ライフサイエンスコーパス: inward rectifier

1 upling between a transport ATPase and a K(+) inward rectifier.

2 f selective pharmacological probes targeting inward rectifiers.

3 prising the sulfonylurea receptor 2B and the inward rectifier 6.1 subunit (SUR2B/Kir6.1).

4 sulfonylurea receptor 1 (SUR1) and potassium inward rectifier 6.2 (Kir6.2), the two adjacent genes on

5 4 subunit and Kir2.1 (Gbetagamma-independent inward rectifier) also resulted in a decrease in channel

6 the diversity in the activation kinetics of inward rectifiers among different plant species.

7 for potassium channels of the voltage-gated, inward rectifier and calcium-activated classes, ClC-type

8 -permeable ion channels, including 20-100 pS inward rectifiers and 150-200 pS apparent Ca(2+)-activat

9 rstanding the overall structural features of inward rectifiers and ATP-binding cassette (ABC) transpo

10 nt consequences between similar mutations in inward-rectifier and voltage-gated K+ channels, which su

11 inhibition of a K(+) current, presumably an inward rectifier, and a Na(+)-dependent component.

12 Inward rectifiers are a class of K+ channels that can co

13 sequence analysis identified two related K+ inward rectifier cDNAs, referred to as Kir1.2 and Kir1.3

14 gulated hyperpolarization-activated chloride inward rectifier channel (Cl.ir) was identified in mamma

15 The G protein-insensitive inward rectifier channel (IRK1) contains the same class

16 inositol 4,5-bisphosphate (PIP(2))-sensitive inward rectifier channel Kir2.1 was expressed in Drosoph

17 We have cloned a novel K+-selective, inward rectifier channel that is widely expressed in bra

18 itable primers on human eosinophils mRNA, an inward rectifier channel, Kir2.1, was identified, which

19 Using genetically targeted PIP2-sensitive inward rectifier channels (Kir2.1) as biosensors, we pro

20 at depolarized membrane potentials, whereas inward rectifier channels conduct greater current at hyp

21 have as few as three, and on average twenty, inward rectifier channels each.

22 s of research on the possible role played by inward rectifier channels in the mechanism of VF, as wel

23 Thus, it may be beneficial to block inward rectifier channels under conditions in which thei

24 Under conditions in which cationic inward rectifier channels were blocked, membrane hyperpo

25 tivity in a manner similar to that seen with inward rectifier channels.

26 the KvAP (voltage-activated) and KirBac1.1 (inward rectifier) channels, as well as models of the por

27 ve investigated the gating properties of the inward rectifier chloride channel (Cl(ir)) from mouse pa

28 ed by channels which are distinct from other inward-rectifier Cl- channels, e.g. ClC-2, phospholemman

29 r identification of a novel chloride (Cl(-)) inward rectifier (Cl.ir) in mammalian heart.

30 An inward rectifier conductance appeared at approximately E

31 The results suggest that inward rectifiers contain an intrapore-binding site for

32 Here, we used a crystal structure of a mouse inward rectifier containing a bound alcohol and structur

33 cells exhibited I(K(V)) and large potassium inward rectifier current (I(K(IR))), and occasionally a

34 nea pig (GP) heart, suggesting a role of the inward rectifier current (I(K1)) in the mechanism govern

35 transient outward current (I(to,f)) and the inward rectifier current (I(K1)) were selectively upregu

36 However, type B cells express an inward rectifier current (Ih) that has different permeat

37 ated (by ?44%), whereas the Ba(2+)-sensitive inward rectifier current (IKir,fb) was upregulated by 79

38 d and moderately prolonged suppression of an inward rectifier current (IRK+).

39 cant changes in I(to), sustained current, or inward rectifier current densities, but peak L-type Ca(2

40 The inward rectifier current I(K1) is tightly regulated regi

41 The inward rectifier current in A cells (IK1) was time-indep

42 tion and pharmacological properties from the inward rectifier current in type A cells.

43 and p.P888L-SAP97 cardiomyocytes, while the inward rectifier current increased in WT-SAP97 but not i

44 oth chambers as well as higher levels of the inward rectifier current only in RV myocytes.

45 Hypercapnic acidosis activated an inward rectifier current that was K+-selective and sensi

46 Kir2.x) channels that underlie the classical inward rectifier current, I(K1).

47 ary endothelial cells (HCEC) contain a large inward rectifier current, IK(IR), that can be abolished

48 otassium channels (I(BK,steady)), and larger inward rectifier currents (I(K1)).

49 h most glial recordings reveal expression of inward rectifier currents (K(IR)), it is not clear how s

50 g substance P mRNA exhibited noninactivating inward rectifier currents, whereas neurons expressing en

51 ssing enkephalin mRNA exhibited inactivating inward rectifier currents.

52 and densities of sodium, L-type calcium, and inward rectifier currents.

53 n in human heart by acutely blocking cardiac inward rectifier currents.

54 y reported 1.8 A resolution structure of the inward-rectifier cytoplasmic pore, adapted to Kir2.1, is

55 ion of promiscuity of SUR1 outside of the K+ inward rectifier family of channels.

56 hibitor of ROMK1, a channel belonging to the inward rectifier family of K+ channels.

57 The KirBac1.1 channel belongs to the inward-rectifier family of potassium channels.

58 differential expression of the two distinct inward rectifiers found in type A and B cells contribute

59 ral integrity of this region is critical for inward rectifier function.

60 the outer mouth of Kir1.1b directly affected inward rectifier gating by external K, independent of pH

61 coexpression of members of the pore-forming inward rectifier gene family (Kir6.1, KCNJ8, and Kir6.2

62 the relative expression levels of different inward rectifier genes.

63 pe I-specific conductance gK,L and/or a slow inward rectifier, gh.

64 G protein-coupled inward rectifiers (GIRKs) are activated directly by G pr

65 ted positive to resting potential and a fast inward rectifier, gK1.

66 The potassium inward rectifier I(K(ir)), activated at similar voltages

67 posure (up to 15 min); the amplitude of slow inward rectifier (I(h)) currents activated from -50 mV w

68 Cer but not sph or SPP inhibits the inward rectifier (I(Kir)) in OLGs.

69 Time-dependent block of the inward rectifier, I(K1), at hyperpolarized potentials de

70 presence of the time- and voltage-dependent inward rectifier (Ih) and the low-threshold calcium curr

71 l, inward Ca2+ currents (ICa) appear and the inward rectifier (IK(IR)), the sole resting conductance,

72 One day later the inward rectifier, IK1, is first observed.

73 expression and physiological role of anionic inward rectifiers in heart are unknown.

74 The strong inward rectifier IRK1 (Kir 2.1) opened and closed with k

75 conductance similar to those of a classical inward rectifier, IRK3.

76 rotein betagamma subunits, whereas classical inward rectifiers (IRKs) are constitutively active.

77 n that channel activity of Kir2 subfamily of inward rectifiers is strongly suppressed by the elevatio

78 IP(3), inositol (1,4,5)-triphosphate; (K)ir, inward rectifier; JNK, c-Jun N-terminal kinase; I(K), in

79 zations from any cause by overexpressing the inward rectifier K channel Kir2.1 in stabilizer cells.

80 nd 3.1 are bacterial homologues of mammalian inward rectifier K channels.

81 els and heterotetrameric G-protein-regulated inward rectifier K channels.

82 rt the intermolecular model for pH gating of inward rectifier K channels.

83 gamma that are crucial for G protein-coupled inward rectifier K(+) (GIRK) channel activation.

84 h we coexpressed rat CXCR4 and the G-protein inward rectifier K(+) (GIRK) channel showed that GABAB a

85 G-protein-gated inward rectifier K(+) (GIRK) channels allow neurotransmi

86 G protein gated inward rectifier K(+) (GIRK) channels open and thereby s

87 tic transmissions in which G-protein-coupled inward rectifier K(+) (GIRK) channels play a role.

88 G protein-coupled inward rectifier K(+) (GIRK) channels regulate cellular

89 ed P2Y receptors to neuronal G protein-gated inward rectifier K(+) (GIRK) channels.

90 ilators in the heart, by activating vascular inward rectifier K(+) (K(ir)) channels, we tested the hy

91 Although strong inward rectifier K(+) (Kir) channels have been reported

92 ac1.1 and KirBac3.1) and eukaryotic (Kir2.1) inward rectifier K(+) (Kir) channels.

93 sm and K(ATP) channels and the minor role of inward rectifier K(+) (Kir2.1) channels in regulating bl

94 of the nucleus basalis (NB) by inhibiting an inward rectifier K(+) channel (Kir).

95 e COOH-terminal region of an ATP-insensitive inward rectifier K(+) channel (Kir2.1).

96 for two representative genes, i.e. the weak inward rectifier K(+) channel (TWIK-1), and phosphate an

97 ular N- and C termini of the G protein-gated inward rectifier K(+) channel GIRK1 at 1.8 A resolution.

98 he effect of TGF-beta(1) on the 14-pS Kir2.3 inward rectifier K(+) channel in rat primary cultured re

99 Here we use human Inward Rectifier K(+) Channel Kir2.1 to map site-specifi

100 sed by mutations in KCNJ2, which encodes the inward rectifier K(+) channel Kir2.1.

101 in SUR1 (Sulfonylurea receptor 1) or KIR6.2 (Inward rectifier K(+) channel member 6.2), which encode

102 ) in KCNJ2, the gene that encodes the strong inward rectifier K(+) channel protein (Kir2.1), in an 11

103 Inward rectifier K(+) channel subfamily 2 (Kir2) channel

104 ABSTRACT: Inward rectifier K(+) channel subfamily 2 (Kir2) channel

105 In the present study, we show that inward rectifier K(+) channel subfamily 2 isoform 1 (Kir

106 ATP-binding cassette protein family, and an inward rectifier K(+) channel subunit (Kir6.x).

107 GIRK (G protein-gated inward rectifier K(+) channel) proteins play critical fu

108 cells were also transfected with the Kir2.3 inward rectifier K(+) channel, which allows for changing

109 G protein-coupled inward rectifier K(+) channels (GIRK channels) are activ

110 gulated in homologs, such as G-protein-gated inward rectifier K(+) channels (GIRK), have differential

111 from the endothelium, and (b) activation of inward rectifier K(+) channels (K(ir)) and Na(+)-K(+) pu

112 Inward rectifier K(+) channels apparent lack of selectiv

113 Inward rectifier K(+) channels commonly exhibit long ope

114 Inward rectifier K(+) channels govern the resting membra

115 nd extracellular K(+) on the distribution of inward rectifier K(+) channels in the glial endfoot and

116 s of metabolic inhibitors on the activity of inward rectifier K(+) channels K(ir)2.1, K(ir)2.2, and K

117 lactotrophs and the subsequent activation of inward rectifier K(+) channels provide an effective and

118 Inhibition of inward rectifier K(+) channels under ischemic conditions

119 A cytoplasmic pore, conserved among inward rectifier K(+) channels, extends the ion pathway

120 modulated N-type Ca(2+) and G-protein-gated inward rectifier K(+) channels.

121 resembles the cytoplasmic pore structures of inward rectifier K(+) channels.

122 We explored the role of inward rectifier K(+) conductances in colonic ICC that m

123 Doubling the magnitude of the inward rectifier K(+) current (I(K1)) increased rotor fr

124 DHF significantly reduced the inward rectifier K(+) current (I(K1)), delayed rectifier

125 oroquine inhibition of cardiac ATP-sensitive inward rectifier K(+) current (I(KATP)) is antifibrillat

126 In contrast, inward rectifier K(+) current and L-type Ca(2+) channels

127 onents of transient outward K(+) current and inward rectifier K(+) current, along with corresponding

128 G protein-regulated inward rectifier K+ (GIRK) channels were over-expressed

129 Heteromultimeric G protein-activated inward rectifier K+ (GIRK) channels, abundant in heart a

130 subunits bind and activate G protein-coupled inward rectifier K+ (GIRK) channels.

131 on of extracellular potassium (K+) activated inward rectifier K+ (Kir) channels and caused membrane p

132 pore, acts as a gate for PIP2 activation of inward rectifier K+ (Kir) channels expressed in Xenopus

133 closest relative, Kir1.3 (Kir1-ATP-regulated inward rectifier K+ [ROMK] family) and displays none of

134 The G-protein gated inward rectifier K+ channel (GIRK) is activated in vivo

135 We report that the IRK3 but not the IRK1 inward rectifier K+ channel activity is inhibited by m1

136 Kir4.1 and Kir5.1, two members of the inward rectifier K+ channel family, are expressed in sev

137 opmental features caused by mutations in the inward rectifier K+ channel gene KCNJ2.

138 ive sequence homology with previously cloned inward rectifier K+ channel genes.

139 a mouse liver cDNA library to identify novel inward rectifier K+ channel genes.

140 The molecular nature of the strong inward rectifier K+ channel in vascular smooth muscle wa

141 Using the Inward Rectifier K+ channel Kir2.1, we validate the prac

142 The inward rectifier K+ channel Kir2.3 is inhibited by hyper

143 which results in the phosphorylation of the inward rectifier K+ channel protein.

144 G protein-gated inward rectifier K+ channel subunits 1-4 (GIRK1-4) have

145 IKAChis composed of two inward rectifier K+ channel subunits, GIRK1 and GIRK4.

146 pore-forming H5 (or P) region of the strong inward rectifier K+ channel, Kir2.1, based initially on

147 ct on a cloned voltage-gated Na+ channel, an inward rectifier K+ channel, or on lymphocyte Ca2+ and C

148 The ROMK subtypes of inward rectifier K+ channels (Kir 1.1, KCNJ1) mediate po

149 Inward rectifier K+ channels control the cell's membrane

150 Here we report that several cloned inward rectifier K+ channels directly bind PIP2, and tha

151 We conclude that Kir2.1 encodes for inward rectifier K+ channels in arterial smooth muscle.

152 dependent lipid kinases is known to activate inward rectifier K+ channels in cardiac membrane patches

153 Structural models of inward rectifier K+ channels incorporate four identical

154 The Kir1.1 (ROMK) subtypes of inward rectifier K+ channels mediate potassium secretion

155 a blocker explains the signature feature of inward rectifier K+ channels, namely, that at a given co

156 Inward rectifier K+ channels, which modulate electrical

157 itical in trafficking and conductance of the inward rectifier K+ channels.

158 age-dependent manner, characteristic of many inward rectifier K+ channels.

159 ies have suggested an important role for the inward rectifier K+ current (I K1) in stabilizing rotors

160 he embryonic myocytes to FGF-1 downregulated inward rectifier K+ current (IK(IR)) density as well as

161 e Ca2+ or transient outward K+ currents, but inward rectifier K+ current (IK1) was significantly decr

162 Cs+ inhibited the inward rectifier K+ current (KIR) and increased the freq

163 polarization-activated current (HCN), but no inward rectifier K+ current.

164 2+, Cs+, Ca2+ and Mg2+ were very similar for inward rectifier K+ currents from native cells and clone

165 cloned Kir2.1 in Xenopus oocytes resulted in inward rectifier K+ currents that strongly resemble thos

166 ndicate that Gi mediates the SRIF effects on inward rectifier K+ currents.

167 Inward-rectifier K(+) (Kir) channels are often activated

168 quired for activation and K(+) conduction in inward-rectifier K(+) (Kir) channels are still debated.

169 Strong inward-rectifier K(+) (Kir) channels play a significant

170 Inward-rectifier K(+) (Kir) channels play many important

171 bee venom, inhibits only certain eukaryotic inward-rectifier K(+) (Kir) channels with high affinity.

172 ffective blockers of K(+) ion efflux through inward-rectifier K(+) (Kir) channels, we examined the in

173 y-which activates capillary endothelial cell inward-rectifier K(+) (KIR2.1) channels to produce a rap

174 ankyrin domain in the cytosolic side of the inward-rectifier K(+) channel AKT1 regulates kinase dock

175 It shares the common inward-rectifier K(+) channel fold with eukaryotic chann

176 KirBac1.1 is a prokaryotic inward-rectifier K(+) channel from Burkholderia pseudoma

177 localize the pH-sensitive gate in the renal inward-rectifier K(+) channel Kir1.1a (ROMK1).

178 containing the ABC transporter SUR1 and the inward-rectifier K(+) channel Kir6.2, in the presence of

179 all-or-none-like conductance changes of the inward-rectifier K(+) channel.

180 lls under resting conditions is dominated by inward-rectifier K(+) channels belonging to the Kir 2 fa

181 (Q)), a honey bee toxin derivative, inhibits inward-rectifier K(+) channels by binding to their exter

182 The ROMK subtypes of inward-rectifier K(+) channels mediate potassium secreti

183 TPN(Q) inhibits the ROMK1 and GIRK1/4 inward-rectifier K(+) channels with affinities very simi

184 nd mutant heteromultimeric G protein-coupled inward-rectifier K+ (GIRK) channels in Xenopus oocytes.

185 uine's effectiveness may be explained by its inward-rectifier K+ channel blockade profile and suggest

186 bitory agents specific to each member of the inward-rectifier K+ channel family.

187 g characteristics of two ion channels in the inward-rectifier K+ channel superfamily were compared at

188 We have purified a protein inhibitor of an inward-rectifier K+ channel, ROMK1, from the venom of th

189 gh-affinity ligands that directly target any inward-rectifier K+ channel.

190 However, it is unknown whether inward-rectifier K+ channels and reentry are also import

191 Inward-rectifier K+ channels are a group of highly speci

192 Blockade of inward-rectifier K+ channels by chloroquine terminates r

193 ROMK inward-rectifier K+ channels control renal K+ secretion.

194 Inward-rectifier K+ channels differ from voltage-activat

195 Each of the four subunits of the inward-rectifier K+ channels has only two instead of six

196 yotic pore into eukaryotic voltage-gated and inward-rectifier K+ channels.

197 very useful molecular probe for studying the inward-rectifier K+ channels.

198 , and synthesized a protein inhibitor of the inward-rectifier K+ channels.

199 Inward-rectifier K+ current (IK1) is believed to be an i

200 sium conductance, and to a lesser extent the inward rectifier (K(IR)) conductance, underlies neuronal

201 ic and functional data showing that the K(+) inward rectifier KAT1 (K(+)Arabidopsis thaliana 1) chann

202 lice variants transiently expressed with the inward rectifier Kir 6.2 formed functional K(ATP) channe

203 To differentiate these possibilities in inward rectifier (Kir) channels, we examined cysteine ac

204 f potassium channels: voltage-gated (Kv) and inward rectifier (Kir) channels.

205 nding of this nucleotide to the pore-forming inward rectifier (Kir) subunit despite the lack of known

206 m conductance predominantly mediated by K(+) inward rectifier (Kir)2.1, which was blocked by the NMDA

207 Although the cationic inward rectifiers (Kir and hyperpolarization-activated I

208 , calcium-operated (BK, -52%, p < 0.05), and inward-rectifier (Kir, -40%, p < 0.05) K+ channels prima

209 xpression of their subunits (e.g., potassium inward rectifier [Kir] 6.2) in adult pathologies are mos

210 These features are those of an "inward rectifier," Kir.

211 Gating of inward rectifier Kir1.1 potassium channels by internal p

212 strong inward rectifier Kir2.1 and the weak inward rectifier Kir1.1.

213 ds to the physiological pH gate of the renal inward rectifier, Kir1.1 (ROMK, KCNJ1).

214 was intermediate between that of the strong inward rectifier Kir2.1 and the weak inward rectifier Ki

215 s well as the fully open state in the strong inward rectifier Kir2.1 channel.

216 potassium channel blocker, barium, with the inward rectifier Kir2.1, we identify mutants bearing pos

217 PIP(2) is the primary agonist for classical inward rectifier (Kir2) channels, through which this lip

218 port a direct interaction between the strong inward rectifier, Kir2.1, and a recently identified spli

219 e cloning of the gene encoding the beta-cell inward rectifier Kir6.2 (Bir), a subunit of the beta-cel

220 at encode the sulfonylurea receptor 1 or the inward rectifier Kir6.2 subunit of the channel, is a maj

221 However, when SURx is combined with an inward rectifier Kir6.2 subunit, ATP-sensitive potassium

222 sette family of proteins, associate with the inward rectifier Kir6.x to form ATP-sensitive potassium

223 eptor 1 (SUR1 or ABCC8) and a K(+)-selective inward rectifier (Kir6.2 or KCNJ11).

224 ) channels consist of pore-forming potassium inward rectifier (Kir6.x) subunits and sulfonylurea rece

225 ), twin-pore domain K channels (TASK, TREK), inward rectifier Kir7.1, Ca(2+)-activated K(+) channels

226 losed-state crystal structure of prokaryotic inward rectifier, KirBac1.1, has implicated four inner h

227 converts the channel from a weak to a strong inward rectifier, on the G156R background restored ion c

228 e affinity of a weak ATP binding site on the inward rectifier or affects linkage between the binding

229 heteromultimers of KIR6.2, a weak potassium inward rectifier, plus SUR2A, a low-affinity sulfonylure

230 regulated (K(ATP)) channels are formed by an inward rectifier pore-forming subunit (Kir) and a sulfon

231 leads to the activation of G-protein-coupled inward rectifier potassium (GIRK) channels and hyperpola

232 G protein gated inward rectifier potassium (GIRK) channels are gated by

233 G-protein-gated inward rectifier potassium (GIRK) channels are regulated

234 onal coupling of mGluR7 to G protein-coupled inward rectifier potassium (GIRK) currents in a heterolo

235 sium (K(ATP)) channel is assembled from four inward rectifier potassium (K(ir)6.x) subunits and four

236 = 0.2 muM), small-molecule inhibitor of the inward rectifier potassium (Kir) channel and diuretic ta

237 Inward rectifier potassium (Kir) channels act as cellula

238 Inward rectifier potassium (Kir) channels are physiologi

239 Inward rectifier potassium (Kir) channels play important

240 Inward rectifier potassium (Kir) channels regulate cell

241 Emerging evidence suggests that mosquito inward rectifier potassium (Kir) channels represent viab

242 Endothelial cells express inward rectifier potassium (Kir) channels, but their rol

243 Strong inward rectifier potassium (Kir2) channels are important

244 engineered excitable donor cells expressing inward rectifier potassium (Kir2.1) and cardiac sodium (

245 vailable on interactions involving SAP97 and inward rectifier potassium (Kir2.x) channels that underl

246 lation of MRF4, as evidenced by induction of inward rectifier potassium and acetylcholine receptor ch

247 ulated potassium (KATP) channel complexes of inward rectifier potassium channel (Kir) 6.2 and sulfony

248 Inward rectifier potassium channel (Kir) Kir2.2 has mult

249 expressing either connexin-43 (Cx43 HEK) or inward rectifier potassium channel 2.1 (Kir2.1) and Cx43

250 itional experiments using the PIP2-sensitive inward rectifier potassium channel Kir2.1 as a biosensor

251 nding partners, kainate receptor GluR6/7 and inward rectifier potassium channel Kir2.1, closely assoc

252 of the sulfonylurea receptor 1, SUR1, and an inward rectifier potassium channel subunit, Kir6.2, regu

253 Loss-of-function mutations in the inward rectifier potassium channel, Kir2.1, cause Anders

254 scarinic m2 ACh receptors (mAChRs) linked to inward rectifier potassium channels (K(ir)) evenly distr

255 effects of e-LXA4 on signaling and on Kv and inward rectifier potassium channels (Kir) in mice bone m

256 Inward rectifier potassium channels (Kir) play critical

257 zation are associated with downregulation of inward rectifier potassium channels (Kir2.1/2.3).

258 s a major contributor to G protein-activated inward rectifier potassium channels in the mammalian bra

259 e m2 muscarinic receptor and G-protein-gated inward rectifier potassium channels show that RGS9-2, vi

260 ceptor channels, and up-regulation of muscle inward rectifier potassium channels.

261 hmias can be perpetuated by up-regulation of inward rectifier potassium channels.

262 ecific residues of the cytoplasmic domain of inward rectifier potassium channels.

263 C) revealed the presence of a Ba2+-sensitive inward rectifier potassium conductance.

264 The inward rectifier potassium current (I(K1)) is reduced by

265 ssium (Kir) 2.x channels mediate the cardiac inward rectifier potassium current (I(K1)).

266 cific outward conductance differences in the inward rectifier potassium current (I(K1)).

267 K+]o should increase the adenosine-activated inward rectifier potassium current (IK,ADO) in AV nodal

268 ed rectifier potassium current (IKr) and the inward rectifier potassium current (IK1) were also downr

269 ration, [K+]o, because of the absence of the inward rectifier potassium current (IK1).

270 ison of predictions across models identified inward rectifier potassium current and the sodium-potass

271 e recently created by genetic suppression of inward rectifier potassium current, I(K1), in guinea pig

272 ing delayed-rectifier potassium current, the inward rectifier potassium current, the acetylcholine ac

273 f adenylyl cyclase and by the stimulation of inward rectifier potassium current.

274 (I(KACh)), or Kir6.2 (I(KATP)) and reducing inward rectifier potassium currents.

275 e trafficking, localization, and activity of inward rectifier potassium Kir2 channels are important f

276 Inward-rectifier potassium (K+) channels conduct K+ ions

277 The defining structural feature of inward-rectifier potassium (Kir) channels is the unique

278 G-protein-regulated inward-rectifier potassium channel 2 (GIRK2) is reported

279 annels are thought to be composed of Kir6.2 (inward-rectifier potassium channel 6.2) and SUR2A (sulfo

280 HERG (human eag-related gene) encodes an inward-rectifier potassium channel formed by the assembl

281 ive hippocampal neurons by overexpressing an inward-rectifier potassium channel.

282 External potassium (K) activates the inward rectifier ROMK (K(ir)1.1) by altering the pH gati

283 ly non-selective members of the prokaryotic 'inward rectifier' subfamily of K(+) channels.

284 odulation of channel complexes formed of the inward rectifier subunit, Kir6.2, and the sulfonylurea s

285 nsitive K(+) channels (K(ATP)) comprise four inward rectifier subunits (Kir6.2), each associated with

286 d SUR2, and against different epitopes of K+ inward rectifier subunits Kir 6.1 and Kir 6.2 of the ATP

287 ylurea receptor, SUR, and pore-forming, K(+) inward rectifier subunits, Kir6.X, giving differing sens

288 currents resulting from expression of these inward-rectifier subunits alone, consistent with a domin

289 properties make the Kv-type EXP-2 channel an inward rectifier that resembles the structurally unrelat

290 stent with a novel function in plants as the inward rectifier that tightly regulates membrane potenti

291 strate the differential sensitivity of these inward rectifiers to metabolic inhibition and internal p

292 operty, called inward rectification, enables inward rectifiers to perform many important physiologica

293 ain the relative insensitivity of eukaryotic inward rectifiers to toxins.

294 from GIRK2 and IRK1, a G protein-insensitive inward rectifier, to determine the region within GIRK2 i

295 )(4) (sulfonylurea receptor type 1/potassium inward rectifier type 6.2) respond to the metabolic stat

296 e glutamate receptors, as well as Shaker and inward rectifier type K(+) channels, and can mediate clu

297 The inactivation of the inward rectifier was correlated with the expression of I

298 The SRIF-induced activation of the inward rectifier was suppressed in locus coeruleus neuro

299 All three of these inward rectifiers were inhibited by lowering the pH of t

300 n Xenopus oocytes is a non-inactivating weak inward rectifier with channel properties similar to TWIK