ライフサイエンスコーパス: HERG

1 KCNH2 that encodes for p.T152HfsX180 Kv11.1 (hERG).

2 eptide corresponding to the E-pore region of HERG.

3 around 13% at 10 muM, comparable to that of hERG.

4 than a 3000-fold selectivity for PDE1B over hERG.

5 interaction between the sigma-1 receptor and hERG.

6 that mediate its interaction with ASIC3 and hERG.

7 d expression level of Nedd4-2, which targets hERG.

8 70-independent quality control E3 ligase for hERG.

9 at position Gly-603 in the S5-pore linker of hERG.

10 izing cell population, and the expression of hERG.

11 o channel-forming subunits encoded by KCNH2 (hERG 1a and 1b) are expressed in cardiac tissue.

12 properties distinct from those of homomeric hERG 1a channels.

13 be copurified with an Ab against the nascent hERG 1a N terminus.

14 how that shRNA specifically targeting either hERG 1a or 1b transcripts reduced levels of both transcr

15 Despite these findings, adoption of hERG 1a/1b heteromeric channels as a model for cardiac I

16 s encoding human ether-a-go-go-related gene (hERG) 1a and 1b subunits, which assemble to produce ion

17 l Per-Arnt-Sim domain, which is omitted from hERG 1b by alternate transcription.

18 These findings establish that hERG 1b is critical for normal repolarization and that l

19 The human ether-a-go-go-related gene encodes hERG, a cardiac voltage-gated K(+) channel that is abnor

20 h tumor gene expression, most notably KCNH2 (HERG, a potassium channel) (P = 9.5 x 10(-7)), indicatin

21 ansitions through early closed states of the hERG activation pathway, and that the weak voltage depen

22 ng and selecting BKIs with minimum levels of hERG activity and frequencies of other safety liabilitie

23 Selected compounds were tested for in vitro hERG activity and in vivo efficacy in the P. berghei mou

24 A balance of low Pgp efflux and hERG activity was achieved by lowering the polar surface

25 ibition in vitro, anti-human Src inhibition, hERG activity, in vivo pharmacokinetic data, and efficac

26 overall profile, specifically with regard to hERG activity, led to alkyl sulfone 16.

27 for target affinity, brain permeability, and hERG activity, novel and diverse compounds based on cycl

28 including optimization of oral exposure and hERG activity.

29 anti-human ether-a-go-go potassium channel (hERG) activity of the first-generation anti-Cryptosporid

30 Reduction of hERG affinity led to greater than a 3000-fold selectivit

31 363, which showed increased potency, reduced hERG affinity, and higher selectivity against the closel

32 lternative, with good blood stability and no hERG affinity, providing new opportunities for the serie

33 e moiety can be very efficient in decreasing hERG affinity.

34 may reveal drug design principles to reduce hERG affinity.

35 erved, while some of the compounds exhibited hERG affinity.

36 hERG alteration by mutation or pharmacological inhibitio

37 comparison of the blocking potencies between hERG and Cav1.2.

38 al and pharmacological properties similar to hERG and could be overexpressed and purified from Pichia

39 eracts through the transmembrane region with hERG and decreases hERG functional expression.

40 eta-arrestin signaling-mediated increases in hERG and IKr were also observed in hERG-HEK cells as wel

41 chimeric channel between protease-sensitive hERG and insensitive human ether-a-go-go (hEAG), as well

42 D2 receptors and negligible interactions at hERG and M1 receptors.

43 n LQT2 patients with functional mutations in hERG and matched healthy participants, testing the hypot

44 oncentrations, verapamil blocked hCav1.2 and hERG, as did vanoxerine and bepridil both of which also

45 A positive hERG assay has been embraced by regulators as a non-clin

46 k interactions with key antitargets (M1R and hERG) associated with side effects.

47 enesis, we identified that calpain-1 cleaves hERG at position Gly-603 in the S5-pore linker of hERG.

48 ed into the extracellular milieu and cleaved hERG at the S5-pore linker.

49 ly we propose that trafficking inhibition of hERG be added to CiPA.

50 Sig1R promoted the formation of hERG/beta1-integrin signaling complexes upon extracellul

51 nd with a balanced profile of BACE1 potency, hERG binding affinity, and Pgp recognition.

52 on of polar groups was effective in reducing hERG binding affinity, this came at the expense of highe

53 ans to increase BACE1 potency while reducing hERG binding affinity.

54 ubility and microsomal stability and reduced hERG binding.

55 ytes by combining effects of a hormone and a hERG blocker, dofetilide, or hERG mutations.

56 False-negative and false-positive hERG blockers were identified accurately.

57 Torsadogenic hERG blockers, such as sotalol and quinidine, produced s

58 Kv11.1 (hERG) blockers with comparable potencies but different b

59 ared vanoxerine with dofetilide, a selective hERG-blocking torsadogen used for intractable AF, verapa

60 ous Nedd4-2, a ubiquitin ligase that targets hERG but not Kv1.5 or EAG channels for ubiquitination an

61 ts suggest that loss of expression of KCNH2 (HERG) by methylation could be a good prognostic marker,

62 Dysfunction of hERG causes long QT syndrome and sudden death, which occ

63 processing, we synthesized a codon-modified HERG cDNA (HERG-CM) where the codons were synonymously c

64 ocyte model modified to include dynamic drug-hERG channel (human Ether-a-go-go-Related Gene) interact

65 ation; reduced channel sialylation increases hERG channel activity during the action potential, there

66 of a model activator (NS1643) action on the hERG channel and its L529I mutant.

67 tested on IKr using HEK293 cells expressing HERG channel and native cardiac myocytes.

68 isk are more likely to be trapped within the hERG channel and show stronger reverse use dependency of

69 ompounds also have high selectivity over the hERG channel and were characterized with respect to thei

70 chronic incubation (for 2-3 weeks) with the hERG channel blocker dofetilide (100 nM), whereas more a

71 used minimal acute cardiotoxicity based on a hERG channel blocking assay and an unappreciable chronic

72 how that APETx2 also inhibits the off-target hERG channel by reducing the maximal current amplitude a

73 e, we tested chimaeras of rat Kv1.2 with the hERG channel for function in Xenopus oocytes and for ove

74 and establish that allosteric modulation of hERG channel function through ligand binding to the PAS

75 Changes in hERG channel function underlie long QT syndrome (LQTS) a

76 changes in surface N-glycosylation modified hERG channel function.

77 Mutations in the intrinsic ligand affected hERG channel gating and LQTS mutations abolished hERG cu

78 The data describe a novel mechanism by which hERG channel gating is modulated through physiologically

79 positive sera showed the predominance of the HERG channel in controlling action potential duration an

80 on in immunized guinea-pigs by targeting the HERG channel independently from fibrosis.

81 ion connecting the S5 and S6 segments of the HERG channel induces high titres of antibodies that inhi

82 Modeling dynamic drug-hERG channel interactions and multi-ion channel pharmaco

83 homology between anti-52-kDa Ro antigen and HERG channel is present.

84 eases inhibit IKr by cross-reacting with the HERG channel likely at the pore region where homology be

85 repolarization, suggesting that the rates of hERG channel opening and, critically, that of deactivati

86 de blockade can concur simultaneously in the hERG channel pore.

87 s, its binding to a H3 receptor as well as a hERG channel prevented it from further development.

88 otential duration by directly binding to the HERG channel protein.

89 For each condition of reduced glycosylation, hERG channel steady-state activation and inactivation re

90 Thus, it is important to understand hERG channel trafficking and its regulation.

91 Inhibition of the HERG channel was assessed by electrophysiology and by co

92 el of receptors including 5-HT2B subtype and hERG channel, which suggests no major cardiac issues.

93 vant concentrations, these drugs blocked the hERG channel.

94 IKr using HEK293 cells stably expressing the hERG channel.

95 d electrophysiological interference with the hERG channel.

96 no relevant affinity for off-target M1R and hERG channel.

97 easure the human ether-a-go-go-related gene (hERG) channel block (the primary mechanism by which drug

98 e are associated with alterations in Kv11.1 (hERG) channel-controlled repolarizing IKr currents of ca

99 activity with a peptide corresponding to the hERG-channel pore-forming region.

100 icantly inhibited IKr and cross reacted with hERG-channel proteins.

101 tabilizes these early closed states, leaving hERG channels able to activate at a rate similar to conv

102 We have previously shown that mature hERG channels are degraded by ubiquitin ligase Nedd4-2 v

103 SGK enhances the expression level of mature hERG channels by inhibiting Nedd4-2 as well as by promot

104 analyses, we demonstrated that internalized hERG channels can effectively recycle back to the plasma

105 s, disruption of the Nedd4-2 binding site in hERG channels did not eliminate the SGK-induced increase

106 Dysfunction of hERG channels due to mutations or certain medications ca

107 ransfection of native (WT) and p.T152HfsX180 hERG channels generated a current that was indistinguish

108 exerted "chaperone-like" effects over native hERG channels in both CHO cells and mouse atrial-derived

109 The homeostasis of hERG channels in the plasma membrane depends on a balanc

110 We reported previously that hERG channels in the plasma membrane undergo vigorous in

111 Slow deactivation of hERG channels is critical for preventing cardiac arrhyth

112 d its relationship to the slow activation of hERG channels is not understood.

113 uggest that Tbx20 controls the expression of hERG channels responsible for the rapid component of the

114 ctivated voltage sensor limits the return of hERG channels to rest.

115 Our recent data indicate that hERG channels undergo enhanced endocytic degradation und

116 y analyzed the KCNH2 (encoding for Kv11.1 or hERG channels) and TBX20 (encoding for the transcription

117 function or decrease the expression level of hERG channels, leading to long QT syndrome.

118 In hERG channels, the intrinsic ligand harbors hereditary m

119 sphine-stabilized AuNPs irreversibly blocked hERG channels, whereas thiol-stabilized AuNPs of similar

120 hed hERG currents and altered trafficking of hERG channels, which explains the LQT phenotype.

121 tly, we characterized mode-shift behavior in hERG channels, which results from stabilization of activ

122 ut not Rab4, is involved in the recycling of hERG channels.

123 in the homeostasis of plasma membrane-bound hERG channels.

124 s, without interacting with M1 receptors and hERG channels.

125 ks the position of the intracellular gate in hERG channels.

126 nterference with key human CYP450 enzymes or hERG channels.

127 he effect of Rab4 on the expression level of hERG channels.

128 itions limits the overall activation rate of hERG channels.

129 Human ether-a-go-go-related gene (hERG) channels lack the proline-valine-proline motif and

130 1 human ether-a-go-go related gene (Kv11.1) (hERG) channels, encoded by the KCNH2 gene, is associated

131 HERG-CM produced typical IKr-like currents; however, cha

132 , we synthesized a codon-modified HERG cDNA (HERG-CM) where the codons were synonymously changed to r

133 Translation efficiency was reduced for HERG-CM, as determined by heterologous expression, in vi

134 iabilities with CYP-metabolizing enzymes and hERG compared with ispinesib and SB-743921, which is imp

135 Dissociation of hERG complexes containing Hsp70 and the E3 ubiquitin lig

136 Simulations of hERG current and ventricular action potentials corrobora

137 A reduction in the hERG current causes long QT syndrome, which predisposes

138 There was no significant change in maximum hERG current density.

139 l was used to test the effects of changes in hERG current.

140 x20 enhanced human KCNH2 gene expression and hERG currents (IhERG) and shortened action-potential dur

141 channel gating and LQTS mutations abolished hERG currents and altered trafficking of hERG channels,

142 e group of small molecules that can activate hERG currents and thus may act as potent antiarrhythmic

143 0/Hsp70 chaperones assist the folding of the hERG cytosolic domains.

144 p70 nucleotide exchange factor Bag1 promotes hERG degradation by the ubiquitin-proteasome system at t

145 The interaction with Bag1 then shifts hERG degradation to the membrane-anchored E3 ligase TRC8

146 hway for hERG regulation; Rab4 decreases the hERG density at the plasma membrane by increasing the en

147 hERG dimers and tetramers became both singly and doubly

148 st to demonstrate that inhibitory Abs to the HERG E-pore region induce QTc prolongation in immunized

149 elevated total and membrane HERG protein and HERG-encoded current density by approximately 30-50%, wh

150 Human ether-a-gogo-related gene (HERG) encodes a potassium channel that is highly suscept

151 The human ether-a-go-go-related gene (hERG) encodes the pore-forming alpha-subunit of the rapi

152 The human ether-a-go-go-related gene (hERG) encodes the pore-forming subunit of the rapidly ac

153 The human ether-a-go-go-related gene (hERG) encodes the pore-forming subunit of the rapidly ac

154 Loss-of-function mutations in hERG (encoding the Kv11.1 voltage-gated potassium channe

155 ic receptor-based DREADD (M3D-arr) in stable hERG-expressing human embryonic kidney (HEK) cells, we d

156 und that M3D-arr activation increased mature hERG expression and current.

157 posure to low K(+) medium but also decreased hERG expression and function in cells under normal cultu

158 , coexpression of RNF207 and HSP70 increased HERG expression compared with HSP70 alone.

159 id not eliminate the SGK-induced increase in hERG expression.

160 lete elimination of SGK-mediated increase in hERG expression.

161 Clarification of protease-mediated damage of hERG extends our understanding of hERG regulation.

162 The fine tuning of metabolism and hERG followed by differentiation of advanced leads that

163 transmembrane region with hERG and decreases hERG functional expression.

164 the plasma membrane is a key determinant of hERG functionality, the mechanisms underlying its regula

165 8 also mediates degradation of the misfolded hERG-G601S disease mutant, but pharmacological stabiliza

166 and abundance of mature ERG proteins in both hERG-HEK cells and neonatal cardiac myocytes through the

167 reases in hERG and IKr were also observed in hERG-HEK cells as well as in neonatal rat ventricular my

168 properties of mutations within an overlooked hERG helix, finding important contributions to channel f

169 of some ion channels and in particular, the hERG (human Ether-a'-go-go-Related Gene) cardiac potassi

170 We further engineered a hERG (human ether-a-go-go-related gene) channel, which,

171 d the hypothesis that anti-Ro Abs target the HERG (human ether-a-go-go-related gene) K(+) channel, wh

172 Drug-induced block of the cardiac hERG (human Ether-a-go-go-Related Gene) potassium channe

173 The HERG (human Kv11.1a) channel has previously been shown t

174 ult of unintentional blockade of the Kv11.1 (hERG [human ether-a-go-go-related gene]) channel are a m

175 rents representing IKr (CHO cells expressing hERG; IC50=219+/-21 mumol/L) and IKs (CHO cells expressi

176 n blotting analysis, we demonstrate that the hERG/IKr channel was selectively cleaved by the serine p

177 ect, and small interfering RNA inhibition of hERG in beta and L cells increased insulin and GLP-1 sec

178 role in the loss-of-expression phenotype of hERG in certain hereditary and acquired LTQ2 syndromes.

179 uggest that the sigma-1 receptor may bind to hERG in the endoplasmic reticulum, aiding its assembly a

180 Although the abundance of hERG in the plasma membrane is a key determinant of hERG

181 on of Rab4 decreases the expression level of hERG in the plasma membrane.

182 +) channel human ether-a-go-go-related gene (hERG) in myeloid leukemia and colorectal cancer cell lin

183 rms of its microsomal stability, and CYP and hERG inhibition, along with an excellent brain penetrati

184 co-2 permeability/efflux, CYP3A4 inhibition, hERG inhibition, and rat microsomal extraction ratio (ER

185 We found that CYP3A4 inhibition, hERG inhibition, Caco-2 permeability, and efflux are unl

186 axin inhibitor lead compound 1, to attenuate hERG inhibition, remove CYP3A4 time-dependent inhibition

187 less prone to off-target activities such as hERG inhibition.

188 tain an acceptable lipophilicity to mitigate hERG inhibition.

189 s which mitigated the residual weak in vitro hERG inhibition.

190 w liabilities associated with metabolism and hERG inhibition.

191 has potent human ether-a-go-go-related gene (hERG) inhibitory activity, associated with long Q-T synd

192 highly specific (zero false positives on 50 hERG-insensitive drugs), low-cost hERG safety assay.

193 hed light on the structural requirements for hERG interaction but most importantly may reveal drug de

194 nd undesired off-target pharmacology such as hERG interactions.

195 Low K(+)-enhanced hERG internalization is accompanied by an increased rate

196 In the present study, we addressed whether hERG internalization occurs under normal K(+) conditions

197 Attenuation of hERG ion channel activity inherent within the initial ch

198 els consistent with in vitro activity on the hERG ion channel.

199 off-target human ether-a-go-go-related gene (hERG) ion channel inhibition were dependent on lipophili

200 ich encodes the cardiac human ether-a-go-go (hERG) ion channel, have been associated with sudden card

201 ge movement can only partly account for slow hERG ionic activation, and that the rate of pore closure

202 BK channel is functionally redundant whereas hERG is essential.

203 fic responses in microculture because mutant hERG is known to be sensitive to environmental condition

204 -1, we identified that the S5-pore linker of hERG is the target domain for proteinase K cleavage.

205 Kv11.1 (hERG) is a voltage-gated potassium channel that shows ve

206 ovement in human ether-a-go-go-related gene (hERG) is slow, as is return of charge upon repolarizatio

207 ded by the human ether-a-go-go-related gene (hERG), is therefore required before drug approval.

208 Although a potent blocker of hERG, it produced no serious adverse events.

209 n the other hand, analog 49e displayed lower hERG K(+) channel block while retaining potent in vitro

210 sistance development, but suffered from high hERG K(+) channel block.

211 d C235 Pf clones, low inhibitory activity in hERG K(+) channel blockage testing, negativity in the Am

212 Relaxation of a hERG K(+) channel model during molecular-dynamics simula

213 mpound 32d, elicited only weak inhibition of hERG K(+) channels and hNaV1.5 Na(+) channels, and no ef

214 Eventually, hERG K-channel block was identified as the main limitati

215 nhibit the human ether-a-go-go-related gene (HERG) K(+) channel at the extracellular pore (E-pore) re

216 target the human ether-a-go-go-related gene (HERG) K(+) channel by inhibiting the corresponding curre

217 ion of the human ether-a-go-go-related gene (hERG) K(+) channel leads to the prolongation of the vent

218 isoforms KCNE3S and KCNE4S, KCNE3L inhibited hERG; KCNE4L inhibited Kv1.1; neither form regulated the

219 adation of human ether-a-go-go-related gene (hERG, KCNH2) transcripts containing premature terminatio

220 man ether-a-go-go-related potassium channel (hERG, Kv11.1) is a voltage-dependent channel known for i

221 tem at the endoplasmic reticulum to regulate hERG levels and channel activity.

222 This scaffold suffers from hERG liabilities which were not remedied through this ro

223 rtain of these compounds exhibited potential hERG liabilities.

224 TgCDPK1 inhibitor 32, which does not have a hERG liability and possesses a favorable pharmacokinetic

225 erivative does not display the same level of hERG liability as observed with 1 and represents a promi

226 3)H]astemizole competitive binding assay for hERG liability screening.

227 Mitigation of a potential Ames and hERG liability ultimately led to two promising compounds

228 ycle in a series of HCV NS5B inhibitors, the hERG liability was reduced.

229 Damage of hERG mediated by proteases such as calpain may contribut

230 with a detailed comparison of average CHEMBL hERG MMPA results versus pairs with extreme transformati

231 bly decorated by sigma-1 receptors; however, hERG monomers were only singly decorated.

232 he direct binding of the sigma-1 receptor to hERG monomers, dimers, and tetramers.

233 is not due to enhanced protein synthesis, as hERG mRNA expression was not altered by low K(+) exposur

234 interactions of oestrogen with the pore loop hERG mutation (G604S).

235 dogenic effects: oestradiol interaction with hERG mutations in the pore loop containing G604 or with

236 a hormone and a hERG blocker, dofetilide, or hERG mutations.

237 IKur current blocker with selectivity versus hERG, Na and Ca channels, and an acceptable preclinical

238 y we measured the concentration-responses of hERG, Nav1.5 and Cav1.2 currents for 32 torsadogenic and

239 Mutations in hERG or drugs can impair the function or decrease the ex

240 ological selectivity or safety risks such as hERG or phospholipidosis.

241 large-conductance KCa1.1, Kv1.2/1.3, Kv7.4, hERG, or inwardly rectifying K(+) channels.

242 The human ether-a-go-go-related gene (hERG; or KCNH2) encodes the voltage-gated potassium chan

243 ariant of the ether-a-go-go related channel (hERG), p.Arg148Trp (R148W) was found at heterozygous sta

244 permeability, reduced Caco-2 efflux, reduced hERG PC activity, and increased selectivity profile whil

245 that proline substitutions within the S6 of hERG perturbed pore gate closure, trapping channels in t

246 associated long-QT syndrome by targeting the hERG potassium channel and inhibiting the related curren

247 A dataset of 55 hERG potassium channel inhibitors collected from Kramer

248 However, inhibition of the hERG potassium channel was identified as a liability for

249 desired property of not inhibiting the human hERG potassium ion channel at concentrations at which th

250 07 and the human ether-a-go-go-related gene (HERG) potassium channel interact and colocalize.

251 The human human ether-a-go-go-related gene (hERG) potassium channel plays a critical role in the rep

252 nt (G601S) human ether-a-go-go related gene (hERG) potassium channel protein.

253 ons in the human ether a go-go-related gene (hERG) potassium channel, many of which cause misfolding

254 log of the human Ether-a-go-go Related Gene (hERG) potassium channel.

255 ade of the human ether-a-go-go related gene (hERG) potassium channel.

256 -activated human ether-a-go-go-related gene (hERG) potassium channels are critical for the repolariza

257 -of-function mutations in human ether go-go (HERG) potassium channels underlie long QT syndrome type

258 ility, good metabolic stability, and a clean hERG profile relative to a previous frontrunner lead com

259 mpounds with improved aqueous solubility and hERG profile while maintaining metabolic stability and i

260 rted compounds, and with a slightly improved hERG profile.

261 on significantly elevated total and membrane HERG protein and HERG-encoded current density by approxi

262 Therefore, the heterozygous carriers of hERG/R148W may be at risk of cardiac sudden death.

263 amount of RNA encoding for either hERG/WT or hERG/R148W or their equimolar mixture.

264 rfering with Rab11 function not only delayed hERG recovery in cells after exposure to low K(+) medium

265 ation is accompanied by an increased rate of hERG recovery in the plasma membrane upon reculture foll

266 3-phosphate 5-kinase and Rab11 to facilitate hERG recycling to the plasma membrane.

267 dd4-2 as well as by promoting Rab11-mediated hERG recycling.

268 damage of hERG extends our understanding of hERG regulation.

269 that beta-arrestin signaling plays a role in hERG regulation.

270 esent study demonstrates a novel pathway for hERG regulation; Rab4 decreases the hERG density at the

271 man ether-a-go-go-related gene K(+) channel (hERG) represents one of the major antitarget concerns in

272 its fast inactivation rate, which is key to hERG's role in cardiac action potential repolarization.

273 deep hydrophobic pockets, which may explain hERG's unusual sensitivity to many drugs.

274 ives on 50 hERG-insensitive drugs), low-cost hERG safety assay.

275 A subtle structural feature of the hERG selectivity filter might correlate with its fast in

276 highly sensitive (zero false negatives on 50 hERG-sensitive drugs) and highly specific (zero false po

277 containing the S1-S6 transmembrane region of HERG showed functional and pharmacological properties si

278 Finally, we used a full-length hERG splicing-competent construct to show that inhibitio

279 We show that PM hERG structural and metabolic stability is compromised b

280 tics, in vivo efficacy, and selectivity over hERG, structure-activity relationship studies around the

281 between pairs of sigma-1 receptors bound to hERG tetramers had two peaks, at approximately 90 and ap

282 uncovered a family of positive modulators of hERG that specifically bind to the PAS domain.

283 e have determined the molecular structure of hERG to 3.8 A using cryo-electron microscopy.

284 al relevance of the unique susceptibility of hERG to proteases, we show that cardiac ischemia in a ra

285 activity, which can in turn yield simplified hERG toxicophores.

286 on potential duration, likely via effects on HERG trafficking and localization in a heat shock protei

287 These findings provide novel insight into hERG trafficking and regulation.

288 Of the MICE drugs only bepridil inhibited hERG trafficking following overnight exposure.

289 governing the recognition of PTC-containing hERG transcripts as NMD substrates have not been establi

290 ated in cardiomyocytes, where levels of both hERG transcripts were reduced by either 1a or 1b shRNA,

291 These results suggest that HERG translation and trafficking rates are independently

292 de study cohorts, pharmacological studies of HERG-type potassium channels, electrophysiological data)

293 perties of this N-terminal, proximal domain, hERG variant were explored in Xenopus oocytes injected w

294 inetics of what we interpret to be intrinsic hERG voltage sensor movement.

295 well culture, the expression of mutant G601S-hERG was reduced in microchannels.

296 While expression of WT-hERG was similar in microchannel and well culture, the e

297 ded by the human ether-a-go-go-related gene (hERG), which is important for the repolarization of the

298 The hERG window current increased significantly by 50-150%,

299 ing that the sigma-1 receptor interacts with hERG with 4-fold symmetry.

300 interaction between the sigma-1 receptor and hERG within the plane of the plasma membrane.

301 h the same amount of RNA encoding for either hERG/WT or hERG/R148W or their equimolar mixture.