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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.
10 s showed high viability (90% on average) and HEK cells within the printed structures were shown to pr
13 vity of I(Kur) generated in vitro in CHO and HEK cells by channels predicted to exhibit or lack this
18 xpressed in cultured hippocampal neurons and HEK cells to understand the role of the variant in the t
20 ions with distinct properties in oocytes and HEK cells, and that subunit linkage can overcome the exp
21 rom wild-type and transgenic mice as well as HEK cells expressing wild-type and mutant K(ATP) channel
26 reviously demonstrated that apoE secreted by HEK cells stably expressing apoE3 or apoE4 (HEK-apoE) bi
28 hronic cell fate changes in OK cells and CaR-HEK cells and that the proximal tubular CaR is likely to
43 ly on ligand-gated ion channels, we employed HEK cells transfected with cDNAs encoding three requisit
45 es were observed between control and exposed HEK cells concerning electrical properties, growth, and
46 values measured in vivo, in UT-B-expressing HEK cell xenografts, were significantly higher (about tw
47 es formed between axons and AMPAR-expressing HEK cells develop significantly fewer inactive presynapt
49 BAPTA, nuclei isolated from mGlu5-expressing HEK cells responded to the addition of glutamate with ra
51 654 and lipid 430 activated TLR2-expressing HEK cells, and this activation was inhibited by anti-TLR
53 1 antagonist iodo-resiniferatoxin (10 nm for HEK cells and 1 microg/50 micro;l for pain behavior).
54 ing single-molecule pull-down (SiMPull) from HEK cell lysate and subunit counting in the plasma membr
56 (d) = 6.1 nM), and in membranes derived from HEK cells stably expressing Na(V)1.5 (K(d) = 0.9 nM).
57 application of GABA to patches excised from HEK cells expressing different mixtures of alpha1 and al
58 or Y857F PDGFRbetas immunoprecipitated from HEK cells, GRK2 tyrosyl phosphorylation was PDGF-depende
59 KCa channels in membrane patches pulled from HEK cells and when they are placed into reconstituted 1-
60 mechanics are greater in tethers pulled from HEK cells transfected with prestin when compared to cont
63 with GLUTs expressed in and solubilized from HEK cells show that HEK cell GLUT1 resolves as 6- and 10
64 ng (HEK-muFAP) and CD26-expressing (HEKCD26) HEK cells and characterized by planar scintigraphy and o
66 bundance of mature ERG proteins in both hERG-HEK cells and neonatal cardiac myocytes through the enha
67 s in hERG and IKr were also observed in hERG-HEK cells as well as in neonatal rat ventricular myocyte
70 tions coexpressed with SCN5A in heterologous HEK cells produced a significantly reduced sodium curren
72 In whole-cell patch-clamp studies on hTRPA1-HEK cells, 15dPGJ(2) evoked currents similar to equimola
75 coimmunoprecipitate with full-length SUR1 in HEK cell lysates, such findings delineate a novel mechan
90 ing events involving NF-kappaB activation in HEK cells and cytokine production (IFN-alpha, TNF, and I
92 llular signal-regulated kinase activation in HEK cells, but failed to diminish cytotoxicity in cultur
93 -driven luciferase reporter gene activity in HEK cells nearly 1 order of magnitude more effectively t
99 ls, and overexpression of moesin and Ano1 in HEK cells alters the subcellular localization of both pr
104 in oocytes and cell surface biotinylation in HEK cells indicated that the WNK-mediated inhibition of
106 rthermore, expression of IRBIT constructs in HEK cells revealed that activation of pNBC1 required onl
107 entry in wild-type cells (HEK-293, COS1), in HEK cells expressing a thapsigargin-sensitive variant of
108 nt receptors in stable cell lines created in HEK cells for agonist-stimulated guanosine 5'-3-O-(thio)
109 ssion of a dominant-negative form of Cul1 in HEK cells demonstrated that EF2K levels are regulated by
110 azithromycin reduced peak SCN5A currents in HEK cells (IC50=110+/-3 mumol/L) and Na(+) current in mo
114 ely 2-fold improvement over previous dyes in HEK cells, dissociated rat cortical neurons, and medicin
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 of glutamate in both receptors expressed in HEK cells as well as in native receptors in cortical neu
119 TRPA1 wild type Lys-179 protein expressed in HEK cells exhibited intact biochemical properties, inclu
121 ly engineered V1442E-Na channel expressed in HEK cells shows marked enhancement of fast inactivation
124 CaM had little effect on NaV1.4 expressed in HEK cells, possibly due to large differences in the endo
125 lyR alpha1 homomeric receptors, expressed in HEK cells, reduced the potencies of glycine, beta-alanin
126 ted activation of TRPC6, stably expressed in HEK cells, was significantly inhibited by FK506, which a
127 n alpha1 beta3 gamma2L GABAA Rs expressed in HEK cells, we found that S-mTFD-MPPB inhibited GABA-indu
139 sensitive to the Kv7 blocker linopirdine in HEK cells heterologously expressing Kv7.4, and in rat re
140 2, the activation of NF-kappaB by H.8/Lip in HEK cells was enhanced upon coexpression of TLR1 but not
141 Our data suggest that the cAMP machinery in HEK cells acts as a low-pass filter disregarding the rel
146 xic up-regulation of HIF-1 alpha observed in HEK cells, was sensitive to pertussis toxin, and involve
147 n-sensitive variant of TRPC3 (TRPC3a), or in HEK cells overexpressing another membrane protein, V1aR.
153 photobleaching experiments were performed in HEK cells expressing prestin-GFP after cholesterol manip
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
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 V5-mediated channel activity was recorded in HEK cells coexpressing TRPV5 and sKL or membranous Kloth
167 ak magnetically mediated calcium response in HEK cells expressing a previously published TRPV4-ferrit
168 ibroblasts, HEK and COS-7 cells, and ROCE in HEK cells mediated by TRPC3, TRPC6, TRPC7, and TRPC5 sho
170 , coexpression of A280V GPD1-L with SCN5A in HEK cells reduced inward Na+ currents by approximately 5
176 e the molecular makeup of the native SOCs in HEK cells and the role of a STIM1-Orai1-TRPC1 complex in
179 nduced currents of ACRs have been studied in HEK cells and neurons, but light-gated channel conductan
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.
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
190 ed, in a cGMP-PKG-specific manner, in intact HEK cells heterologously expressing alpha(1c) and beta(2
194 cium current in both human embryonic kidney (HEK) cells and cardiomyocytes, although the mechanism of
195 very of endotoxin to human embryonic kidney (HEK) cells and cell activation at picomolar concentratio
196 in TRPV1-transfected human embryonic kidney (HEK) cells and DRG neurons and potentiated capsaicin-ind
198 receptor-transfected human embryonic kidney (HEK) cells and rat trigeminal ganglion cells) on the sil
199 smission to cultured human embryonic kidney (HEK) cells expressing full-length, mutant human alpha-sy
201 tion were studied in human embryonic kidney (HEK) cells expressing human Na channels and by modeling
203 ter ovary (CHO), and human embryonic kidney (HEK) cells in order to compare widely used mammalian exp
204 Ca(2+) transient in human embryonic kidney (HEK) cells over-expressing Ca(v)2.2 but not Ca(v)2.1 (P/
206 (0.5 mm CaCl(2)) in human embryonic kidney (HEK) cells permanently expressing the human CaR (HEK-hCa
207 the longer TRPC3a in human embryonic kidney (HEK) cells showed that it mediates Ca2+ entry in respons
208 s and in transfected human embryonic kidney (HEK) cells stably expressing Kir 2.1 and 2.3 channels.
211 dy, we used cultured human embryonic kidney (HEK) cells stably transfected with human P2X(7) receptor
212 h were recorded from human embryonic kidney (HEK) cells that had been transiently transfected with mo
214 opioid receptors and human embryonic kidney (HEK) cells transfected with a cloned mu opioid receptor,
216 d three new lines of human embryonic kidney (HEK) cells) expressing: (1) wild-type dog NCX1 (dog NCX1
217 nel was expressed in human embryonic kidney (HEK) cells, and activity was monitored using the giga-se
218 (TLR2) expressed in human embryonic kidney (HEK) cells, inducing IL-8 production, and engaged mouse
219 ectroscopy on mobile human embryonic kidney (HEK) cells, neurons cells from mice, and yeast cells (S.
220 demonstrate that in human embryonic kidney (HEK) cells, rescue of SOCs required co-transfection of l
221 b, when expressed in human embryonic kidney (HEK) cells, was unstable due to degradation by proteasom
222 able hERG-expressing human embryonic kidney (HEK) cells, we demonstrate that beta-arrestin signaling
229 ross-correlation spectroscopy (FCCS) of live HEK cells transfected with 2 spectrally different OLIG2
230 in hyperammonemic murine skeletal myotubes, HEK cells, and skeletal muscle from hyperammonemic rats
233 rowth and increase migration of noncancerous HEK cells; indeed, both properties were almost doubled w
234 ing single NRVMs to a dynamic clamp model of HEK cell ionic current reproduced the cardiac maximal di
235 sly shown that reovirus-induced apoptosis of HEK cells is initiated by death receptor activation but
236 the extracted electrical characteristics of HEK cells exposed during 72 h to a 0.5 T uniform static
238 Immunoadsorption of hsp90 from cytosol of HEK cells expressing the truncated CYP2E1(Delta3-29) yie
242 Applying whole-cell patch-clamp recording of HEK cells, we found that wild-type but not disease mutan
246 nilloid 4 (TRPV4) in Xenopus laevis oocytes, HEK cells and nociceptive neurons, and stimulated neuron
249 data shows our M2e-MAbs bind to M2e peptide, HEK cells expressing the M2 channel, as well as, influen
250 or shedding of meprin A, we generated stable HEK cell lines expressing meprin beta alone and both mep
254 rexpressed PPIP5K1 from osmotically stressed HEK cells (0.2 M sorbitol; 30 min) revealed a persistent
257 in and solubilized from HEK cells show that HEK cell GLUT1 resolves as 6- and 10-nm Stokes radius pa
259 e number of GFP-tagged Kv2.1 channels on the HEK cell surface was compared with K(+) channel conducta
261 cell lines transformed by Ad5 DNA and three HEK cell lines transformed by the SV40 early region did
263 uman embryonic kidney) cells and transfected HEK cells that stably express wild-type (WT) and mutant
265 ippocampal neurons and to CASPR2-transfected HEK cells led to some internalization of the IgG, but wi
266 confirm PASK binding to NKCC1 in transfected HEK cells and further suggest that this binding is not a
267 onance energy transfer assays in transfected HEK cells showed that RGS6 prefers Galpha(o) over Galpha
269 coimmunoprecipitation studies in transfected HEK cells, implying a direct interaction between the pro
271 ized to Kv2.1 surface density in transfected HEK cells, was used to determine the expression levels o
277 urons, whole-cell patch clamp of transfected HEK cells revealed that Nav1.7 activation was unaltered
280 n the activation of NF-kappaB of transfected HEK cells, we discovered that some oligodeoxynucleotides
283 Here, serum starvation of ROMK-transfected HEK cells led to an increase of ROMK current density; su
285 x more active on TLR8- than TLR7-transfected HEK cells (EC50, approximately 50 nM vs. approximately 5
286 68 by PKA in ARVM or transiently transfected HEK cells increased its palmitoylation, but PKA activati
290 ) or that were transfected to express TRPV4 (HEK cells), pretreatment with a PAR2 agonist enhanced Ca
295 oprecipitation studies, carried out in whole HEK cell lysates, confirmed in vivo binding between thes
298 eceptors was underscored in experiments with HEK cells, which lack the P2X7 receptor and showed strik
300 he conformation of intracellular apoE within HEK cells and astrocytes adopts a directional pattern; i