ライフサイエンスコーパス: GIRK channel

1 tween positions 67 and 323 do not activate a GIRK channel.

2 egative regulator of G protein activation of GIRK channels.

3 pocket located in the cytoplasmic domains of GIRK channels.

4 ed on the neurotransmitter system coupled to GIRK channels.

5 immobile GPCRs, G-protein heterotrimers, and GIRK channels.

6 hydrate was preserved despite the absence of GIRK channels.

7 odulation of voltage-gated Ca2+ channels and GIRK channels.

8 ave implications for G protein regulation of GIRK channels.

9 volved in the interaction of Gbetagamma with GIRK channels.

10 ction surface of the Gbetagamma complex with GIRK channels.

11 acting surface contains sites for activating GIRK channels.

12 n agreement with the data on native neuronal GIRK channels.

13 hat the halide atom is critical for blocking GIRK channels.

14 n is observed for activation of postsynaptic GIRK channels.

15 adenosine-induced activation of postsynaptic GIRK channels.

16 s; in the same neurons, MCH had no effect on GIRK channels.

17 ess active than the wild type in stimulating GIRK channels.

18 ties were consistent with those of K-ATP and GIRK channels.

19 with inhibition, rather than activation, of GIRK channels.

20 different from that observed in nonselective GIRK channels.

21 ells by the combined activation of K-ATP and GIRK channels.

22 contributions to the temporal regulation of GIRK channels.

23 l for G(beta)gamma and ethanol activation of GIRK channels.

24 mportant interactions between Gbetagamma and GIRK channels.

25 s in both the RT and VB nuclei by activating GIRK channels.

26 less ability than the wild type to activate GIRK channels.

27 beta1, form dimers that bind to and activate GIRK channels.

28 at GIRK1 was an integral component of native GIRK channels.

29 ve antagonists of other Gbetagamma dimers on GIRK channels.

30 of a family of potassium ion channels called GIRK channels.

31 ting Gi/o deactivation by R7 RGS proteins on GIRK channels.

32 ing the activation of an effector other than GIRK channels.

33 tory effects of neurotransmitters acting via GIRK channels.

34 agonist modified CXCL12-evoked activation of GIRK channels.

35 tivation of the (kappa)2 opioid receptor and GIRK channels.

36 ns participate in multi-ligand regulation of GIRK channels.

37 on-dependent internalization of GABA(B)R and Girk channels.

38 ction between receptor and alcohol gating of GIRK channels.

39 ludes the Gbeta5 subunit that interacts with GIRK channels.

40 G protein-regulated inwardly rectifying K+ (GIRK) channel.

41 gated inwardly rectifying potassium (Kir3 or GIRK) channels.

42 ck G-protein-coupled inwardly rectifying K+ (GIRK) channels.

43 ronal G protein-gated inward rectifier K(+) (GIRK) channels.

44 ivate G protein-coupled inward rectifier K+ (GIRK) channels.

45 otein-coupled inwardly rectifying potassium (GIRK) channels.

46 by activating inwardly rectifying potassium (GIRK) channels.

47 of G protein-gated inwardly rectifying K(+) (GIRK) channels.

48 G-protein-activated, inwardly rectifying K+ (GIRK) channels.

49 G-protein-activated, inwardly rectifying K+ (GIRK) channels.

50 te G protein-gated Inwardly Rectifying K(+) (GIRK) channels.

51 to G-protein-gated inwardly rectifying K(+) (GIRK) channels.

52 ein-activated inwardly rectifying potassium (GIRK) channels.

53 otein-coupled inwardly rectifying potassium (GIRK) channels.

54 the G protein-gated Inwardly-rectifying K+ (GIRK) channels.

55 an important functional role that regulates GIRK channel activation by Gbetagamma and that subtle ch

56 GIRK channel activation has also been implicated in the

57 We reconstituted GIRK channel activation in cells where we could quantify

58 Finally, GIRK channel activation is sufficient to cause a non-pho

59 activation increases basal GIRK current and GIRK channel activation mediated by adenosine A(1) recep

60 erotrimer expression at the plasma membrane, GIRK channel activation, and heterotrimer dissociation.

61 between beta-strands, substantially reduced GIRK channel activation, suggesting that these residues

62 ck inhibition to VTA DA neurons, mediated by GIRK channel activation, tempers the locomotor stimulato

63 and Phe(61), can impair Gbetagamma-mediated GIRK channel activation.

64 he nonsyndromic pacemaker disease because of GIRK channel activation.

65 in the suprachiasmatic nucleus (SCN) through GIRK channel activation.

66 f the genioglossus is functionally linked to GIRK channel activation.

67 of G-protein-gated inwardly rectifying K(+) (GIRK) channel activation and undergoes only small struct

68 G protein-coupled inwardly rectifying K(+) (GIRK) channel activation.

69 for G protein-coupled inward rectifier K(+) (GIRK) channel activation.

70 Spiking was also inhibited by the direct GIRK channel activator ML297, whereas blocking these cha

71 essential role of LGN for maintaining basal GIRK channel activity and for harnessing neuronal excita

72 nhibition, bath application of TRH decreased GIRK channel activity in cell-attached patches.

73 ause bath application of ACh did not inhibit GIRK channel activity in cell-attached patches.

74 Finally, although the dependence of GIRK channel activity on PIP2 is clear, it is not known

75 The wild type beta(1)gamma(2) induced robust GIRK channel activity with an EC(50) of about 4 nm.

76 dylinositol bisphosphate to directly inhibit GIRK channel activity.

77 s completely abolished Gbeta1 stimulation of GIRK channel activity.

78 would allow intracellular Na(+) to modulate GIRK channel activity.

79 er, whether activity-dependent regulation of GIRK channels affects excitatory synaptic plasticity is

80 G-protein-gated inward rectifier K(+) (GIRK) channels allow neurotransmitters, through G-protei

81 G protein-gated inwardly rectifying K+ (GIRK) channels also depend on ATP hydrolysis for gating

82 ) in G-protein-gated inwardly rectifying K+ (GIRK) channels alters ion selectivity and reveals sensit

83 This slow response is partially sensitive to GIRK channel and D2 dopamine receptor block.

84 tion appears to specify interactions between GIRK channels and organizational elements involved in ch

85 planation for G alpha-specific activation of GIRK channels and other G betagamma-sensitive effectors.

86 hibits MCH neurons through H3R by activating GIRK channels and suggest that that inhibition of the MC

87 protein-regulated inwardly rectifying K(+) (GIRK) channels and delayed GIRK channel closure.

88 -protein-coupled inward rectifier potassium (GIRK) channels and hyperpolarization, but in response to

89 G protein-gated inward rectifying potassium (GIRK) channels and internalizes with kinetics similar to

90 G-protein-coupled inwardly rectifying K(+) (GIRK) channels and small conductance Ca(2+)-activated K(

91 pyridine), but blockers of calcium channels, GIRK channels, and SK-type potassium channels were ineff

92 latonin was blocked by coadministration of a GIRK channel antagonist tertiapin-q (TPQ).

93 eceptor, because postsynaptic G-proteins and GIRK channels appear to be fully functional.

94 The GIRK channels are activated by a number of inhibitory ne

95 the canonical G protein-activation pathway, GIRK channels are activated by small molecules but less

96 Chinese hamster ovary cells expressing only GIRK channels are also blocked by SCH23390.

97 es depotentiation of LTP, demonstrating that GIRK channels are critical for depotentiation, one form

98 GIRK channels are directly bound and activated by the G

99 While most neuronal GIRK channels are formed by GIRK1 and GIRK2 subunits, di

100 We conclude that GIRK channels are important functional effectors of the

101 These results are the first to show that GIRK channels are necessary for the effects of melatonin

102 The GIRK channels are regulated by diverse intra- and extrac

103 It is unknown whether GIRK channels are subject to regulation by guanine disso

104 GIRK channels are tetramers comprising combinations of s

105 Girk channels are tetramers consisting of various combin

106 GIRK channels are tetramers containing various combinati

107 iated Src kinase activation, suggesting that GIRK channels are upstream of Src family tyrosine kinase

108 protein-gated inwardly rectifying potassium (GIRK) channels are a family of K(+)-selective ion channe

109 citable cells inwardly rectifying potassium (GIRK) channels are activated by G betagamma dimers deriv

110 G protein-gated inwardly rectifying K+ (GIRK) channels are activated independently by Gbetagamma

111 protein-gated inwardly rectifying potassium (GIRK) channels are critical regulators of neuronal excit

112 protein-gated inwardly rectifying potassium (GIRK) channels are expressed in lamina II of the mouse s

113 G protein gated inward rectifier potassium (GIRK) channels are gated by direct binding of G protein

114 protein-gated inwardly rectifying potassium (GIRK) channels are important gatekeepers of neuronal exc

115 G-protein-gated inwardly rectifying K(+) (GIRK) channels are widely expressed in the brain and are

116 tein-coupled inward rectifier K(+) channels (GIRK channels) are activated directly by the G protein b

117 to the metabotropic receptor activating the GIRK channels, as direct activation of GIRK channels by

118 G-protein-coupled receptors that signal via GIRK channels, as indicated by greater antinociceptive e

119 ify the chemical features that contribute to GIRK channel block, we tested several structurally relat

120 Remarkably, GIRK2 null mutation or GIRK channel blockade abolishes depotentiation of LTP, d

121 Selective atrial GIRK channel blockade may effectively treat AF during co

122 otein-coupled inwardly rectifying potassium (GIRK) channel blockade.

123 The GIRK channel blocker rTertiapin-Q diminished the NECA-ev

124 Tertiapin (10-100 nmol/L), a selective GIRK channel blocker, counteracted adenosine-induced act

125 Furthermore, these GIRK channel blockers completely blocked Gi-mediated Src

126 a P2Y(12) receptor-selective antagonist, the GIRK channel blockers did not affect the ADP-induced ade

127 concentrations, the 2 structurally distinct GIRK channel blockers, SCH23390 and U50488H, caused comp

128 protein-activated inwardly rectifying K(+) (GIRK) channels, both residing in dendritic spines as wel

129 a low receptor reserve for the activation of GIRK channels but a >90% receptor reserve for the inhibi

130 s direct effects of G(beta)gamma subunits on GIRK channels, but mechanisms involved in GIRK channel i

131 membrane-permeant local anesthetics inhibit GIRK channels by antagonizing the interaction of PIP(2)

132 ible with 'membrane delimited' activation of GIRK channels by G proteins and the characteristic burst

133 Li(+) did not impair direct activation of GIRK channels by Gbetagamma, suggesting that inhibition

134 and biophysical bases for the inhibition of GIRK channels by intracellular protons are illustrated.

135 d sufficient for the selective activation of GIRK channels by ML297.

136 actions may be a common mechanism for gating GIRK channels by molecules as different as Na+ or the G[

137 teraction between the beta subunit and brain GIRK channels by mutating the outer surface of the betag

138 g the GIRK channels, as direct activation of GIRK channels by nonhydrolyzable GTP also potentiated th

139 hosphorylation underscores the inhibition of GIRK channels by SP, and Ser-185 in GIRK1 and Ser-191 in

140 am signaling events, including activation of GIRK channels by the Gbetagamma dimer resulting in membr

141 d a dual regulation of G protein-gated K(+) (GIRK) channels by Li(+), and identified the underlying m

142 that increased binding of Gbetagamma to the GIRK channel can effectively compete with the G(q)-media

143 otein-coupled inwardly rectifying potassium (GIRK) channels can be activated or inhibited by differen

144 G protein-coupled inwardly rectifying K+ (GIRK) channels can be activated or inhibited by distinct

145 protein-regulated inwardly rectifying K(+) (GIRK) channels can operate as dynamic integrators of alp

146 r, disrupting the ion selectivity in another GIRK channel, chimera I1G1(M), generates a GIRK channel

147 attached lipid instead of palmitate rendered GIRK channel closure insensitive to depalmitoylation inh

148 rectifying K(+) (GIRK) channels and delayed GIRK channel closure.

149 These data indicate that functional GIRK channels composed of GIRK2 and GIRK3 subunits exist

150 7 selectively activates recombinant neuronal GIRK channels containing the GIRK1 subunit in a manner t

151 otein-coupled inwardly rectifying potassium (GIRK) channels contribute to the resting membrane potent

152 GIRK channels control spike frequency in atrial pacemake

153 y subunits, rather than G(beta)gamma dimers: GIRK channel current inhibition was diminished by Pasteu

154 Inhibition of GIRK channel currents by TRH and constitutively active G

155 Inhibition of GIRK channel currents by TRH primarily involved signalin

156 Under these conditions, noradrenaline-evoked GIRK channel currents displayed: (1) a prominent lag pha

157 HT (5-hydroxytryptamine; serotonin) enhanced GIRK channel currents, whereas thyrotropin-releasing hor

158 TRH) inhibited both basal and 5-HT-activated GIRK channel currents.

159 contrast, beta5-containing dimers inhibited GIRK channel currents.

160 he deactivation kinetics of baclofen-induced GIRK channel currents.

161 ound that beta5gamma2 could bind to the same GIRK channel cytoplasmic domains as other, activating Gb

162 GIRK channels decrease cellular excitability by hyperpol

163 rein, we show that GABABR signaling to Kir3 (GIRK) channels decreases with NMDAR blockade.

164 ve reported activity-dependent regulation of GIRK channel density in cultured hippocampal neurons tha

165 rovide a mechanism for dynamic regulation of GIRK channel density in the plasma membrane.

166 unit on the recombinant P/Q-type channel and GIRK channel expressed in HEK293 cells and on native non

167 protein-gated inwardly rectifying potassium (GIRK) channels expressed in the brain is unknown.

168 Given the importance of GIRK channels for neuronal excitability (with >600 publi

169 strate that mouse VTA GABA neurons express a GIRK channel formed by GIRK1 and GIRK2 subunits.

170 Here, we report that GIRK channels formed by GIRK1 and GIRK2 subunits are fou

171 the functional and biochemical properties of GIRK channels formed by the co-assembly of GIRK2 and GIR

172 ir3.2 and Kir3.1/Kir3.4 heterotetramers, the GIRK channels found in the brain and the heart, respecti

173 ole of caspase-3 mediated down-regulation of GIRK channel function and expression in hippocampal neur

174 ions that selectively enhanced or suppressed GIRK channel function in midbrain DA neurons correlated

175 hese findings demonstrate that regulation of GIRK channel function is a dominant factor in gonadotrop

176 tanding many studies reporting modulation of GIRK channel function, whether neuronal activity regulat

177 -mutant studies, these findings suggest that GIRK channels gate by moving from the open conformation

178 by the modulatory affects of RGS proteins on GIRK channel gating.

179 for understanding multiligand regulation of GIRK channel gating.

180 otein-coupled inwardly rectifying potassium (GIRK) channels, GIRK1/4, heterologously expressed in sym

181 ls targeting an integral subunit of neuronal GIRK channels (GIRK2) to probe the impact of GIRK channe

182 Whereas GIRK4 is associated with the cardiac GIRK channel, Girk4 expression has been detected in a fe

183 ies such as epilepsy and addiction, in which GIRK channels have been implicated.

184 etagamma-activated inwardly rectifying K(+) (GIRK) channels have distinct gating properties when acti

185 G-protein-activated inward-rectifying K(+) (GIRK) channels hyperpolarize neurons to inhibit synaptic

186 Because activation of GIRK channels hyperpolarizes neuronal membranes, the NMD

187 Mice lacking GIRK channels in DA neurons exhibited increased locomoto

188 Our data suggest that GIRK channels in dorsal hippocampal pyramidal neurons ar

189 irk1 or Girk2, nor the selective ablation of GIRK channels in GABA neurons, diminished morphine-induc

190 Moreover, direct activation of GIRK channels in midbrain GABA neurons did not enhance m

191 led m2-muscarinic acetylcholine receptors to GIRK channels in Xenopus oocytes to evaluate the effect

192 otein-coupled inwardly rectifying potassium (GIRK) channels in hypothalamic POMC neurons through a me

193 ein-activated inwardly rectifying potassium (GIRK) channels in neuronal PC12 cells, resulting in loss

194 e distribution of G-protein-gated potassium (GIRK) channels in the mouse spinal cord and measured the

195 protein-gated inwardly rectifying potassium (GIRK) channels in these cells.

196 ng G-protein-gated inwardly rectifying K(+) (Girk) channels in VTA DA neurons.

197 otein-coupled inwardly rectifying potassium (GIRK) channels in Xenopus oocytes.

198 ereas Gbeta1-4 subunits activate heteromeric GIRK channels independently of receptor activation, Gbet

199 t influence G-protein heterotrimer action in GIRK-channel induced pacemaker membrane hyperpolarizatio

200 on GIRK channels, but mechanisms involved in GIRK channel inhibition have not been fully elucidated.

201 Moreover, TRH- R1-mediated GIRK channel inhibition was diminished by minigene const

202 ries did not contribute to receptor-mediated GIRK channel inhibition, bath application of TRH decreas

203 potential physiological significance of the GIRK channel inhibition.

204 ed to test G protein mechanisms that mediate GIRK channel inhibition.

205 ein-dependent inwardly rectifying potassium (GIRK) channel inhibitor, abolishes histaminergic inhibit

206 However, the GIRK channel inhibitors did not affect platelet aggregat

207 Furthermore, the GIRK channel inhibitors reversed SFLLRN-induced platelet

208 ndicate that receptor-mediated inhibition of GIRK channels involves PLC activation by G(alpha) subuni

209 e notion that the subunit composition of VTA GIRK channels is a critical determinant of DA neuron sen

210 responses as m1 mAChR-mediated inhibition of GIRK channels is mimicked by PMA and Ca2+ ionophore.

211 The surface expression of neuronal GIRK channels is regulated by the psychostimulant-sensit

212 The inhibition of GIRK channels is somewhat selective because members of t

213 ith either RGS7 or RGS9, the acceleration of GIRK channel kinetics was strongly increased over that p

214 of either RGS7 or RGS9 modestly accelerated GIRK channel kinetics.

215 -expression of Gbeta5 alone had no effect on GIRK channel kinetics.

216 The gating properties of GIRK channels (Kir3.1/Kir3.2a) activated by muscarinic m

217 king G protein-coupled inward rectifying K+ (GIRK) channels largely abolished the mutation-induced en

218 nous LHR expressed in GnRH neurons activates GIRK channels, leading to suppression of membrane excita

219 amate release and postsynaptic activation of GIRK channels, leading to the dampening of both spindle-

220 protein-gated inwardly rectifying potassium (GIRK) channels leads to a hyperpolarization of the neuro

221 Here we show that the GIRK channels linked to GABAB receptors differed in two

222 in levels coupled with known function of the GIRK channel may suggest an important contribution of GI

223 This study suggests that GIRK channels may be an alternative therapeutic target f

224 We identify a powerful cholinergic-GIRK channel mechanism operating at the hypoglossal moto

225 firing, suggesting the involvement of a non-GIRK channel mechanism.

226 ium (GIRK) channels, we investigated whether GIRK channels mediate any of the functional responses of

227 GIRK channels mediate the actions of inhibitory brain ne

228 ein-activated inwardly rectifying potassium (GIRK) channels mediate slow synaptic inhibition and cont

229 Neuronal G-protein-gated potassium (GIRK) channels mediate the inhibitory effects of many ne

230 ring modes drive bidirectional plasticity of GIRK channel-mediated currents.

231 GIRK channel modulation was reconstituted in PTX-treated

232 protein-activated inwardly rectifying K(+) (GIRK) channels near excitatory synapses on dendritic spi

233 GIRK channels (GIRK2) to probe the impact of GIRK channels on associative learning and memory.

234 the effect of the DA neuron-specific loss of GIRK channels on D2R-dependent regulation of VTA DA neur

235 How GIRK channels open upon contact with Gbetagamma remains

236 G protein gated inward rectifier K(+) (GIRK) channels open and thereby silence cellular electri

237 For example, Kir3 (GIRK) channels open on binding to the G protein betagamm

238 Further mutagenesis indicates that GIRK channel opening involves a rotation of the transmem

239 rimer, modulate effectors (N-type Ca(2+) and GIRK channels), or couple to receptors.

240 taining dimers inhibit Gbetagamma-stimulated GIRK channels, perhaps by directly binding to the channe

241 In conclusion, activity-dependent GIRK channel plasticity may represent a slow destabiliza

242 ich G-protein-coupled inward rectifier K(+) (GIRK) channels play a role.

243 G-protein-coupled inward rectification K(+) (GIRK) channels play an important role in modulation of s

244 significant changes in expression of Gi/o or GIRK channel proteins.

245 there should be PKC phosphorylation sites in GIRK channel proteins.

246 G protein-independent pathways of activating GIRK channels provides a unique strategy for developing

247 G protein-coupled inward rectifier K(+) (GIRK) channels regulate cellular excitability and neurot

248 protein-activated inwardly rectifying K(+) (GIRK) channels regulate neuronal excitability by mediati

249 ural or functional diversity in the neuronal GIRK channel repertoire.

250 Certain transmitters inhibit Kir3 (GIRK) channels, resulting in neuronal excitation.

251 detect movements of the cytoplasmic tails of GIRK channels (Riven et al., this issue of Neuron).

252 might provide the basis for designing novel GIRK channel-selective blockers.

253 lation or pharmacologic inhibition of spinal GIRK channels selectively blunted the analgesic effect o

254 rd and that pharmacologic ablation of spinal GIRK channels selectively blunts the analgesic effect of

255 CR4 and the G-protein inward rectifier K(+) (GIRK) channel showed that GABAB antagonist and agonist m

256 athway for morphine-dependent enhancement of GIRK channel signaling in hippocampal neurons.

257 cuss recent advances in our understanding of Girk channel structure, organization in signaling comple

258 data support the contention that the unique GIRK channel subtype in VTA DA neurons, the GIRK2/GIRK3

259 Altogether, our data show that different GIRK channel subtypes can couple to GABAB receptors in v

260 layer of the cerebellum along with neuronal GIRK channel subunits 1 and 2 where RGS6 forms a complex

261 l neurons elevates surface expression of the GIRK channel subunits GIRK1 and GIRK2 in the soma, dendr

262 We found that the GIRK channel subunits GIRK1 and GIRK2 were concentrated

263 urons natively expressed RGS6, GABA(B)R, and GIRK channel subunits, and cerebellar granule neurons fr

264 upled inwardly rectifying potassium channel (GIRK) channel subunits.

265 e wondered whether NMDAR-induced increase in GIRK channel surface density and current may contribute

266 terotrimers are more effective activators of GIRK channels than G(s) heterotrimers when comparable am

267 r GIRK channel, chimera I1G1(M), generates a GIRK channel that is also inhibited by extracellular loc

268 dies show that toluene has effects on BK and GirK channels that are opposite to those of ethanol, sug

269 ein-activated inwardly rectifying potassium (GIRK) channels that mediate membrane hyperpolarization a

270 ts are known to bind the N- and C-termini of GIRK channels, the mechanism underlying G(betagamma) act

271 ng G protein-gated inwardly rectifying K(+) (GIRK) channels, thereby moderating the influence of exci

272 eins modulate inwardly rectifying potassium (GIRK) channels through direct interactions.

273 transfection assay in cell lines expressing GIRK channels to examine effects of dimers containing th

274 mpetitively with the intracellular domain of GIRK channels to facilitate rapid activation and deactiv

275 Dose-dependent contributions of GIRK channels to the analgesic effects of the -opioid re

276 DNX activated GIRK channels to the same extent as QP, whereas DHX and

277 r new hope for the selective manipulation of Girk channels to treat a variety of debilitating afflict

278 with G protein-gated inwardly rectifying K+ (GIRK) channels to stimulate their activity.

279 nes, the NMDA receptor-induced regulation of GIRK channel trafficking may represent a dynamic adjustm

280 unction, whether neuronal activity regulates GIRK channel trafficking remains an open question.

281 channels suggests a model for activation of GIRK channels using this hydrophobic alcohol-binding poc

282 ibition may be communicated at a distance to GIRK channels via unbinding and diffusion of phosphatidy

283 Function of all GIRK channels was enhanced by intoxicating concentration

284 NPY activation of GIRK channels was mediated via NPY1 receptors, whereas i

285 ay that led to the ACh-induced inhibition of GIRK channels was unaffected by pertussis toxin pretreat

286 between endogenous muscarinic receptors and GIRK channels, we found that firing of individual CHIs r

287 beta2 with multiple Ggamma subunits activate GIRK channels, we hypothesized that specificity might be

288 te the effect of extracellular pH (pH(o)) on GIRK channels, we performed experiments on heteromeric G

289 known to activate G-protein-gated potassium (GIRK) channels, we investigated the hypothermic response

290 rotein-gated, inwardly rectifying potassium (GIRK) channels, we investigated whether GIRK channels me

291 -linking, and inwardly rectifying potassium (GIRK) channels were used as rapid indicators of G-protei

292 binding property of mutant Gbeta2 to cardiac GIRK channels when compared with native Gbeta2.

293 Therefore, these channels are GIRK channels, which are constitutively active at rest i

294 d leads to a sustained activation of cardiac GIRK channels, which is likely to hyperpolarize the myoc

295 protein-gated inwardly rectifying potassium (GIRK) channels, which help control neuronal excitability

296 urons through the Y1R-mediated activation of GIRK channels, while the alphaMSH analog, MTII, had no e

297 The whole-cell current of GIRK channels with a constitutively active gate, GIRK2(V

298 I(4,5)P2, PI(3,4)P2 and PI(3,5)P2, activated GIRK channels with similar potencies.

299 Mobile and immobile MORs activated GIRK channels with the same onset kinetics and agonist s

300 Bupivacaine inhibited GIRK channels within seconds of application, regardless