ライフサイエンスコーパス: TEA

1 TEA acts as a fast blocker (resulting in decreased curre

2 TEA and PEA had similar serum sIgA.

3 TEA cluster 1 had the most subjects with a history of in

4 TEA cluster 2, the smallest cluster, had the most subjec

5 TEA cluster 3, the largest cluster, had normal lung func

6 TEA domain (TEAD) transcription factors are essential fo

7 TEA domain (TEAD) transcription factors serve important

8 TEA domain transcription factor-1 (TEAD-1) is essential

9 TEA inhibited total Kv current with an IC50 = 0.54 mm an

10 TEA transcription activates promoters associated with re

11 TEA(+) decreases the association rate of 21-amino-9alpha

12 TEA, guanidine, and tetramethylguanidine inhibition was

13 (TEA-thiolate(+) = -S(CH(2))(11)N(CH(2)CH(3))(3)(+); SC6F

14 is purpose a MtBE-H2O (1:1) system with 10mM TEA and HCl was applied leading to a phenolic fraction,

15 4 patients survived to hospital discharge (2 TEA alone, 3 TEA/LCSD combined, and 4 LCSD alone), 1 of

16 tional mechanistic details of the Pd(OAc)(2)/TEA-catalyzed aerobic alcohol oxidation system are discl

17 s to 15nS-V and becomes sensitive to Ca(2+), TEA, BK, and SK blockers.

18 ent is small (3nS-V), insensitive to Ca(2+), TEA, BK, and SK blockers.

19 und to be -0.11, -0.25, and -0.47 V vs E(1/2,TEA) (term is defined later in experimental), respective

20 21 TEA and 52 PEA children were recruited (28 PEA-OIT, 24 P

21 The highly cationic nanoparticle [Au(225)(TEA-thiolate(+))(22)(SC6Fc)(9)] adsorbs so strongly on P

22 rvived to hospital discharge (2 TEA alone, 3 TEA/LCSD combined, and 4 LCSD alone), 1 of the TEA alone

23 inhibitor, tetraethylammonium (TEA), and (4) TEA + l-NAME.

24 genic embryos show that a binding site for a TEA Domain (TEAD) transcription factor is essential for

25 (+) current in SCs was composed (> 70%) of a TEA (2 mm)-sensitive component that was mediated by the

26 there was a reduction in the prevalence of a TEA-sensitive 113 pS channel in neurones from TG2576 mic

27 First, by activating TEA-inhibitable K(+)(Ca) channels, endothelium-derived h

28 In addition, TEA-soy sizes had a BOD5/COD ratio of 0.44, much higher

29 T) infants evaluated at term equivalent age (TEA) and healthy full-term newborns using proton magneti

30 luded for cranial US at term-equivalent age (TEA).

31 The T early alpha (TEA) promoter in the murine Tcra locus generates noncodi

32 alpha-TEA stimulated both apoptosis and autophagy in murine ma

33 a-tocopheryl ether linked acetic acid (alpha-TEA) have been developed.

34 vative alpha-tocopheryloxyacetic acid (alpha-TEA) induces tumor cell apoptosis and may offer a simple

35 ltridecyl)chroman-6-yloxy acetic acid (alpha-TEA), induce human breast, prostate, colon, lung, cervic

36 Although both VES and alpha-TEA can induce A2780 and subline A2780/cp70 ovarian canc

37 more sensitive to growth inhibition by alpha-TEA than VES.

38 ignaling programs are activated during alpha-TEA-induced tumor cell killing.

39 f caspase-dependent apoptosis enhanced alpha-TEA-induced autophagy.

40 We suggest that the ability of alpha-TEA to stimulate autophagy and enhance cross-priming of

41 the ether-linked acetic acid moiety of alpha-TEA were demonstrated by high-performance liquid chromat

42 arrest within 24 h of treatment, only alpha-TEA is an effective inducer of apoptosis.

43 VES or alpha-TEA treatment of cp70 cells with 5, 10, or 20 microg/ml

44 Taken together, these data show alpha-TEA to be a potent and stable proapoptotic agent for hum

45 id chromatography analyses that showed alpha-TEA to remain intact, whereas VES was hydrolyzed to the

46 Here we report that alpha-TEA also triggers tumor cell autophagy and that it impro

47 Cell exposure to alpha-TEA generated double-membrane-bound vesicles indicative

48 cancer cell lines are exceptions, with alpha-TEA exhibiting greater proapoptotic effects.

49 ation with dendritic cells pulsed with alpha-TEA-generated autophagosomes reduced lung metastases and

50 to the same extent as tetra-ethyl ammonium (TEA) but did not affect the membrane potential.

51 methylhistamine (RAMH), tetraethyl ammonium (TEA), and 4-aminopyridine (4-AP) were applied in the sup

52 Transient epileptic amnesia (TEA) is a recently recognised form of epilepsy of which

53 was to compare thoracic epidural analgesia (TEA) to intravenous patient-controlled analgesia (IV-PCA

54 Our Tissue Enrichment Analysis (TEA) can be found within WormBase, and can be downloaded

55 crude reaction mixture with Bu(2)SnCl(2) and TEA at room temperature enabled facile isolation of mult

56 Furthermore, blockade of 4-AP- and TEA-sensitive K+ channels in the presence of TTX signifi

57 evated and prolonged the effects of BDNF and TEA on actin polymerization.

58 tic analysis of currents elicited by CCh and TEA allowed an estimate of receptor affinity for TEA of

59 Addition of Cs(+) and TEA(+) to the growth medium confirmed the key role of th

60 ls insofar as it is insensitive to Cs(+) and TEA(+), but resembles voltage-independent channels of gl

61 IBTX and TEA/4-AP did not affect the basal [Ca(2+) ]i in isolated

62 ng of the coupling between permeant ions and TEA blockade.

63 lation of the TS evoked EPSPs and IPSPs, and TEA and 4-AP increased the average amplitude and decreas

64 (15 mM poly-L-SUCL, 25 mM each of NH4OAc and TEA (pH 8.0); 80% (v/v) methanol sheath liquid containin

65 Both L-NMMA and TEA attenuated bradykinin-mediated vasodilation in healt

66 l-NNA and TEA, as well as their combination, lowered CVC in young

67 enicillamine (SNAP) was inhibited by ODQ and TEA but was insensitive to PD98059.

68 =20:1) and blocked by internal paxilline and TEA.

69 sodium current (I(Na)) and 4AP-sensitive and TEA-resistant potassium current (I(K)).

70 chloride (3 stocks), acetone (7 stocks), and TEA (3 stocks), respectively, and 0% for a validation se

71 s between the behaviour of internal TBSb and TEA suggesting these molecules bind to distinct but inte

72 S-IPSCs persisted in the presence of TTX and TEA but not 4-AP.

73 inhibitor of the interaction between YAP and TEA domain transcription factor 4 [TEAD4]).

74 coactivator Yes-associated protein (YAP) and TEA domain family members (TEAD).

75 se Yes, the Yes-associated protein (YAP) and TEA domain TEAD2 transcription factor pathway are activa

76 s the value of thoracic epidural anesthesia (TEA) and left cardiac sympathetic denervation (LCSD) in

77 Whole-cell currents were inhibited by 4-AP, TEA, charybdotoxin and iberiotoxin implicating functiona

78 ning K(+) current with the addition of 4-AP, TEA-Cl, and glibenclamide; and 4) blocking I(Ca) with ca

79 ls, with Ca(2+)-sensitive K(+) and both 4-AP/TEA-sensitive and -insensitive currents; type 3 cells, w

80 nsensitive currents; type 3 cells, with 4-AP/TEA-sensitive and -insensitive K(+) and small Na(+) curr

81 sion for transcriptomic endotypes of asthma (TEA), gene signatures that discriminate phenotypes of di

82 AA (p < 0.025) and higher Cho (p < 0.001) at TEA when compared to healthy controls.

83 ectedly, S1P also enhances MRTF-A binding at TEA sites.

84 infants showed a larger ventricular size at TEA compared with term infants (P < .001).

85 owever, scarce reciprocal inhibition between TEA and Arg was found, while the biguanide metformin was

86 hare an evolutionarily conserved DNA-binding TEA domain, which binds to the MCAT cis-acting regulator

87 ) a site near the cytoplasmic end that binds TEA and K+ (but not Rb+) ions; K+ ions binding to this s

88 The K(+) channel blocker TEA could also reverse the inhibitory effect of Y-27632

89 For the Na pump, both TEA and TPA inhibited, but TMA did not.

90 which has been shown to interfere with both TEA binding and the interaction of K+ with an external b

91 under mild conditions (TMS-Cl/TEA or TMS-Br/TEA in refluxing CHCl(3)) that do not cause demetalation

92 t responses were not affected by apamin, but TEA evoked similar changes.

93 did not affect the rise in [Ca(2+) ]i , but TEA/4-AP strongly ( approximately 3-fold) enhanced [Ca(2

94 ing rate constant for receptors activated by TEA alone.

95 The I(A) amplitude was not affected by TEA at any concentration or membrane potential.

96 etigabine-facilitated efflux were blocked by TEA (IC(50)s=0.4 and 0.3mM, respectively) and the neurot

97 A mechanism in which receptors blocked by TEA can close would account for the experimental finding

98 nd high conductance channels were blocked by TEA or 4-AP or 140 mM RbCl.

99 as insensitive to PD98059 but was blocked by TEA.

100 e-wide gene expression during development by TEA/ATTS family of transcription factors.

101 emical step is reductive quenching of Fl* by TEA because of the latter's greater concentration.

102 Occupancy by TEA completely prevented MTSET modification of a cystein

103 +) (and with extracellular Na(+) replaced by TEA), Fe(2)(+) carried detectable, whole-cell, inward cu

104 Hepatic accumulation of [(14)C]TEA in 14-day BDL rats was reduced to 29.6 +/- 10.9% of

105 e model substrate tetraethylammonium ([(14)C]TEA) was administered intravenously to BDL and control r

106 lled by using the tetraethylammonium cation (TEA(+)) and/or iodide anion (I(-)) as chemical inputs.

107 n coapplied with 1 mM carbamylcholine (CCh), TEA decreased the effective opening rate demonstrating t

108 regulator (CFTR(inh)-172), or K(+) channels (TEA or XE991).

109 the BK calcium-dependent potassium channels (TEA (1 mM), paxilline (10 muM) and iberiotoxin (100 nM))

110 the ionic salt tetraethylammonium chloride (TEA(+)Cl(-)) or the zwitterion tricine(+/-).

111 Tetraethylammonium chloride (TEA) was used to inhibit K(+)(Ca) channel activation and

112 be deprotected under mild conditions (TMS-Cl/TEA or TMS-Br/TEA in refluxing CHCl(3)) that do not caus

113 ot influenced by l-NNA (all concentrations), TEA (4-400 mum) or their combination (400 mum) (P > 0.05

114 At millimolar concentrations, TEA inhibited nicotinic receptor currents by depressing

115 udied under similar experimental conditions (TEA(o) and K(i)).

116 cantly abrogated the concentration-dependent TEA inhibition.

117 oxygen species (ROS)-mediated, TAZ-dependent TEA domain transcription factor (TEAD) trans-activation.

118 ounded by the upstream INT1-2 and downstream TEA elements.

119 e), (2) tetraethylammonium (TEA), (3) EMLA + TEA (Combo), and (4) Ringer solution (Control).

120 tage and [Ca(2+)](i) and blocked by external TEA but not by charybdotoxin, iberiotoxin, apamin, or 4-

121 In the presence of external TEA, the internal TBSb on-rate decreased with increased

122 hannels, and the mechanism by which external TEA slows C-type inactivation, have been considered well

123 nded on a residue required for extracellular TEA action, suggesting that the identified compound targ

124 or CDC5, the cellular differentiation factor TEA domain 4, and the proapoptotic factor BNIP 2.

125 MinK-55C is distant from the pore: one finds TEA does not affect Cd(2+) block if channels are formed

126 allowed an estimate of receptor affinity for TEA of about 1 mM, while an upper limit of 10 s-1 could

127 The basis for TEA inactivity in DN thymocytes is unclear, because Edel

128 ixture (2:1 ratio by volume up to 60 mL) for TEA and cisplatin-ethiodized oil emulsion (0.5 mg cispla

129 Pmp22 enhancers contain binding motifs for TEA domain (Tead) transcription factors of the Hippo sig

130 YAP in MKs and demonstrate a requirement for TEA domain (TEAD) transcriptional factors to comediate Y

131 eggin polyoxoanions of the general formula, (TEA)Hp Naq [H2 M12 (XO4 )O33 (TEA)]r H2 O where p, q, r=

132 NAME (P < 0.001 from control, P < 0.001 from TEA).

133 gnals but failed to alter membrane function (TEA uptake).

134 anism involving activation of PKA and highly TEA-sensitive K(+)-currents.

135 and several potassium channels (iberiotoxin, TEA, 4-amino-pyridine), but blockers of calcium channels

136 ia of Genes and Genomes was used to identify TEA clusters.

137 y deficit have recently been demonstrated in TEA: (i) accelerated long-term forgetting (ALF): the exc

138 Median overall survival in TEA and TACE was 24.3 months (95% confidence interval [C

139 cell invasiveness, associated with increased TEA domain-dependent transcription and CCN2/CTGF express

140 a KCNQ1 mutant (K318I, V319Y) that increases TEA affinity; the second proposes that Cd(2+) binds betw

141 ive to conventional K(+) channel inhibitors (TEA, 4-AP and Ba(2+)) but completely inhibited by tetrac

142 Critical was the role of the intracellular TEA(+)-binding site.

143 Unlike the tetraethylammonium ion (TEA), neither JC638.2alpha nor C16 monostring TA279 prod

144 ies of the current (permeability to Na+, K+, TEA+, and Cs+; voltage insensitivity; and dependence on

145 ffects of inhibitors of BK (IBTX) and BK/Kv (TEA/4-AP) on [Ca(2+) ]i responses to a wide range of hyp

146 In contrast, at more distal locations, TEA transcription inhibits promoter activity through tra

147 cells was enhanced nearly twofold by 1.0 mM TEA, with a decrease in the paired pulse ratio (PPR), ef

148 The currents were mostly blocked by 1 mm TEA, activated rapidly at voltages more positive than -2

149 In 10 mM TEA, potassium currents were reduced in all the bipolar

150 e observed at concentrations as high as 5 mM TEA or in the presence of a mutation which selectively i

151 n or 10 nM dendrotoxin-K and blocked by 5 mM TEA(+).

152 lular solution or during superfusion of 5 mm TEA, suggesting the presence of an additional BK-channel

153 hannel blocker; and (iv) 10 mm l-NNA + 50 mm TEA.

154 l-NAME), and nearly abolished with l-NAME + TEA (13 +/- 2%; P = 0.001 from sulfaphenazole + l-NAME),

155 ions of N(G)-monomethyl-l-arginine (L-NMMA), TEA, fluconazole, and their combination.

156 Lanthanides and Zn2+ (but not TEA+) suppressed the open probability without affecting

157 (+) channel blocker barium chloride (but not TEA, glybenclamide or tertiapin-Q) significantly occlude

158 eral formula, (TEA)Hp Naq [H2 M12 (XO4 )O33 (TEA)]r H2 O where p, q, r=[2,3,8] for 1 and [4,1,4] for

159 The ability of TEA transcription to coordinate the activity of multiple

160 ing FBF in all subjects, and the addition of TEA further reduced FBF after fluconazole, suggesting th

161 % of the plateau phase, as administration of TEA in combination with l-NAME abolished the majority of

162 /- 5.3 Hz), both sensitive to application of TEA (0.5 mm) and 4-aminopyridine (4-AP; 30 mum).

163 The neuroanatomical bases of TEA and its associated memory deficits are unknown.

164 opiate use further supported the benefit of TEA on patient experience.

165 These actions involve binding of TEA(+) to different, but weakly interacting, sites in th

166 annels also blocked by low concentrations of TEA.

167 nt study, we investigated both the effect of TEA(+) on [(3)H]ryanodine binding and the actions of thi

168 ntibody mimicked and occluded the effects of TEA and 4-AP in NTS and dorsal column nuclei neurones, b

169 e knock-out (DKO) mice, the large effects of TEA were absent, spike-evoked GABA release was larger, a

170 Evaluation of TEA clusters in children confirmed that TEA clusters 1 a

171 between the IC(50) values for inhibition of TEA transport by 14 different compounds and their calcul

172 Initiation of TEA and LCSD in patients with refractory VT was associat

173 After initiation of TEA, 6 patients had a large (> or =80%) decrease in VT b

174 A and MOR), less than the interconversion of TEA(+) in solution, a heteroatom-dependent (Al, B, Co, M

175 dine binding was observed in the presence of TEA(+), suggesting that the cation and alkaloid compete

176 t repolarization remained in the presence of TEA, MgTX, or both.

177 entical rates in the absence and presence of TEA.

178 Here, we have analyzed the significance of TEA transcription for Tcra locus regulation through the

179 an external binding site similar to that of TEA in the Kv2.1 outer pore, but with much higher affini

180 for YAP activation and the transcription of TEA domain (TEAD) family members.

181 tant displayed markedly reduced transport of TEA and cimetidine while retaining transport of 1-methyl

182 ent promoter that lies only 4 kb upstream of TEA promoter.

183 ails of the study illustrate that the use of TEA results in an active catalyst that has only one liga

184 or cysteine had a relatively minor effect on TEA potency.

185 ctivity through competing with the oncogenic TEA domain family of transcription factors (TEAD) for YA

186 Addition of calpain inhibitors after BDNF or TEA treatment maintained RhoA levels elevated and prolon

187 de levels (P = 0.04) compared with the other TEA clusters.

188 inding of YAP to its transcriptional partner TEA domain family member 4 (TEAD4); TEAD4 binding requir

189 tion that is pore-independent and, perforce, TEA-insensitive.

190 t not by MPP+ (1-methyl-4-phenylpyridinium), TEA (tetraethylammonium), decynium-22, carnitine, PHA (p

191 hoice of the N-protecting group (see scheme; TEA = triethylamine, TMS = trimethylsilyl).

192 VLM neurones indicate that a 4-AP sensitive, TEA insensitive current, with biophysical properties con

193 expressed in the heteromers includes shifted TEA sensitivity compared with KCNQ2 homomers.

194 Industrial weaving results showed TEA-soy protein had relative weaving efficiency 3% and 1

195 eater compared to TEA, EMLA and Combo sites (TEA, 630 +/- 512, P = 0.003; EMLA, 421 +/- 216, P < 0.00

196 e reactions of impurities unique to specific TEA and chloroform stocks, and thus indicative of their

197 seen for the uptake of the hOCT1 substrates TEA(+) and ASP(+).

198 In major HPB surgery, TEA provides a superior patient experience through impro

199 significant difference in overall survival, TEA demonstrated better complete tumor response, longer

200 TEAD (TEA/ATTS domain) transcription factors are the most dist

201 complex with the transcription factor TEAD (TEA domain family member) directly induce LATS2 expressi

202 In addition to a highly conserved TEAD1 (TEA domain family member 1)-binding MCAT motif, nucleoti

203 h muscle development and uses its N-terminal TEA domain (TEAD) to bind M-CAT elements.

204 Tetraethylammonium (TEA) is frequently used to inhibit delayed rectifier K(+

205 ly to skin surface), (2) tetraethylammonium (TEA), (3) EMLA + TEA (Combo), and (4) Ringer solution (C

206 apamin with glucose and tetraethylammonium (TEA) caused a similar elevation in [Ca(2+)](i), which wa

207 ovement of Ca2+, K+, and tetraethylammonium (TEA+) through the model RyR2 pore were simulated with ex

208 h 4-aminopyridine (4-AP)/tetraethylammonium (TEA)-sensitive and CdCl(2)-sensitive inward currents; ty

209 he external pore blocker tetraethylammonium (TEA) and depended on a residue required for extracellula

210 otassium channel blocker tetraethylammonium (TEA), and the selective adenosine triphosphate (ATP)-sen

211 ve K(+) channel blocker, tetraethylammonium (TEA), and a large-conductance Ca(2+)-activated K(+) (BK(

212 cetylcholine receptor by tetraethylammonium (TEA) and related quaternary ammonium derivatives.

213 type for organic cations tetraethylammonium (TEA) was also transported by SlCAT2.

214 reaction gel containing tetraethylammonium (TEA) cations.

215 rans-ions), and external tetraethylammonium (TEA), an I(Ks) pore-blocker.

216 ssibility, extracellular tetraethylammonium (TEA) and tetramethylammonium application produces potent

217 rations of extracellular tetraethylammonium (TEA; IC(50) = 11.8 mM), but no specific antagonists were

218 on is composed of a fast tetraethylammonium (TEA)-sensitive component, determining the width and ampl

219 or some substrates (e.g. tetraethylammonium (TEA)), they have distinct selectivities for others (e.g.

220 ugh inhibition of highly tetraethylammonium (TEA)-sensitive ion channels that contribute to action po

221 a KCa channel inhibitor, tetraethylammonium (TEA), and (4) TEA + l-NAME.

222 Intracellular tetraethylammonium (TEA) inhibition was studied at the single-channel level

223 h were inhibited by 5 mM tetraethylammonium (TEA(+)) chloride.

224 S inhibitor; (iii) 50 mm tetraethylammonium (TEA), a non-specific KCa channel blocker; and (iv) 10 mm

225 ted the effect of 1.0 mM tetraethylammonium (TEA; which blocks Kv3 channels) on inhibitory synaptic c

226 opyridine (4-AP) but not tetraethylammonium (TEA) or dendrotoxin (DTX).

227 ced the effectiveness of tetraethylammonium (TEA(+)) as a blocker of K(+) translocation.

228 of the rapid transfer of tetraethylammonium (TEA(+)) at the 1,2-dichloroethane/water interface.

229 ride salts, specifically tetraethylammonium (TEA), tetrapropylammonium (TPA), tetrabutylammonium (TBA

230 ded, economical template tetraethylammonium (TEA(+) ) has been systematically examined by experimenta

231 The location of the tetraethylammonium (TEA) binding site in the outer vestibule of K+ channels,

232 ntercation compared with tetraethylammonium (TEA(+)), due to the coordination of Li(+) to the carbona

233 slices with BDNF or with tetraethylammonium (TEA), which induces a chemical form of LTP, produces a r

234 [Cl(-)], [Na(+)], and [tetraethylammonium] ([TEA(+)]), but dependent on [H(+)].

235 ter pore, but with much higher affinity than TEA.

236 position equivalent to Shaker T449, and that TEA prevents a constriction that underlies inactivation

237 The prevailing model has been that TEA is coordinated by four amino acid side chains at the

238 We conclude that TEA modulates, in a concentration dependent manner, tau(

239 n of TEA clusters in children confirmed that TEA clusters 1 and 2 are associated with a history of in

240 Our results demonstrate that TEA(+) inhibits both K(+) translocation through RyR, and

241 onal experiments in Shaker demonstrated that TEA bound well to C-type inactivated channels, but did n

242 se results add weight to the hypothesis that TEA is a syndrome of mesial temporal lobe epilepsy.

243 ch higher than 0.03 for PVA, indicating that TEA-soy sizes were easily biodegradable in activated slu

244 these findings rule out the possibility that TEA binding involves an intimate interaction with the fo

245 tudies over a wide voltage range reveal that TEA block has a complex voltage-dependence that also dep

246 The data show that TEA is a weak agonist of the nicotinic receptor.

247 These data suggest that TEA and LCSD may be effective additions to the managemen

248 Together, these data suggest that TEA is stabilized in a more external position in the out

249 function with TCRalpha promoters such as the TEA promoter to drive TCRalpha-chain gene assembly in th

250 profile in the circulation to determine the TEA cluster assignment in a cohort of children with asth

251 ring vertebrate neural tube development, the TEA domain transcription factor (TEAD) is the cognate DN

252 ocus, where cohesion-binding sites flank the TEA promoter and the Ealpha enhancer, and demarcate Tcra

253 e 0- to 48-hour pain scores was lower in the TEA group (78.6 vs 105.2 pain-hours, P = 0.032) with a 3

254 to NO2 and subsequent NO2 collection in the TEA solution is >98% under a variety of controlled condi

255 A/LCSD combined, and 4 LCSD alone), 1 of the TEA alone patients underwent an urgent cardiac transplan

256 Thus, the inactivity of the TEA promoter in DN thymocytes is due primarily to intrin

257 a transcription terminator downstream of the TEA promoter.

258 vided that a sufficient concentration of the TEA reducing agent was present in solution.

259 ate constant and transfer coefficient of the TEA(+) transfer are compared with previously reported va

260 Reducing the TEA concentration from 40 mM to 1 mM significantly decre

261 Remarkably, the TEA promoter on this allele exhibits normal developmenta

262 fect in I(A) kinetics demonstrating that the TEA effects were not due to a reduction of extracellular

263 harmacological studies demonstrated that the TEA-sensitive component of I(K,slow), I(K,slow2,) is sel

264 locus (TCRalpha/delta(5DeltaT)) in which the TEA promoter lies in the same location as the Vdelta5 ge

265 clear translocation and interaction with the TEA domain (TEAD) transcription factor complex, which le

266 ethylammonium, and tetrapropylammonium, TMA, TEA, and TPA, respectively) did not inhibit PMCA.

267 sponse to L-NMMA was greater (P=0.04) and to TEA was lower (P=0.04) in healthy subjects compared with

268 growth by competing with YAP for binding to TEA-domain proteins (TEADs).

269 ax s) were significantly greater compared to TEA, EMLA and Combo sites (TEA, 630 +/- 512, P = 0.003;

270 on strategy, 140 patients were randomized to TEA (N = 106) or intravenous patient-controlled analgesi

271 et initial Valpha-to-Jalpha recombination to TEA-proximal Jalpha segments and promote the ordered usa

272 sensitive to charybdotoxin and resistant to TEA.

273 potassium currents, which were sensitive to TEA and 4-AP, respectively.

274 etely inactivated at -40 mV and sensitive to TEA and DTX but less so to 4-AP.

275 e large conductance channel was sensitive to TEA, iberiotoxin, was activated in excised inside-out pa

276 enge, patients were classified as transient (TEA) or persistent (PEA) egg-allergic.

277 ssed by tetraethylammonium cation transport (TEA).

278 ent NO2 collection in a 20% triethanolamine (TEA) solution as nitrite and nitrate for delta(15)N anal

279 gradable sizing agents from triethanolamine (TEA) modified soy protein could substitute poly(vinyl al

280 ons of commercial stocks of triethanolamine (TEA), thionyl chloride, chloroform, and acetone.

281 the photosensitizer (PS) and triethylamine (TEA) as the sacrificial electron donor, these complexes

282 orate) under mild conditions (triethylamine (TEA) or molecular sieves) easily led to the correspondin

283 in acetonitrile (with 0.25 M triethylamine (TEA)) thus identified as P(-) (singly reduced, nonproton

284 demonstrated the potential of triethylamine (TEA) for shifting the charge state pattern toward lower-

285 ster salts in the presence of triethylamine (TEA).

286 diethylmethylamine (DEMA) or triethylamine (TEA) through a T mixer coupled to a time-of-flight mass

287 Eight patients underwent TEA, and 9 underwent LCSD (3 patients had both procedure

288 of 54.2+/-16.6 years; 13 men) who underwent TEA, LCSD, or both to control ventricular tachycardia (V

289 ckel-Onsager theory of electrophoresis, when TEA(+)Cl(-) was added to the buffer.

290 hese results argue against the model whereby TEA slows inactivation via a foot-in-the-door mechanism

291 re, the initial peak was just 17 +/- 2% with TEA + l-NAME (P < 0.001 from l-NAME).

292 zole (P = 0.02 from control), 71 +/- 3% with TEA (P = 0.01 from control), and further to 38 +/- 2% wi

293 Thus, these findings are consistent with TEA, guanidine, and tetramethylguanidine inhibiting from

294 Resting FBF decreased with TEA and L-NMMA in all subjects (P<0.001); however, the v

295 s persistently and significantly higher with TEA at 3 months (62 of 88 [70%] vs 39 of 76 [51%], P = .

296 r intralesional progression were longer with TEA than TACE (TTP, 34.6 months [95% CI: 28.2, 41] vs 26

297 ctive memory performance in 41 patients with TEA.

298 ter refrigerated storage, since samples with TEA and GRA extract showed the lowest values.

299 r TBARS values were obtained in samples with TEA and GRA extracts.

300 ediated vasodilation remained unchanged with TEA in healthy subjects but was significantly attenuated