ライフサイエンスコーパス: be blocked by

1 GFP respond to 10 muM 5-HT and this response is blocked by 1 muM ondansetron, a 5-HT3 antagonist, and

2 the end of the long pulse nearly doubled and was blocked by 100 mum tannic acid.

3 the metallic anode if the anions of the salt are blocked by a ceramic electrolyte in a polymer/cerami

4 eutrophilia and mucosal chemokine production are blocked by a small-molecule BRD4 bromodomain inhibit

5 reducing their activity in a manner that can be blocked by a 5-HT1A antagonist.

6 The actions of miRNAs can be blocked by a new class of drugs, antagomirs, some of

7 imarily IPSPs in premotor neurons that could be blocked by a nicotinic receptor antagonist.

8 GluA1 S845 phosphorylation could be blocked by a PKA inhibitor, and GluA1 T840 dephosphor

9 ted in the downregulation of Mfn2, which can be blocked by a proteasome inhibitor.

10 itor, and GluA1 T840 dephosphorylation could be blocked by a protein phosphatase 1/2A (PP1/PP2A) inhi

11 s phosphorylation at Ser-1303 by Dapk1, that is blocked by a neuroprotective cell-permeable peptide m

12 to CaV2.2 channel-mediated responses, as it is blocked by a omega-conotoxin GVIA application.

13 Finally, the acquisition of conditioning is blocked by a PDK1 inhibitor.

14 This inhibition is blocked by a PLC inhibitor (U73122, 1-(6-{[(17beta)-3

15 Instead, constitutive AMPAR trafficking is blocked by a Rac1 inhibitor and is regulated by a dyn

16 ion in CLL cells and that such proliferation is blocked by a TLR7/8/9 inhibitor, by DNase, and by the

17 Likewise, (11)C-JNJ-54173717 PET signal was blocked by a chemically distinct P2X7R ligand, indic

18 blished enabling us to demonstrate that pain was blocked by a cyclooxygenase-2 inhibitor, suggesting

19 use HSCs, the inhibited CCN2 3'-UTR activity was blocked by a miR-199a-5p antagomir.

20 ctivity depended on a 3' ssDNA extension and was blocked by a polyethylene glycol linker, indicating

21 as dependent on group I mGluR activation and was blocked by a proteasome inhibitor (MG-132).

22 uced colonic anion secretion and this effect was blocked by a specific neuropeptide Y receptor Y1 (NP

23 duced colonic anion secretion, although this was blocked by a specific neuropeptide Y receptor Y1 rec

24 These effects were blocked by a CB2 receptor antagonist (SR144528) or

25 formation of capillary tubes; these effects were blocked by a neutralizing antibody against GM-CSF.

26 lly, the treatment's neuroprotective effects were blocked by a p-Akt inhibitor.

27 When the completion of germination is blocked by ABA, radicle elongation and cell divisions

28 For example, when type I IFN signaling was blocked by Abs in Rag1(-/-) mice, the mice showed dr

29 ends on VAChT expression in Kenyon cells and is blocked by ACh receptor antagonism.

30 Finally, the depression-like behaviors were blocked by acute injection of the 5HT2A/C agonist (

31 oblast as ischemia-induced VEGFR2 expression was blocked by ADAM17-siRNA.

32 on of shed syndecan-1 (sSDC1) to the nucleus was blocked by addition of exogenous heparin or heparan

33 Furthermore, sensitization was blocked by all inhibitors tested except the inactive

34 A23187 resulted in PTP1B cleavage, which can be blocked by ALLN.

35 AMPAR recycling was blocked by alterations in the GTPase, TC10, which co

36 by Pep19 in 3T3-L1 differentiated adipocytes is blocked by AM251, a cannabinoid type 1 receptors anta

37 hese currents showed a pH50 value of 6.6 and were blocked by amiloride.

38 in arterioles isolated from HFD rats, which was blocked by AMP-activated protein kinase (AMPK) inhib

39 resealing caused cell swelling, which could be blocked by an isosmotic addition of a pore-impermeabl

40 phobic track leading to the active site that is blocked by an evolutionarily conserved motif which we

41 After CNS injury, axon regeneration is blocked by an inhibitory environment consisting of th

42 ge was inhibited using eculizumab, and C5aR1 was blocked by an antagonist.

43 This effect was blocked by an Avpr1b antagonist.

44 ribosomes in dendrites when memory formation was blocked by an inhibitor of translation initiation.

45 F by ~10% after 60 min exposure, but effects were blocked by an anti-aflatoxin antibody only with A.

46 owed statistically significant increases and were blocked by an excess of authentic standard GSK14821

47 sociated fibroblasts (CAFs), and this effect was blocked by anakinra.

48 t prostate cancer (PCa) and its activity can be blocked by androgen-deprivation therapies (ADTs).

49 e effects were mediated by 5-HT because they were blocked by antagonists of 5-HT2A and 5-HT1A recepto

50 The increased thrombin flux after 500 s was blocked by anti-FXIa antibody (O1A6), consistent wit

51 in bone marrow cells from naive mice, which was blocked by anti-IL-5 antibody.

52 However, killing could be blocked by antibodies against FasL, which identified

53 BCs to endothelial cells when MUC1 and CD43 were blocked by antibodies.

54 Furthermore, LPS-induced apoptosis was blocked by antioxidant N-acetylcysteine or NF-kappaB

55 The inhibitory phase was blocked by apamin, revealing a distinct excitatory c

56 This enhancement is blocked by application of a group I mGluR1-specific a

57 Plasma membrane recruitment of DCC or UNC5B was blocked by application of the netrin-1 VI-V peptide,

58 s report, we expand the list of viruses that are blocked by ARB in a laboratory setting to include Eb

59 scarinic receptor stimulation as all effects were blocked by atropine.

60 The protection was blocked by auranofin and required an intact selenocy

61 on calcium entry via voltage-gated channels, is blocked by BAPTA chelation, and recruits intracellula

62 on, even in the absence of osmostress, which is blocked by Bcl-xL co-expression.

63 lation of the proapoptotic molecule Bid, and was blocked by Bcl2 overexpression.

64 s from patients and that this activation can be blocked by BCR inhibitors.

65 ation induced by ilimaquinone and nocodazole is blocked by betagamma inhibition, demonstrating that b

66 opolar cytokinesis when myosin contractility is blocked by blebbistatin [4].

67 ents that is still present when active force is blocked by Blebbistatin.

68 impermeable to sodium and chloride ions, and are blocked by blockers of voltage-gated ion channels.

69 U50,488-induced reinstatement was blocked by BNST nor-BNI injections, and BNST U50,488

70 1A, contributed to tumor cell migration that was blocked by C-DIM/NR4A1 antagonists.

71 stretch-activated cation channels that could be blocked by Ca(2+) and by FM1-43.

72 BV-2 microglia rapidly released Gal-3, which was blocked by calcineurin inhibitors.

73 thickening of cortical actin fibres and this was blocked by candesartan.

74 eration of platelet intracellular ROS, which was blocked by CD36 inhibitors, mimicked by CD36-specifi

75 ly administered fluorophore-tagged exendin-4 was blocked by central pretreatment with the competitive

76 genesis and p-Creb expression; these effects were blocked by co-addition of protein kinase A inhibito

77 tive stress-induced apoptosis; these actions were blocked by co-administration of the 5-HT4R antagoni

78 These pro- and anti-nociceptive effects were blocked by co-injection of a TRPV channel inhibitor

79 ting of the SCN circadian clock by melatonin was blocked by coadministration of a GIRK channel antago

80 ce by compensatory ERK activation, which can be blocked by combined inhibition of Her2 and MEK.

81 Sustained HER3-AKT activation was blocked by combining erlotinib with either anti-HER2

82 trimers and by A769662, the effects of which were blocked by compound C.

83 ynthase kinase 3 beta, or caspases, toxicity is blocked by compounds targeting cyclin-dependent kinas

84 rophy in PlGF mice, but not when hypertrophy was blocked by concomitant expression of PlGF and RGS4,

85 um concentration ([Ca(2+)]i) which could not be blocked by conventional channel blockers.

86 d that the effect of chronic C3 exposure can be blocked by cotreatment with a C3aR antagonist and by

87 y increased paracellular permeability, which was blocked by cotreatment with LPA, but not LPA1 knockd

88 Raptor) in microglia, whose mTORC1 signaling was blocked, by crossing Raptor loxed (Raptor(flox/flox)

89 was prevented or reversed when the h-current was blocked by Cs(+).

90 PAFR was blocked by CV-3988, and oxidative stress was attenua

91 L12-dependent nuclear import of LASP-1 could be blocked by CXCR4 antagonist, AMD-3100.

92 effect on electrical activity in alpha-cells was blocked by CYN 154806, an antagonist of the somatost

93 etic or pharmacologic targeting of the EGFR, was blocked by Dasatinib, highlighting the central role

94 n of PAR1 observed in Rab11B-deficient cells is blocked by depletion of Rab11A and the autophagy rela

95 after intracerebroventricular infusion of E2 was blocked by DH infusion of an ERK or mTOR inhibitor.

96 nteraction with Huwe1 and polyubiquitylation were blocked by disruption of casein kinase 1 (CK1) acti

97 Associative LTF is blocked by dn classical calpain, whereas non-associat

98 assical calpain, whereas non-associative LTF is blocked by dn small optic lobe (SOL) calpain.

99 AK, and occludin and FAK phosphorylation can be blocked by DSP and occludin antibodies.

100 Activation of SC signaling by glutamate was blocked by EGTA and dizocilpine and by silencing exp

101 scription of HIF-1alpha mRNA, a process that is blocked by either inhibition or knockdown of signal t

102 Enhanced cytosolic calcium in CBE-N2a cells was blocked by either ryanodine or dantrolene, antagonis

103 at, whose development prior to fertilization is blocked by epigenetic regulators belonging to the Pol

104 When oxidative stress was blocked by exposing mice to N-acetylcysteine, induct

105 cCDCP1 is capable of dimerization, which can be blocked by expression of the extracellular portion of

106 This constriction is blocked by fibrous organelles, structures that pass t

107 d MMP9 expression stimulated by high glucose was blocked by FOXO1 deletion or FOXO1 knockdown.

108 This effect of BPA was blocked by Fulvestrant, a full estrogen antagonist,

109 nce in ketamine-treated rats and this effect was blocked by GABAA receptor antagonism.

110 Pitavastatin-induced apoptosis was blocked by geranylgeraniol and mevalonate, products

111 a cells on insulin release from islets could be blocked by GLP-1 receptor antagonist.

112 These effects were blocked by granisetron (5-HT3 antagonist) and were

113 oth cases, prolonged epileptiform discharges were blocked by group I mGluR antagonists (LY367385 + MP

114 This critical disease process is blocked by haptoglobin.

115 tibody-independent Tau uptake into BV2 cells was blocked by heparin, consistent with a previously des

116 lloproteinase (TIMP)-1 and collagen-I, which were blocked by HIF-1alpha shRNA.

117 rphologic analysis revealed that sweat ducts were blocked by hyperkeratotic or parakeratotic plugs.

118 affected by NF-kappaB or Sp1 inhibitors, but was blocked by hypoxia-inducible factor-1alpha (HIF-1alp

119 Furthermore, TH1 differentiation was blocked by Id2 deficiency, which led to E-protein-de

120 ng in increased NRAS expression, which could be blocked by inactivation of Usp9x and therapeutic comb

121 rk suppression underlying lateral inhibition was blocked by inactivation of somatostatin-expressing i

122 ociated with increased c-Jun mRNA levels and was blocked by inactivation of the JNK1/2 signaling path

123 tory and invasive potentials in vitro, which are blocked by inhibiting MMP-12, PI3-K, p38 or JNK acti

124 Rescue of K590A could be blocked by inhibiting ER to Golgi transport using bre

125 loss of neurons or synapses may potentially be blocked by inhibiting neuraminidases, Gal-3, or MerTK

126 ansion of lung cancer stem-like cells, which is blocked by inhibiting mitochondrial respiration.

127 gene transcription or protein synthesis, but was blocked by inhibiting postsynaptic G-protein activit

128 enhanced association of Spns2 with S1P1 that was blocked by inhibiting SphK1 activity with PF-543.

129 Pi-dependent effects on Ca(2+) were blocked by inhibiting the phosphate carrier.

130 urthermore, all pro-ovulatory actions of sLh are blocked by inhibition of Tnfalpha secretion or PG sy

131 In neural cells, exosome formation can be blocked by inhibition or silencing of neutral sphingo

132 enescence by chronic inflammatory conditions is blocked by inhibition of tmTNF-alpha cleavage.

133 osis of PC12 cells or primary neurons, which was blocked by inhibition of MerTK.

134 dependent inhibition of mTORC1 or mTORC2 but was blocked by inhibition of mTORC1/2.

135 d intracellular S1P levels in HLMVECs, which was blocked by inhibition of SphK1.

136 We found that NO-mediated angiogenesis was blocked by inhibition of VEGF with sFlt1 (from 881 +

137 These effects were blocked by inhibition of beta2-AR or the PKA pathwa

138 soconstriction, yet not TRPC6 translocation, were blocked by inhibition or deficiency of sphingosine

139 by stomatal closure and that both responses are blocked by inhibitors of ROS-producing respiratory b

140 phenotype on zebrafish development that can be blocked by inhibitors of PAK or MEK.

141 ng requires dynamic actin polymerization and is blocked by inhibitors of both Arp2/3 and formins.

142 Finally, the D2R-induced ADP is blocked by inhibitors of cAMP/PKA signaling, insensit

143 fatty acids, and phosphatidylcholine, which is blocked by inhibitors of fatty-acid synthase, PI 3-ki

144 nd PGC-1alpha and NDUFS1 mRNA expression and was blocked by inhibitors of Gbetagamma, Akt, NOS, and s

145 These latter effects of A1AT-FA were blocked by inhibitors of peroxisome proliferator-ac

146 romolecules in a selective manner, which can be blocked by injection of mannose receptor ligands.

147 Functional rotation is thought to be blocked by insertion of the latter half of the CTD in

148 e that the antidepressant effects of GLYX-13 are blocked by intra-medial prefrontal cortex (intra-mPF

149 CA1 and mitochondria in astrocytic processes were blocked by ionotropic glutamate receptor (iGluR) an

150 cPLA2alpha(+/+)macrophages, COX-2 expression was blocked by IP, EP2, and EP4 receptor antagonists, in

151 lation-induced stress granule (SG) formation was blocked by ISRIB.

152 histamine on fibroblast proliferation could be blocked by JAK3/STAT6 signaling selective antagonist.

153 ER stress, NFkappaB, and TGF-beta1 signaling were blocked by JNK specific siRNA.

154 The IL-6 effect was blocked by JSI-124 but not PD-98059.

155 lted in increased proliferation, which could be blocked by knockdown of Yap.

156 e self-renewal capacity of cancer stem cells was blocked by LF3 in concentration-dependent manners, a

157 019S LRRK2 and actin-regulatory proteins can be blocked by LRRK2 kinase inhibitors, although we did n

158 ce of its entry into autophagic vacuoles and was blocked by lysosomal cathepsin B and L inhibition.

159 ression by transforming growth factor-beta I was blocked by Meg3 silencing through the inhibition of

160 cular endothelial cells and this interaction was blocked by microglial depletion.

161 Moreover, SPCA1a is blocked by micromolar concentrations of the commonly

162 duction of microRNA-146a, and RvD2's actions were blocked by microRNA-146a inhibition.

163 nociceptive and antiallodynic effects, which were blocked by MOP or NOP receptor antagonists.

164 synthase activation during renal IR that can be blocked by MR antagonism with BR-4628.

165 nse to exogenous purines and these responses were blocked by MRS-2500.

166 nd FGF2 induced pS6 in Muller glia, and this was blocked by mTor inhibitor.

167 These structural effects were blocked by mTOR complex/signaling inhibitors like r

168 ing cholinergic waves, MC calcium transients were blocked by muscarinic acetylcholine receptor antago

169 n of CFC regardless of whether its retrieval was blocked by muscimol.

170 ecrease in catalytic-domain homo-FRET, which was blocked by mutating the T-site (I205K).

171 analysis, and show that multimerization can be blocked by mutations in a specific region of Domain I

172 str3-positive cilia and this recruitment can be blocked by mutations in Sstr3 that impact agonist bin

173 ses spreading and contractions, but this can be blocked by myosin-II inhibition.

174 ve oxygen species in uterine arteries, which was blocked by N-acetylcysteine.

175 channels (NaV1.1-NaV1.4, NaV1.6-NaV1.7) that are blocked by nanomolar concentrations and TTX-resistan

176 ll death in five different cell types, which is blocked by necrostatin-1.

177 azole propionic acid receptor activation and are blocked by neuronal silencing.

178 This interaction can be blocked by NKp30 blocking Ab and an inhibitory ligand

179 ndritic amplification in mitral cells, which was blocked by NMDA and mGluR1 receptor antagonists, con

180 remaining NO signals (mostly mitochondrial) were blocked by nNOS deletion, but not by inhibiting the

181 ane microdomains called lipid rafts, and can be blocked by non-specific depletion of plasma membrane

182 nduced responses and nuclear export of NR4A1 are blocked by NR4A1 antagonists, the p38 inhibitor SB20

183 s produced when processing at the S1/S0 site is blocked by O-linked glycosylation in third instar lar

184 ubset of cellular mRNAs whose nuclear export is blocked by ORF10 with the 3' UTRs of ORF10-targeted t

185 GE2-initiated cAMP production in these cells was blocked by our recently developed novel selective EP

186 Different PKMs or calpain isoforms were blocked by overexpressing specific dominant-negativ

187 ependent, purinergic signaling pathways that are blocked by P2 antagonists.

188 CREB phosphorylation was blocked by p38 inhibitors and induced by the p38 act

189 shortening and MRI contrast enhancement that is blocked by particle formation in solution but yields

190 sed Cl(-)/HCO3 (-) exchange and the increase was blocked by pendrin inhibition.

191 Agonist-induced rosette formation is blocked by pertussis toxin, dependent on PI3K activit

192 or PG synthesis and all actions of rTnfalpha are blocked by PG synthesis inhibitors.

193 imals lacking fibronectin receptors, and can be blocked by pharmacological inhibition of the CamKinas

194 this initiation of maladaptive signaling can be blocked by pharmacological therapies that elevate cGM

195 nctions in endothelial cells in vitro, which is blocked by pharmacological inhibition of acid sphingo

196 LRx triggers degradation of the ECM, which is blocked by pharmacological inhibition or genetic abla

197 peptide S-induced anxiolysis, as this effect was blocked by pharmacological and chemogenetic inhibiti

198 pendent on signaling via SMAD2 and SMAD3 and was blocked by pharmacological inhibitors.

199 tors, while metastasis of astrocytomas might be blocked by PKCe stimulators.

200 ertal development and that this increase can be blocked by pre-pubertal, but not post-pubertal, gonad

201 This increase in activity is blocked by pretreating the slices with the glial meta

202 Induction of pCREB signal by forskolin was blocked by pretreatment of cells with lactate.

203 URB694 self-administration was blocked by pretreatment with an antagonist for eithe

204 analgesic response in tail flick test which was blocked by pretreatment with norbinaltorphimine (nor

205 d to saline (-1 +/- 2mmHg; P < 0.001), which was blocked by pretreatment with the apelin receptor ant

206 Locomotor effects were blocked by pretreatment with the dopamine D1-like r

207 The inhibitory effects of iTregs are blocked by preventing direct cellular contact or by

208 ATR-Chk1 inhibitor-induced origin firing is blocked by prior exposure to DNA damaging agents show

209 ional recovery following MSC transplantation was blocked by PrP(C) downregulation.

210 ely 0.1 mum with stimulation at 50 Hz, 10 s) were blocked by removal of Ca(2+) from the extracellular

211 d KLF5 production and SMC de-differentiation were blocked by resveratrol via its inhibition of the Ak

212 To test this hypothesis, RhoA-ROCK signaling was blocked by RhoA deletion from postnatal neurons or t

213 This shift was blocked by ribavirin (RBV), an antiviral drug that r

214 The single neuron intrinsic oscillations were blocked by riluzole, and are thus dependent on pers

215 rate in vivo in VTA dopamine neurons, which was blocked by rolipram pretreatments.

216 was independent of IL-1beta stimulation and was blocked by SAHA, suggesting that SAHA inhibits IL-6

217 These effects were blocked by selective antagonists of alpha6-containi

218 also activated nitric oxide production that was blocked by sigma1-receptor knockdown or Akt inhibiti

219 enic endothelial tube formation, which could be blocked by silencing SP4.

220 In both cases, junctional disassembly can be blocked by simultaneous induction of myosin contracti

221 TNF-alpha-activated NF-kappaB pathway, which was blocked by SO2.

222 istin stimulated GH-release, a response that was blocked by somatostatin.

223 When IGF1R engagement with Sdc1 is blocked by SSTNIGF1R, ASK1 becomes activated, and ini

224 horylation and DNA binding of STAT3 and this was blocked by STAT3 inhibitors but not by rapamycin.

225 H2O2 production is blocked by stigmatellin, indicating its origin from c

226 oximately 90% of the initial outward current was blocked by substitution of Cl(-) ions or application

227 bly, IGF1R kinase activity in both fractions is blocked by synstatinIGF1R (SSTNIGF1R), a peptide that

228 demonstrated that viral spread of mut-Ad3GFP was blocked by synthetic HD5 whereas that of the wild-ty

229 , we demonstrate that MDM2-ALT1 splicing can be blocked by targeting SRSF1 sites on exon 11 using ant

230 hen a fraction of ryanodine receptors (RyRs) are blocked by tetracaine or ruthenium red, Ca sparks la

231 he frequency of Ca(2+) waves and this effect was blocked by tetracaine and ryanodine but not 2-aminoe

232 ne cells (DACs): (1) ipRGC signaling to DACs is blocked by tetrodotoxin both in vitro and in vivo, in

233 s of Scn8a(N1768D/+) CA1 hippocampal neurons were blocked by tetrodotoxin, riluzole, and SN-6, implic

234 ines TNF-alpha, IL-12, and IL-6; this effect was blocked by TGF-betaR1 inhibition (P < 0.0001).

235 elevated by epinephrine/norepinephrine that are blocked by the antioxidant N-acetyl cysteine and iro

236 cluster formation is redox sensitive and can be blocked by the antioxidant MitoQ.

237 ation in human melanoma cell lines which can be blocked by the CXCR4-selective antagonist AMD3100.

238 A-5) and that NKG2D ligand up-regulation can be blocked by the expression of viral dsRNA-binding prot

239 These neuroprotective effects could be blocked by the PI3-K/Akt inhibitor LY294002, indicati

240 bitory effect of rapamycin and FK506 but can be blocked by the presence of mycophenolate mofetil.

241 induced by alkalinization of the skin could be blocked by the protease-activated receptor 2 antagoni

242 ges; structures of E,E,E-3a show rotation to be blocked by the shorter P(CH2)4CH horizontal lineCH(CH

243 in IgE binding and that the interaction can be blocked by the therapeutic anti-IgE antibody omalizum

244 erein each window of the molecular container is blocked by the bridges of adjacent containers, effect

245 n into membrane vesicles of Escherichia coli is blocked by the compound N,N'-dicyclohexylcarbodiimide

246 channel of the proteasome core particle (CP) is blocked by the convergent N termini of alpha-subunits

247 strated that the resolution of lung fibrosis is blocked by the failure of adenosine levels to subside

248 ffer in comparison with HEPES, and that this is blocked by the specific TMEM16A inhibitor T16inh-A01.

249 osterone-stimulated MR nuclear translocation was blocked by the 11beta-HSD2 inhibitor carbenoxolone.

250 ribosomes in LA dendrites when consolidation was blocked by the cap-dependent initiation inhibitor 4E

251 Memory impairment during nicotine withdrawal was blocked by the CB1R antagonist rimonabant or the gen

252 5212-mediated inhibition in CFA-treated rats was blocked by the CB2 receptor-selective antagonist SR1

253 The effect of Na2S was blocked by the CFTR inhibitor CFTR_inh172, the adeny

254 n MRL/Fas(lpr/lpr) and C57/Sle1Sle2Sle2 mice was blocked by the CID 1067700 compound, which specifica

255 diated methylation inhibited CS activity and was blocked by the CS substrate oxaloacetate.

256 inducible gene I-like receptor (RLR) pathway was blocked by the CV-A16, CV-A6, and EV-D68 3C(pro) pro

257 CB1 activation is mediated by 2-AG since it was blocked by the diacylglycerol lipase inhibitor DO34.

258 o the dorsal striatum, and the latter effect was blocked by the dopamine D2-like receptor antagonist

259 er social isolation or acute physical stress was blocked by the glucocorticoid synthesis inhibitor, m

260 r pre-incubation with histamine; this effect was blocked by the HRH1 antagonist pyrilamine.

261 of depolarization-induced calcium transients was blocked by the IP3 antagonist, and not observed in t

262 especially the atypical PKCzeta level which was blocked by the knockdown of Galphaq and Galpha12.

263 y an accelerating decline rate of BACE1, and was blocked by the lysosomal inhibitor chloroquine, rath

264 cue- but not stress-induced alcohol seeking was blocked by the mGluR2 positive allosteric modulator.

265 ted by K(+) inward rectifier (Kir)2.1, which was blocked by the NMDA receptor antagonist D-AP5.

266 Moreover, when TRIM5 activity was blocked by the nonimmunosuppressive analog of cyclos

267 ast, a third, slower component of exocytosis was blocked by the peptide, as was the functional replen

268 oxLDL-induced ROS generation was blocked by the reduced NAD phosphate oxidase 2 (NOX2

269 This effect was blocked by the selective Hcrt-1/Ox-A antagonist SB33

270 alpha-MG induced secretion, and the response was blocked by the SGLT1 inhibitor phlorizin or by repla

271 odilation after fluvoxamine treatment, which was blocked by the sigma1-receptor antagonist or various

272 t on extracellular regulated kinase (ERK1/2) was blocked by the Src family kinase inhibitor PP2, indi

273 inhibitory effect of SNAP on N-type currents was blocked by the sulfhydryl-specific modifying reagent

274 Gene expression was blocked by the TGF-beta receptor I kinase inhibitor

275 that was absent in TRPV1 knock-out mice, and was blocked by the TRPV1 antagonist AMG9810.

276 imulation by luminal glucose (20%) secretion was blocked by the voltage-gated Ca channel inhibitor, n

277 This effect was blocked by the Y1 receptor antagonist BIBO3304 trifl

278 infection was established, but virus spread was blocked, by the anti-CD81 mAb.

279 , and phosphorylation of Akt in ASMCs, which were blocked by the calpain inhibitor MDL28170.

280 and proinflammatory cytokine mRNA expression were blocked by the Cx43 blockers Gap26 and carbenoxolon

281 unc18-1 and syntaxin-1A diffusional switches were blocked by the expression of Munc18-1(Delta317-333)

282 both cue- and stress-induced alcohol seeking were blocked by the GABAB receptor positive allosteric m

283 leukemia (CLL) cells and that these effects were blocked by the humanized anti-ROR1 mAb cirmtuzumab

284 During 6-s pacing cycle length, EADs were blocked by the Ito blocker 4-aminopyridine, but rea

285 intestinal barrier dysfunction and VH, which were blocked by the LPS antagonist LPS-RS or by TLR4 kno

286 Abnormalities were blocked by the mTORC1 inhibitor sirolimus.

287 These effects were blocked by the nicotinic acetylcholine receptor (nA

288 e-induced changes in DAT conformation, which were blocked by the specific sigma1R antagonist CM304.

289 es, membrane stretch-induced cation currents were blocked by the TRPM4 inhibitor 9-phenanthrol in bot

290 urthermore, SRWe-stimulated IL-33 production was blocked by TLR4 antibody and NF-kB inhibitor in mous

291 and inflammatory cytokine expression, which were blocked by TLR4 inhibitor, TAK242, and by TLR4 abla

292 activity of L lactis G121-treated human DCs was blocked by TLR8-specific inhibitors, mediated by L l

293 PI3K/Akt phosphorylation, and tube formation was blocked by treating HUVECs with an Akt inhibitor.

294 The effects of islet-derived IP-10 could be blocked by treatment of donor islets and recipient mi

295 Low-glucose induction of miR-708 was blocked by treatment with the chemical chaperone 4-p

296 nd mouse embryonic fibroblasts, effects that were blocked by treatment with IGF1 receptor inhibitor.

297 These effects were blocked by treatment with Na2S or by overexpression

298 e insulin exposure (or GSK-3beta inhibition) is blocked by tumor-promoting isoforms of APC that reduc

299 Crosslinking was blocked by U18666A derivatives that block cholestero

300 2+) levels in response to nitrate treatments were blocked by U73122, a pharmacological inhibitor of p