ライフサイエンスコーパス: HEK cell

1 HEK cell uptake with capsid delivery system was 7.8-, 7.

2 HEK cells also have a simplified morphology compared to

3 HEK cells express only a small amount of mature alpha6be

4 HEK cells lack calcium currents, thereby circumventing t

5 HEK cells transfected to express SMAD9(V90M) had reduced

6 HEK cells transfected with the reporter showed an increa

7 tor NF-kappaB by human embryonic kidney 293 (HEK) cells transfected with toll-like receptor (TLR) 2.

8 a-stimulated 293 human embryonal kidney (293-HEK) cells expressing HLA-Cw*0702.

9 cells that possess gBK, as well as HLA-A2(+) HEK cells transfected with the gBK gene.

10 ength human isoforms from suspension-adapted HEK cells.

11 Cos-7 and HEK cells were transfected with a cDNA encoding full-len

12 s showed high viability (90% on average) and HEK cells within the printed structures were shown to pr

13 3Ralpha2 expressed on the surface of CHO and HEK cells as well as several glioma cell lines.

14 vity of I(Kur) generated in vitro in CHO and HEK cells by channels predicted to exhibit or lack this

15 expression of beta-subunits between CHO and HEK cells.

16 In ESCs and HEK cells, the RNA ends of more than 5% of MARGI read pa

17 on rat or guinea pig striatal membranes and HEK cells expressing cDNA for the human dopamine transpo

18 cell membranes from portal vein myocytes and HEK cells expressing the channel.

19 olling AMPA receptor function in neurons and HEK cells to that of TARPs.

20 xpressed in cultured hippocampal neurons and HEK cells to understand the role of the variant in the t

21 echanism was observed in primary neurons and HEK cells.

22 ions with distinct properties in oocytes and HEK cells, and that subunit linkage can overcome the exp

23 rom wild-type and transgenic mice as well as HEK cells expressing wild-type and mutant K(ATP) channel

24 of gamma(6) with the Cav3.1 channel in both HEK cells and atrial myocytes.

25 sms underlying this Kv2.1 clustering in both HEK cells and cultured hippocampal neurons.

26 Aspirin was hydrolyzed by HEK cells transfected with PAFAH1B2 or PAFAH1B3, and the

27 reviously demonstrated that apoE secreted by HEK cells stably expressing apoE3 or apoE4 (HEK-apoE) bi

28 citrate, suggesting that iron is taken up by HEK cells as Fe(2+).

29 hronic cell fate changes in OK cells and CaR-HEK cells and that the proximal tubular CaR is likely to

30 ntly inhibited cell death in both OK and CaR-HEK cells.

31 licited substantially more cell death in CaR-HEK cells than in nontransfected HEK-293 cells.

32 modulate CaR responsiveness in HEK-293 (CaR-HEK) cells.

33 In CB1-HEK cells, 4-hour pretreatment with cannabinoid agonists

34 enuated inverse agonism by rimonabant in CB1-HEK cells.

35 urface of live human embryonic kidney cells (HEK cells).

36 the rSK3 gene in mammalian cell lines (CHO, HEK cells) caused the appearance of a K(+) conductance w

37 e the voltage sensitivities in patch-clamped HEK cells for 10 new VF dyes.

38 lant-produced hOPN as compared to commercial HEK cell-produced hOPN determined by MTT assay.

39 d hOPN had a structure similar to commercial HEK cell-produced hOPN.

40 In contrast, HEK cells expressing the variant Lys-179 TRPA1 failed to

41 DeltaV340 or the G678V mutations and control HEK cells.

42 Temperature jumps in control HEK cells cause a monophasic increase in membrane capaci

43 The cotransfected HEK cells were then treated with doxorubicin for inducti

44 Treatment of cultured HEK cells with recombinant STC1 activated AMPK and incre

45 ly on ligand-gated ion channels, we employed HEK cells transfected with cDNAs encoding three requisit

46 Using a well-established HEK cell biosensor assay, we show that tau from cases wi

47 es were observed between control and exposed HEK cells concerning electrical properties, growth, and

48 values measured in vivo, in UT-B-expressing HEK cell xenografts, were significantly higher (about tw

49 patch-clamp analysis of Ca(v)2.2 expressing HEK cells revealed an up-regulation of Ca(2+) currents d

50 es formed between axons and AMPAR-expressing HEK cells develop significantly fewer inactive presynapt

51 s shown to activate TRPV1 channel-expressing HEK cells.

52 BAPTA, nuclei isolated from mGlu5-expressing HEK cells responded to the addition of glutamate with ra

53 th in neurons and in NgR/p75(NTR)-expressing HEK cells.

54 654 and lipid 430 activated TLR2-expressing HEK cells, and this activation was inhibited by anti-TLR

55 In contrast, TLR4-expressing HEK cells failed to be activated by either lipid 654 or

56 1 antagonist iodo-resiniferatoxin (10 nm for HEK cells and 1 microg/50 micro;l for pain behavior).

57 ing single-molecule pull-down (SiMPull) from HEK cell lysate and subunit counting in the plasma membr

58 Nuclear mGlu5 receptors derived from HEK cells or cortical cell types bound [3H]quisqualate.

59 (d) = 6.1 nM), and in membranes derived from HEK cells stably expressing Na(V)1.5 (K(d) = 0.9 nM).

60 application of GABA to patches excised from HEK cells expressing different mixtures of alpha1 and al

61 or Y857F PDGFRbetas immunoprecipitated from HEK cells, GRK2 tyrosyl phosphorylation was PDGF-depende

62 KCa channels in membrane patches pulled from HEK cells and when they are placed into reconstituted 1-

63 mechanics are greater in tethers pulled from HEK cells transfected with prestin when compared to cont

64 ere confirmed by macroscopic recordings from HEK cells in the presence of GABA or pentobarbital.

65 with GLUTs expressed in and solubilized from HEK cells show that HEK cell GLUT1 resolves as 6- and 10

66 rane stretch to cellular area change in HeLa/HEK cells.

67 bundance of mature ERG proteins in both hERG-HEK cells and neonatal cardiac myocytes through the enha

68 s in hERG and IKr were also observed in hERG-HEK cells as well as in neonatal rat ventricular myocyte

69 Patch clamp analysis in stable hERG-HEK cells showed effects on current amplitude, inactivat

70 G channels stably expressed in HEK 293 (hERG-HEK) cells.

71 tions coexpressed with SCN5A in heterologous HEK cells produced a significantly reduced sodium curren

72 glandin A(2)-evoked calcium influx in hTRPA1-HEK cells with similar potency and efficacy.

73 In whole-cell patch-clamp studies on hTRPA1-HEK cells, 15dPGJ(2) evoked currents similar to equimola

74 ar myocytes, IC50=66.5+/-4 mumol/L) and IK1 (HEK cells expressing Kir2.1, IC50=44+/-3 mumol/L).

75 atic domains were recombinantly expressed in HEK cell lines.

76 tization of WT receptor was recapitulated in HEK cell membranes, and ectopic arrestin2 promoted desen

77 coimmunoprecipitate with full-length SUR1 in HEK cell lysates, such findings delineate a novel mechan

78 In HEK cells and rat hippocampal neurons, SAP97 in the comp

79 In HEK cells expressing Kv7.4, co-expression of KCNE4 incre

80 In HEK cells stably transfected with B1R, co-expression of

81 In HEK cells, both parental GluT1- and GluT1.HA.H6-mediated

82 In HEK cells, leptin induced a significant hyperpolarizing

83 In HEK cells, mutation of Tyr-1336 eliminates the potentiat

84 In HEK cells, oocytes, and neurons co-expressing TGR5 and T

85 In HEK cells, the phase of Ba2+-sensitive admittance was 3.

86 en probability of 0.6 in oocytes and 0.01 in HEK cells.

87 r4.1 physically associate with caveolin-1 in HEK cells and in kidney extracts.

88 Finally, expression of mARC-1 in HEK cells using a lentivirus vector was used to confirm

89 ed plasma membrane-associated PI(4,5)P(2) in HEK cells within seconds without activating PLC.

90 so showed use dependent block of Na(v)1.6 in HEK cells.

91 ing events involving NF-kappaB activation in HEK cells and cytokine production (IFN-alpha, TNF, and I

92 capable of inducing NF-kappa B activation in HEK cells transfected with TLR5.

93 -driven luciferase reporter gene activity in HEK cells nearly 1 order of magnitude more effectively t

94 in shark and human cotransporter activity in HEK cells.

95 Expression of the mutated allele in HEK cells revealed a mislocalization of the protein in t

96 -1 degradation in primary hepatocytes and in HEK cells overexpressing the IL-1beta receptor.

97 of interaction were observed in vitro and in HEK cells.

98 ls, and overexpression of moesin and Ano1 in HEK cells alters the subcellular localization of both pr

99 Overexpression of Ano1 in HEK cells or Xenopus oocytes is sufficient to generate C

100 enic acid in a functional Ca+2 flux assay in HEK cells expressing GPR40 receptor.

101 Specificity of each sensor was assessed in HEK cells with either the T2 or T3 enzymes deleted.

102 /L Ba2+ (in GP heart cells) or 1 mM Ba2+ (in HEK cells).

103 in oocytes and cell surface biotinylation in HEK cells indicated that the WNK-mediated inhibition of

104 Kv7.4 and Gbetagamma subunits colocalized in HEK cells and renal artery smooth muscle cells.

105 rthermore, expression of IRBIT constructs in HEK cells revealed that activation of pNBC1 required onl

106 entry in wild-type cells (HEK-293, COS1), in HEK cells expressing a thapsigargin-sensitive variant of

107 nt receptors in stable cell lines created in HEK cells for agonist-stimulated guanosine 5'-3-O-(thio)

108 ssion of a dominant-negative form of Cul1 in HEK cells demonstrated that EF2K levels are regulated by

109 azithromycin reduced peak SCN5A currents in HEK cells (IC50=110+/-3 mumol/L) and Na(+) current in mo

110 all sensory neurons and Ca(v)3.2 currents in HEK cells at subanesthetic concentrations.

111 1 induced Ca(2+)-activated Cl(-) currents in HEK cells that were >1 nA in amplitude.

112 locks epibatidine-induced inward currents in HEK cells transfected with alpha3beta4 nAChR.

113 S-Nitrosylation was also detectable in HEK cells expressing recombinant human cardiac calcium c

114 ely 2-fold improvement over previous dyes in HEK cells, dissociated rat cortical neurons, and medicin

115 ased relative to that of wtSOD1 expressed in HEK cells and a motor neuron cell line.

116 HA-tagged BCRP mutants were expressed in HEK cells and tested for their ability to efflux mitoxan

117 A, S364C, S364N, and S364D were expressed in HEK cells and Xenopus laevis oocytes to measure radioact

118 TRPA1 wild type Lys-179 protein expressed in HEK cells exhibited intact biochemical properties, inclu

119 stoma cell lines and 5-HT(3A)Rs expressed in HEK cells in a competitive manner.

120 ly engineered V1442E-Na channel expressed in HEK cells shows marked enhancement of fast inactivation

121 urface levels of assembled AChR expressed in HEK cells to 138% of wild-type levels.

122 Expressed in HEK cells, an exposure to the oxidant H(2)O(2) or diamid

123 CaM had little effect on NaV1.4 expressed in HEK cells, possibly due to large differences in the endo

124 lyR alpha1 homomeric receptors, expressed in HEK cells, reduced the potencies of glycine, beta-alanin

125 ted activation of TRPC6, stably expressed in HEK cells, was significantly inhibited by FK506, which a

126 n alpha1 beta3 gamma2L GABAA Rs expressed in HEK cells, we found that S-mTFD-MPPB inhibited GABA-indu

127 nd erg3 currents heterologously expressed in HEK cells.

128 racellular loop (YFP-NCX1) were expressed in HEK cells.

129 s observed for IRP1(S138E) when expressed in HEK cells.

130 posed of only 5-HT(3A) subunits expressed in HEK cells.

131 for CCh-induced TRPC6 currents expressed in HEK cells.

132 ronal nicotinic receptor stably expressed in HEK cells.

133 In conclusion, hClC-Kb expression in HEK cells is susceptible to proteasome degradation, and

134 PC6 and the endogenous immunophilin found in HEK cells.

135 GLUT1-GLUT3 chimeras with parental GLUT1 in HEK cells.

136 e in that it is not properly glycosylated in HEK cells.

137 In contrast, overexpression of GSAP in HEK cells expressing amyloid precursor protein or in N2a

138 r stable expression of human NBC3 (hNBC3) in HEK cells resulted in a Na(+)-dependent, DIDS (4,4'-diis

139 n of hTid-1 mediates its binding to Hsp70 in HEK cells.

140 sensitive to the Kv7 blocker linopirdine in HEK cells heterologously expressing Kv7.4, and in rat re

141 2, the activation of NF-kappaB by H.8/Lip in HEK cells was enhanced upon coexpression of TLR1 but not

142 Our data suggest that the cAMP machinery in HEK cells acts as a low-pass filter disregarding the rel

143 +RMR in a dose- and time-dependent manner in HEK cells.

144 hway with a half-life of less than 25 min in HEK cells.

145 M for receptors in oocytes versus 2300 nM in HEK cells.

146 Furthermore, we observed in HEK cells cotransfected with wild-type, Y14D, or Y14F Ca

147 xic up-regulation of HIF-1 alpha observed in HEK cells, was sensitive to pertussis toxin, and involve

148 n-sensitive variant of TRPC3 (TRPC3a), or in HEK cells overexpressing another membrane protein, V1aR.

149 We found that SK1 overexpression in HEK cells or its down-regulation in glioma or breast can

150 s and reproduced by expressing the P2X7Rs in HEK cells.

151 -dependent activation of the Gi/o pathway in HEK cells.

152 ild type (WT) and Y857F mutant PDGFRbetas in HEK cells, which lack endogenous PDGFRs.

153 photobleaching experiments were performed in HEK cells expressing prestin-GFP after cholesterol manip

154 within the C-terminus are phosphorylated in HEK cells in response to PMA.

155 resulting in 3-fold larger photocurrents in HEK cells compared with channelrhodopsin-2.

156 Activation of PKG in HEK cells transfected with alpha(1c) and beta(2a) subuni

157 ivation curve to more positive potentials in HEK cells.

158 ation of glycosylated AT1R in proteasomes in HEK cells and human renal proximal tubule cells heterolo

159 sed for both visualization of the protein in HEK cells and fluorescent resonance energy transfer (FRE

160 ogy using the full length S31N M2 protein in HEK cells showed no blockade.

161 However, D564G LH/CG R in HEK cells was not desensitized, and synthetic 3i D564G p

162 pecifically interacted with CLR and RAMP1 in HEK cells coexpressing rat CLR and RAMP1, determined by

163 rry-STIM1 and Orai1-GFP at varying ratios in HEK cells and quantified CRAC current (I(CRAC)) activati

164 iplet NR1/NR2C/NR3A recombinant receptors in HEK cells and compared their currents with those of NMDA

165 ession of various mammalian C5a receptors in HEK cells confirms that cytotoxicity toward neutrophils

166 of GABA(A) alpha1beta2-subunit receptors in HEK cells is constitutive, positively modulated by activ

167 V5-mediated channel activity was recorded in HEK cells coexpressing TRPV5 and sKL or membranous Kloth

168 ibroblasts, HEK and COS-7 cells, and ROCE in HEK cells mediated by TRPC3, TRPC6, TRPC7, and TRPC5 sho

169 AP, tau = 14.1 +/- 1.5 and 11.5 +/- 6.1 s in HEK cells and neurons, respectively).

170 , coexpression of A280V GPD1-L with SCN5A in HEK cells reduced inward Na+ currents by approximately 5

171 alysis of AngII and SII-induced signaling in HEK cells stably expressing AT(1A) receptors.

172 rylation can inhibit melanopsin signaling in HEK cells.

173 l C (7) is an activator of cAMP signaling in HEK cells.

174 Similarly, expression of SLC26A9 in HEK cells resulted in a large Cl(-) current.

175 e the molecular makeup of the native SOCs in HEK cells and the role of a STIM1-Orai1-TRPC1 complex in

176 r their interaction with the native STIM1 in HEK cells.

177 /AMPAR complexes with known stoichiometry in HEK cells.

178 nduced currents of ACRs have been studied in HEK cells and neurons, but light-gated channel conductan

179 Expression studies in HEK cells indicate that none of the mutations hinders ra

180 Expression studies in HEK cells reveal decreased expression of epsilonN436del-

181 ence of TLR4 through transfection studies in HEK cells, which do not normally express this protein, a

182 th the beta1b and alpha2/delta-1 subunits in HEK cells, altering both activation and inactivation pro

183 ome, but not all, of the actions of TARPs in HEK cells; their role in neurons, however, is more limit

184 ribed in this report, we demonstrate that in HEK cells IDE has little impact on insulin clearance.

185 Our initial analysis showed that in HEK cells transfected with SPTLC1 mutants, dSL generatio

186 NKCC1 constructs and cotransfected these in HEK cells, we observed FRET between dimer pairs, and the

187 2 or PKC induced phosphorylation of TRPV1 in HEK cells, suggesting a direct regulation of the channel

188 Expression of this variant in HEK cells produces a decreased density of Ca(2+)-activat

189 crease the palmitoylation of S68A PLM-YFP in HEK cells.

190 ed, in a cGMP-PKG-specific manner, in intact HEK cells heterologously expressing alpha(1c) and beta(2

191 subunit cDNA into a human embryonic kidney (HEK) cell line stably expressing alpha1beta3gamma2 recep

192 manently transfected human embryonic kidney (HEK) cell lines.

193 ed into human tsA201 human embryonic kidney (HEK) cell lines.

194 Using the human embryonic kidney (HEK) cell recombinant system and dissociated neurons, we

195 n Xenopus oocytes or human embryonic kidney (HEK) cells (150 mM external KCl), the unitary conductanc

196 cium current in both human embryonic kidney (HEK) cells and cardiomyocytes, although the mechanism of

197 very of endotoxin to human embryonic kidney (HEK) cells and cell activation at picomolar concentratio

198 in TRPV1-transfected human embryonic kidney (HEK) cells and DRG neurons and potentiated capsaicin-ind

199 Human embryonic kidney (HEK) cells and ovine mesenchymal stem cells (oMSCs) were

200 receptor-transfected human embryonic kidney (HEK) cells and rat trigeminal ganglion cells) on the sil

201 smission to cultured human embryonic kidney (HEK) cells expressing full-length, mutant human alpha-sy

202 In human embryonic kidney (HEK) cells expressing human EP1 receptors, we now show t

203 tion were studied in human embryonic kidney (HEK) cells expressing human Na channels and by modeling

204 In cultured human embryonic kidney (HEK) cells expressing NgR, p75(NTR) was required for MAG

205 ulin (IgG)-producing human embryonic kidney (HEK) cells from non-IgG-producing control cells.

206 stably expressed in human embryonic kidney (HEK) cells in a concentration-dependent manner with an a

207 ter ovary (CHO), and human embryonic kidney (HEK) cells in order to compare widely used mammalian exp

208 Ca(2+) transient in human embryonic kidney (HEK) cells over-expressing Ca(v)2.2 but not Ca(v)2.1 (P/

209 Human Embryonic Kidney (HEK) cells overexpressing TLRs 2, 4 or 5 and surface pla

210 (0.5 mm CaCl(2)) in human embryonic kidney (HEK) cells permanently expressing the human CaR (HEK-hCa

211 the longer TRPC3a in human embryonic kidney (HEK) cells showed that it mediates Ca2+ entry in respons

212 s and in transfected human embryonic kidney (HEK) cells stably expressing Kir 2.1 and 2.3 channels.

213 In human embryonic kidney (HEK) cells stably expressing the cardiac Na(+) channel,

214 dy, we used cultured human embryonic kidney (HEK) cells stably transfected with human P2X(7) receptor

215 h were recorded from human embryonic kidney (HEK) cells that had been transiently transfected with mo

216 opioid receptors and human embryonic kidney (HEK) cells transfected with a cloned mu opioid receptor,

217 ROMK1 expression in human embryonic kidney (HEK) cells transfected with ROMK1.

218 SLC26a5)-transfected human embryonic kidney (HEK) cells under whole-cell voltage clamp.

219 idue of other GPCRs, human embryonic kidney (HEK) cells were transfected with wild-type (WT) and D564

220 primary cultures of human embryonic kidney (HEK) cells with sheared adenovirus (Ad)5 DNA.

221 d three new lines of human embryonic kidney (HEK) cells) expressing: (1) wild-type dog NCX1 (dog NCX1

222 nel was expressed in human embryonic kidney (HEK) cells, and activity was monitored using the giga-se

223 (TLR2) expressed in human embryonic kidney (HEK) cells, inducing IL-8 production, and engaged mouse

224 ectroscopy on mobile human embryonic kidney (HEK) cells, neurons cells from mice, and yeast cells (S.

225 demonstrate that in human embryonic kidney (HEK) cells, rescue of SOCs required co-transfection of l

226 b, when expressed in human embryonic kidney (HEK) cells, was unstable due to degradation by proteasom

227 able hERG-expressing human embryonic kidney (HEK) cells, we demonstrate that beta-arrestin signaling

228 rons and transfected human embryonic kidney (HEK) cells, where it is nonconducting.

229 tem cells (ESCs) and human embryonic kidney (HEK) cells.

230 tethers formed from human embryonic kidney (HEK) cells.

231 rons and transfected human embryonic kidney (HEK) cells.

232 or TRPV4-expressing human embryonic kidney (HEK) cells.

233 ceptors expressed in human embryonic kidney (HEK) cells.

234 DNA transfected into human embryonic kidney (HEK) cells.

235 est MA currents in a small fraction of naive HEK cells similar to the published work.

236 We found that in neuron-HEK cell heterosynapses, GABAergic events mediated by al

237 rowth and increase migration of noncancerous HEK cells; indeed, both properties were almost doubled w

238 ing single NRVMs to a dynamic clamp model of HEK cell ionic current reproduced the cardiac maximal di

239 sly shown that reovirus-induced apoptosis of HEK cells is initiated by death receptor activation but

240 the extracted electrical characteristics of HEK cells exposed during 72 h to a 0.5 T uniform static

241 Cotransfection of HEK cells with both the truncated CYP2E1 and the hsp70-d

242 Immunoadsorption of hsp90 from cytosol of HEK cells expressing the truncated CYP2E1(Delta3-29) yie

243 t blocked nicotine-induced depolarization of HEK cells with an IC50 of approximately 430 nM.

244 We now show that reovirus infection of HEK cells is associated with selective cytosolic release

245 However, after isolation of HEK cells expressing hTRPC3 in stable form, TRPC3a gave

246 Applying whole-cell patch-clamp recording of HEK cells, we found that wild-type but not disease mutan

247 Transfection of HEK cells with GATA4 plasmids activated Bcl2 promoter an

248 Transfection of HEK cells with SR-BI and CD36 significantly enhanced vit

249 The results obtained on HEK cells expressing Dronpa photoswitchable fluorescent

250 nilloid 4 (TRPV4) in Xenopus laevis oocytes, HEK cells and nociceptive neurons, and stimulated neuron

251 sulfonation) in myocytes, perfused heart, or HEK cells.

252 ect on IL-8 secretion from infected parental HEK cells.

253 or shedding of meprin A, we generated stable HEK cell lines expressing meprin beta alone and both mep

254 as well as when they are expressed in stable HEK cell lines.

255 the protein, these antibodies did not stain HEK cells expressing KCNQ1b.

256 Moreover, MSU does not stimulate HEK cells expressing TLR1-11 to activate NF-kappaB.

257 rexpressed PPIP5K1 from osmotically stressed HEK cells (0.2 M sorbitol; 30 min) revealed a persistent

258 tation of amyloid precursor protein (APP(sw) HEK cells) as a cellular model of familial AD.

259 wever, improved MMP and ATP level in APP(sw) HEK cells.

260 in and solubilized from HEK cells show that HEK cell GLUT1 resolves as 6- and 10-nm Stokes radius pa

261 The HEK cell experiments further demonstrated that cofactor

262 e number of GFP-tagged Kv2.1 channels on the HEK cell surface was compared with K(+) channel conducta

263 he WT-CryAB-overexpressing cells than in the HEK cells.

264 cell lines transformed by Ad5 DNA and three HEK cell lines transformed by the SV40 early region did

265 Soluble, recombinant CPM bound to HEK cells expressing B1Rs without stimulating receptor s

266 uman embryonic kidney) cells and transfected HEK cells that stably express wild-type (WT) and mutant

267 e Kv2.1 surface clusters in both transfected HEK cells and hippocampal neurons.

268 ocally coimmunoprecipitated from transfected HEK cells and from the native pancreas and submandibular

269 confirm PASK binding to NKCC1 in transfected HEK cells and further suggest that this binding is not a

270 Moreover, when expressed in transfected HEK cells, both enzymes result in significant increases

271 coimmunoprecipitation studies in transfected HEK cells, implying a direct interaction between the pro

272 In transfected HEK cells, Kv2.1 channels within cluster microdomains ar

273 ized to Kv2.1 surface density in transfected HEK cells, was used to determine the expression levels o

274 These clusters also form in transfected HEK cells.

275 prestin-prestin interactions in transfected HEK cells.

276 man intestinal epithelium and in transfected HEK cells.

277 Similar results were obtained in transfected HEK cells.

278 expression in MyoD- or myogenin-transfected HEK cells.

279 urons, whole-cell patch clamp of transfected HEK cells revealed that Nav1.7 activation was unaltered

280 Patch clamp studies of transfected HEK cells showed that both mutations resulted in a drama

281 R 8 domain confers resistance of transfected HEK cells to type 1 PRRSV.

282 n the activation of NF-kappaB of transfected HEK cells, we discovered that some oligodeoxynucleotides

283 s with EAAC1 in C6 glioma and/or transfected HEK cells.

284 Prestin-transfected HEK cells, however, additionally show a biphasic increas

285 Here, serum starvation of ROMK-transfected HEK cells led to an increase of ROMK current density; su

286 conventional and WT-CryAB stably transfected HEK cells.

287 x more active on TLR8- than TLR7-transfected HEK cells (EC50, approximately 50 nM vs. approximately 5

288 68 by PKA in ARVM or transiently transfected HEK cells increased its palmitoylation, but PKA activati

289 ial Vaniloid-1 (TRPV1) and TRPM8 transfected HEK cells.

290 d on the highest uptake in VMAT2-transfected HEK cells and desirable optical properties.

291 y nucleotide binding also within transfected HEK cells and neurons.

292 ) or that were transfected to express TRPV4 (HEK cells), pretreatment with a PAR2 agonist enhanced Ca

293 estin when compared to control untransfected HEK cells.

294 fluence TLR2-dependent cell activation using HEK cells and BEAS-2B cells.

295 ed in our classic BS cohort and others using HEK cells expressing hClC-Kb-GFP.

296 oprecipitation studies, carried out in whole HEK cell lysates, confirmed in vivo binding between thes

297 Additional experiments with HEK cells suggest that proteasomal malfunction observed

298 eceptors was underscored in experiments with HEK cells, which lack the P2X7 receptor and showed strik

299 In studies with HEK cells engineered to express various TLRs, we show th

300 he conformation of intracellular apoE within HEK cells and astrocytes adopts a directional pattern; i