activator, and chronic treatm
21 ardiac conduction blocks can be prevented by retigabine, a Kv7 channel opener.
22 technique was used to examine the effects of retigabine, a novel anticonvulsant drug, on the electror
23 on this principle, we tested the efficacy of retigabine, a potassium channel opener, to suppress the
24                               Application of retigabine, a recently marketed KV 7 channel opener, par
25                       Our findings show that retigabine, a selective agonist of the KV7 family of pot
26                                              Retigabine, a small molecule that activates KCNQ2-5 chan
27  specific chemical interactions required for retigabine action.
28            In conclusion, we have shown that retigabine acts as a KCNQ potassium channel opener.
29                                              Retigabine also had a marked effect on KCNQ current kine
30                        Intra-LHb infusion of retigabine also reduced ethanol consumption and preferen
31                               Application of retigabine also reversed the loss of force (rescue) for
32                              To determine if retigabine altered ex vivo bladder sensory outflow, we m
33 al moieties of the KCNQ2-5 channel activator retigabine, an anticonvulsant approved by the U.S. Food
34                                              Retigabine, an M-channel opener that does not open recep
35             In addition, potency of numerous retigabine analogues correlates with the negative electr
36 ity relationship studies, a small library of retigabine analogues has been designed, synthesized, and
37 bed cryoEM structure of Kv7.2 complexed with retigabine and on previous structure-activity relationsh
38 c-scale interaction essential for effects of retigabine and provide stringent constraints that may gu
39  KCNQ2/Q3 channels as a molecular target for retigabine and suggest that activation of KCNQ2/Q3 chann
40                                              Retigabine and zinc pyrithione are two activators for KC
41                          Here we report that retigabine and zinc pyrithione recognize two different s
42                                An activator (retigabine) and an inhibitor (XE991) of the M-current we
43 nsing domains (VSDs) in response to voltage, retigabine, and PIP2.
44                           In the presence of retigabine at 0 mV the combined duration and contributio
45  that SF0034 was five times more potent than retigabine at shifting the voltage dependence of KCNQ2/3
46                         To elucidate how the retigabine binding site is coupled to changes in voltage
47 eveal an important role for PIP2 in coupling retigabine binding to altered VSD function.
48                                              Retigabine binds to the pore-forming domain, causing a h
49                                              Retigabine can prevent the episodic loss of force in Hyp
50                                              Retigabine completely prevents the loss of force induced
51                                  Compared to retigabine, compound 60 displayed a higher brain/plasma
52  focused on two possible mechanisms by which retigabine could cause urinary retention: by decreasing
53 resent study, we sought to determine whether retigabine could enhance current through M-like currents
54 els and coapplication of zinc pyrithione and retigabine could restore a disease mutant channel simila
55 ent for use as anti-epileptic drugs, such as retigabine (D-23129, N-(2-amino-4-(4-fluorobenzylamino)-
56    Pharmacological restoration of Eepd1 with Retigabine dihydrochloride effectively mitigates obesity
57 cker linopirdine and anticonvulsant enhancer retigabine display increased and decreased potency, resp
58 x was potentiated by the anticonvulsant drug retigabine (EC(50)=0.5 microM).
59 lishes channel potentiation, indicating that retigabine effects rely strongly on formation of a H-bon
60                In differentiated PC12 cells, retigabine enhanced a linopirdine-sensitive current.
61                       The mechanism by which retigabine enhanced KCNQ2/Q3 currents involved large, dr
62 stinct ways and that the KCNQ channel opener retigabine exerts rescuing effects.
63 channel openers, including FDA-approved drug retigabine (ezogabine), show antidepressant efficacy.
64                   Both potassium-induced and retigabine-facilitated efflux were blocked by TEA (IC(50
65    We investigated four M channel enhancers (retigabine, flupirtine, zinc pyrithione and H(2)O(2)) fo
66                       In control experiments retigabine had no effect on either resting membrane pote
67            This effect was limited to IPSCs; retigabine had no significant effect on excitatory posts
68  analogues of the prototypical Kv7 activator retigabine have been synthesized and tested by electroph
69       Although KCNQ channel openers, such as retigabine, have emerged as anti-epilepsy drugs, their e
70 ions to -85 mV in the presence of 100 microM retigabine (IC(50) = 5.2 microM).
71  transfer were all significantly enhanced by retigabine in a dose-dependent manner.
72 on can explain the anticonvulsant actions of retigabine in animal models of epilepsy.
73 re potent and less toxic anticonvulsant than retigabine in rodents.
74          In contrast, the Kv7 channel opener retigabine increased I(M) amplitude and I(hold).
75                                              Retigabine increased mean maximal Po to 0.38 +/- 0.04 an
76          Consistent with the hypothesis that retigabine increases inhibitory neurotransmission via a
77 contrast, treatment of VPA-treated mice with retigabine induced anticonvulsant effects even when admi
78 rization and increased AP frequency, whereas retigabine induced hyperpolarization and arrested firing
79                                              Retigabine-induced currents in CHO-KCNQ2/Q3 cells were i
80                                              Retigabine inhibited voltage-dependent Ca(2+) channel (V
81                                              Retigabine is a novel anticonvulsant with an unknown mec
82                                              Retigabine is a recently approved anticonvulsant that ac
83                                              Retigabine is the prototype Kv7 activator clinically app
84 teromeric channel showed that application of retigabine leads to a concentration-dependent hyperpolar
85           It has recently been reported that retigabine modulates a potassium channel current in nerv
86 ut mice, and that the decay was sensitive to retigabine modulation, unlike in wild-type mice.
87                                              Retigabine [N-(2-amino-4-[fluorobenzylamino]-phenyl) car
88          However, the K(V) 7 channel agonist retigabine nearly abolished sensory nerve outflow from t
89 local infusion or systemic administration of retigabine normalized neuronal hyperactivity and depress
90 resent study we have examined the effects of retigabine on recombinant human KCNQ2 and KCNQ3 potassiu
91 KCNQ channel opener ezogabine (also known as retigabine) on reward circuitry and clinical symptoms in
92 glion neurons did not reduce the efficacy of retigabine or flupirtine to hyperpolarize the resting me
93                                              Retigabine or similar drugs may be used as a personalize
94  or absence of the specific M-channel opener retigabine, or agonists of bradykinin B2 or purinergic P
95  increased H-bonding propensity, strengthens retigabine potency.
96                                 In addition, retigabine potentiated inhibitory postsynaptic currents
97                                   Therefore, retigabine potently reduces excitability in neural circu
98 used to determine whether pre-treatment with retigabine prevented the loss of force, or post-treatmen
99 osteric non-opioid analgesics Flupirtine and Retigabine, previously shown to exhibit neuroprotective
100                  These results indicate that retigabine primarily affects urinary bladder function by
101                      A K(+) channel agonist, retigabine, protects muscle from K(+)-sensitive weakness
102                                              Retigabine raised the threshold for activation of arteri
103 hat pharmacological Kv7 channel opening with retigabine reduced neuronal hyperexcitability in human a
104 orted mutation that abolishes sensitivity to retigabine, remains fully sensitive to these compounds.
105                       The antiepileptic drug retigabine rescued KCNQ3 currents that were abolished by
106 f or treatment with the hyperpolarizing drug retigabine restores opioid responsiveness and blocks spo
107 nel blocker XE991 or the KCNQ channel opener retigabine reverses the effects on consolidation caused
108                                              Retigabine (RTG) is a first-in-class antiepileptic drug
109 e we show that the novel anti-epileptic drug retigabine (RTG) modulates channel function of pore-only
110 SM cells, suggesting that these cells lacked retigabine-sensitive K(V) 7 channels.
111 olybasic motif in the proximal C terminus of retigabine-sensitive KCNQ channels that contributes to V
112                             Moreover, unlike retigabine, SF0034 did not shift the voltage dependence
113                                              Retigabine shifted the voltage dependence of channel act
114 with its known action on potassium channels, retigabine significantly hyperpolarized the resting memb
115                                              Retigabine stabilizes the conducting conformation of the
116              We found that co-application of retigabine strongly decreased the nicotine-induced incre
117  paired-pulse depression, was not altered by retigabine, suggesting that its effect on IPSCs is prima
118       Exposure to the KCNQ channel activator retigabine suppressed the type II fiber's response to ha
119                     Application of 10 microM retigabine to oocytes expressing the KCNQ2/3 heteromeric
120                               Application of retigabine to speed KCNQ channel activation accelerated
121                                The effect of retigabine was associated with a slowing of M-like tail
122 zylamino)-phenyl)-carbamic acid ethyl ester (retigabine) was abrogated.
123                                   Ezogabine (retigabine) was recently approved as an add-on drug for
124 he 3-position of the tri-aminophenyl ring of retigabine, we synthesized a small-molecule activator (S
125                               The effects of retigabine were blocked by co-incubation with XE-991, su
126                           Similar effects of retigabine were observed in oocytes expressing KCNQ2 alo
127 nsensitive to another Kv7 channel activator, retigabine, were also insensitive to ML213 (10 muM).
128                   K(V) 7 activators, such as retigabine, were used to treat epilepsy but caused urina
129                                              Retigabine, which opens KCNQ channels, diminishes axonal

 
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