ライフサイエンスコーパス: be blocked by

1 responses in astrocytes of the rat brainstem were blocked by (1) antagonists of connexin channels, co

2 When autophagy was blocked by 3-methyladenine (3MA) or by Atg5 siRNA, I

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

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

5 pressing gB(275D) proceeded slowly and could be blocked by a macropinocytosis inhibitor, entry of wil

6 aversions, while the anorexia it causes can be blocked by a monoclonal antibody directed at GFRAL or

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

8 The effects on CD4+ T cell anergy could be blocked by a PLA2G1B-specific neutralizing mAb in vit

9 matin structure and that these effects could be blocked by a small molecule predicted to reverse the

10 ve and reparative response in OPCs, but this is blocked by a local cellular niche where reactive astr

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

12 This increase is blocked by a nicotinic ACh receptor (nAChR) antagonis

13 ound that HCMV infection of epithelial cells is blocked by a synthetic OR14I1 peptide and inhibitors

14 ent effect, as well as CREB phosphorylation, was blocked by a construct derived from the PRG:Galpha(s

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

16 line (BV2) treated with DHA, and the effect was blocked by a miR-124 inhibitor.

17 e marrow progenitors; however, this increase was blocked by a neutralizing antibody to integrin alpha

18 ion and concurrent NF-kappaB activity, which was blocked by a pan PKC inhibitor (Go6983) or an inhibi

19 Redistribution was blocked by a peptidase-resistant version of ZIP and

20 Microglial repair of leaky blood vessels was blocked by a peptide that inhibits the interaction b

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

22 induced redistribution of TJ proteins, which was blocked by a Rho-kinase inhibitor.

23 and pharmacologic stimulation of beta-cells were blocked by a 5-HT(3)R antagonist and were enhanced

24 on-facilitating effects of Ppid upregulation were blocked by a GR antagonist.

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

26 ions of P-gp but not BCRP transport activity were blocked by a peroxisome proliferator-activated rece

27 CXCL7, and IL-33 by mouse platelets were all were blocked by a selective CysLT(2)R antagonist and inh

28 e FO- and anethole-induced calcium responses were blocked by a selective TRPA1 channel antagonist, HC

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

30 The effects of both Slit2 fragments were blocked by Abs to the Slit2 receptor Roundabout hom

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

32 deubiquitinase whose lysosomal localization is blocked by active Rag heterodimer in response to amin

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

34 activity caused by HSV-1 infection could not be blocked by ACV treatment.

35 myocytes resulted in cell hypertrophy, which was blocked by addition of monensin, an inhibitor of end

36 n vitro induced apoptosis of macrophages and was blocked by administration of cell-permeable glutathi

37 ated potassium conductance, G(BK) , that can be blocked by agents that disrupt calcium influx or buff

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

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

40 ted by ALX in 1/32 sera, and binding to PHMB was blocked by ALX (1/5) and by OCT in another (1/5).

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

42 In all cases, cell death was blocked by AMD3100, a CXCR4 entry inhibitor, but not

43 e p53-mediated repression of DNMT3A activity is blocked by amino acid substitutions within this inter

44 However, the lethal function of T can be blocked by an antiholin (RI) during lysis inhibition

45 with accelerated tumor progression that can be blocked by an arginase inhibitor.

46 tivates hPXR in HepG2 cells, with activation being blocked by an hPXR-specific antagonist, SPA70; 3)

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

48 culum (ER) accumulation and, accordingly, it was blocked by an inhibition of translation.

49 s effect, along with the effect on encoding, was blocked by an inhibitor of the Ca(2+)-dependent enzy

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

51 e behavior, and these antidepressant effects were blocked by an AMPA receptor antagonist.

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

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

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

55 ease of endogenous 5-HT, and these responses were blocked by antagonists of 5-HT(7) receptors.

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

57 infected BSCs to activate primary astrocytes was blocked by anti-IFN-beta antibodies.

58 The proangiogenic activity of the CgA(1-373) was blocked by anti-neuropilin-1 antibodies as well as b

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

60 This transmission cycle can be blocked by antibodies targeting proteins exposed on t

61 erves as an exemplar, whereby CTLA4 activity is blocked by antibodies in cancer immunotherapy and aug

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

63 Viral replication can be blocked by antiretroviral therapy.

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

65 These ALD-induced changes were blocked by applying the mineralocorticoid receptor

66 Responses were blocked by atropine or DAU 5884, but not AF-DX 116.

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

68 l but variable fraction of reservoir viruses is blocked by autologous contemporaneous immunoglobulin

69 This process is blocked by bafilomycin A1 that binds and inhibits the

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

71 These effects of leptin were blocked by bath applying a competitive NMDAR antago

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

73 JNK activator (anisomycin)-induced autophagy was blocked by Beclin1 knockdown in OCPs.

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

75 ain of pro-apoptotic Bcl-2 proteins, and can be blocked by BH3 mimetic Bcl-2 inhibitors.

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

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

78 This effect is blocked by both alpha-bungarotoxin and apamin, indica

79 1A, contributed to tumor cell migration that was blocked by C-DIM/NR4A1 antagonists.

80 ulated increase in [Ca(2+)](i) and secretion was blocked by Ca(2+) chelator 1,2-bis(2-aminophenoxy)et

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

82 emble into a functional calcium channel that is blocked by calmodulin in the resting state.

83 inal fragment of EMCN by TNF-alpha treatment was blocked by chemical inhibition of ADAM10 alone or in

84 effects of intra-mPFC infusion of 8-OH-DPAT are blocked by co-infusion of an AMPA receptor antagonis

85 ion reduced cue-induced reinstatement, which was blocked by co-infusion of the CaN inhibitor, FK-506.

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

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

88 e effects of WAY163909 on all these measures were blocked by co-administration with a 5-HT(2C)R antag

89 The effects of retigabine were blocked by co-incubation with XE-991, suggesting sp

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

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

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

93 we analyzed IHCs in which Galphai signaling was blocked by Cre-induced expression of the pertussis t

94 y invasive and metastatic behavior which can be blocked by CRISPR/Cas9-mediated MALT1 knockout.

95 This recruitment was blocked by CXCL14 neutralizing antibody and converse

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

97 6 cells caused naive cells to migrate, which was blocked by depleting CXCL1 and IL-8 from the conditi

98 nd reward-associated behaviors were shown to be blocked by direct antagonism of GHSR(1a).

99 cose and the selective P2Y(11) agonist NF546 is blocked by disruption of A-kinase anchoring protein 5

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

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

102 Macropinocytosis was blocked by dominant-negative vacuolar protein sortin

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

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

105 trabeculae of patients with SDB, which could be blocked by either AIP or KN93 (N-[2-[[[(E)-3-(4-chlor

106 ascent PRPH2 into the cone outer segment can be blocked by either cone dystrophy-causing C-terminal m

107 ependent killing using the modified Ham test is blocked by either C5 or factor D inhibition.

108 These effects are blocked by exogenous NRG1 as well as PV targeted rec

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

110 orhabditis elegans ACD-1 Na(+) leak channels are blocked by extracellular protons.

111 tifier potassium current in the human heart, are blocked by fentanyl with a 3-fold greater potency th

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

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

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

115 This action of FGF23 is blocked by genetic ablation of MFS2.

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

117 Beneficial effects of NaHS were blocked by Glib.

118 that the antidepressant actions of ketamine were blocked by GluN2B-NMDAR knockdown on GABA (Gad1) in

119 al. report that infection by Vibrio cholerae is blocked by gut microbiome-mediated hydrolysis of bile

120 This interaction is blocked by heparin, a sulfated glycosaminoglycan.

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

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

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

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

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

126 Glutamate secretion could be blocked by inhibiting either glutaminase or KV1.3 cha

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

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

129 d stress-impaired synaptic plasticity, which was blocked by inhibiting neural lactate uptake.

130 C-JUN as a downstream target of WNT5B, which was blocked by inhibiting RAC1, a prominent regulator of

131 The increase of angiogenin can be blocked by inhibition of HIF-1 signaling via echinomy

132 , epithelial cells enter S phase but mitosis is blocked by inhibition of mitotic gene expression.

133 ent on significant correction of F508del and was blocked by inhibition of corrected channel function,

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

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

136 n macrophages in vitro and that this process was blocked by inhibition of the dynamin-dependent endoc

137 caused sustained [Ca(2+)](i) elevation that was blocked by inhibition of TRPV4 channel opening.

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

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

140 netic alterations and that these effects can be blocked by inhibitors of DNA methylation.

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

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

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

144 ersisted even when DNA synthesis and mitosis were blocked by inhibitors.

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

146 T1B-deficient CD4+ T cells to Rag1(-/-) mice was blocked by injection of an antibody against integrin

147 In subgroups, leukocyte homing was blocked by integrin antibodies (n = 5).

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

149 ent to produce extinction deficits, and this is blocked by intra-BLA propranolol.

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

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

152 from the Bcl-2-Beclin1 complex, which could be blocked by JNK1 inhibition.

153 cess retraction and membrane ruffling, which were blocked by joint application of P2Y1 and P2Y13 rece

154 F-kappaB subunit p50 translocation to nuclei was blocked by KPNB1 inhibition, which led to an increas

155 GC Tfh and GC B cell development were blocked by loss of SAP in K/BxN mice.

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

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

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

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

160 Increased expression of SARS-CoV-2 receptors was blocked by mitoTEMPO, a mitochondrial superoxide sca

161 MitoROS and ATF4-CHOP were blocked by MitoTEMPO, a mitochondrial antioxidant,

162 ic uptake in CXCR4-expressing cells that can be blocked by more than 90% using a higher-affinity anta

163 ility, and optogenetically-driven immobility is blocked by morphine.

164 organogenesis stages, and that this increase is blocked by morpholino-directed depletion of 12-LOX.

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

166 qE and gene expression phenotypes of spa1-1 are blocked by mutation of CrCO, a B-box Zn-finger trans

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

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

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

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

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

172 osphorylation and ZIP-induced redistribution was blocked by nitrosyl-mutant GluA1-C875S or serine-mut

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

174 VID-19 plasma triggered NET formation, which was blocked by nNIF.

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

176 Second, the heat increase is blocked by nocodazole, which inhibits DNA replication

177 unable to complete translation because they are blocked by non-recycled ribosomes at stop codons.

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

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

180 express UDP-specific P2Y6 receptors that can be blocked by off-target effects of CysLT1R antagonists.

181 This effect was blocked by ouabain.

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

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

184 nd p-Akt2-S474), but these changes could not be blocked by overexpression of Cdc42-T17N.

185 ICWs were blocked by P2Y1 antagonists or CRISPR-Cas9 knockout

186 induced microglial process extension, which was blocked by P2Y12 receptor antagonists.

187 Both events are blocked by pan-caspase inhibition, indicating that K

188 s analysis show that EXO1-mediated resection is blocked by PARP-1.

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

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

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

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

193 Store-operated whole-cell cation currents were blocked by Pico145, a highly selective and potent T

194 sustained elevation in tonic current, which was blocked by PKA and PKC inhibition.

195 store-operated PIP(2) and TRPC1 interactions were blocked by PKCdelta inhibition, and PKCdelta was re

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

197 ng of QX-RBD to trachea and kidney could not be blocked by preincubation with synthetic alpha-2,3-lin

198 dition of PrCYP79D73-enriched microsomes but was blocked by pretreatment with 4-phenylimidazole, an i

199 neuron population activity, and this effect was blocked by pretreatment with an mGluR2/3 antagonist.

200 nsistently inhibited mTORC1 signaling, which was blocked by pretreatment with ferrous sulfate.

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

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

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

204 so found that the pH response of RTN neurons was blocked by preventing 5-HT synthesis and enhanced by

205 we also show that the GPR56-TG2 interaction was blocked by previously-reported synthetic proteins, t

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

207 g with glycocalyx shedding (from 6 h), which were blocked by probenecid.

208 With analogy to how neuronal channels are blocked by protein toxins, a uniporter interaction d

209 to hemin in vitro and that this interaction is blocked by PyoG, confirming the role of Hur in hemin

210 Slit2-S-induced chemorepulsion was blocked by Ras and Rac inhibitors, not affected by P

211 neous binding of IgE to FcepsilonRI and CD23 is blocked by reciprocal allosteric inhibition, suggesti

212 rapid (but not slow) depletion of ER stores was blocked by removing external Na(+) and in mutants of

213 ex of gonadal or neural crest cells, and may be blocked by repressive guidance signals elevated in th

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

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

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

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

218 This interaction is blocked by securin, providing a second mechanism by w

219 timulated cAMP increases and these increases were blocked by selective antagonists of both adenosine

220 rrently, it is still unclear how HIV-1 entry is blocked by SERINC5.

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

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

223 This normalization was blocked by simultaneous inactivation of area 25, but

224 wever, this aHipp-mediated anxiolytic effect was blocked by simultaneous pharmacological inactivation

225 tracellular Ca2+ and IL-17 expression, which was blocked by SOCE inhibitors 2APB, YM58483/BTP2, or An

226 lls from AKI patients increased IL-17, which was blocked by SOCE inhibitors.

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

228 dent and agonist-selective manner that could be blocked by specific antagonists.

229 ivity for potassium over sodium; ion passage is blocked by specific chemical modification at the pore

230 The anti-inflammatory effects of alpha-MSH were blocked by specific p-CREB inhibition.

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

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

233 es in nonpolar solvents, where oxygen attack is blocked by strong ion pairing.

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

235 overall cardiac and aortic VEGFA that could be blocked by systemic chloroquine treatment.

236 phosphorylation and endolysosomal maturation were blocked by TAK1 inhibition.

237 ion was induced by estradiol, an effect that was blocked by tamoxifen and not observed in ERalpha-neg

238 ivation of the IL-6/IL-6Ralpha/STAT3 pathway was blocked by TCZ in human and baboon cells but not in

239 leum induced nNOS S1412 phosphorylation that was blocked by tetrodotoxin and by inhibitors of the pro

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

241 3-dependent stores and primary ADP secretion are blocked by the NAADP receptor antagonist Ned-19, and

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

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

244 d by the Arf-like small GTPase Arl8b and can be blocked by the Rab7 GTPase competitive inhibitor CID1

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

246 Interestingly, the reduction of PCSK9 can be blocked by the treatment of berberine, a natural chol

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

248 that glucocorticoid-induced DPP4 expression is blocked by the GR antagonist RU-486 and by GR siRNA t

249 ponent of the heat flow towards an ice shelf is blocked by the marked step shape of the ice front, an

250 Extinction with social support is blocked by the protein synthesis inhibitors anisomyci

251 hyA mutant, in which dTDP-glucose production is blocked by the rfbA rffH mutations, lacks a LMW-dT po

252 t growth induced by IGF-1R and ErbB3 ligands is blocked by the tetravalent bispecific antibody target

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

254 lcium activation was observed at EW16, which was blocked by the addition of 1 mumol/L tetrodotoxin.

255 with fluorescently labeled LF(E687A) Uptake was blocked by the broad-spectrum MMP inhibitor GM6001.

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

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

258 5212-mediated inhibition in CFA-treated rats was blocked by the CB2 receptor-selective antagonist SR1

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

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

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

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

263 to the PKA inhibitors (H-89, KT270) but that was blocked by the Epac inhibitor ESI 05.

264 Moreover, NF-kB/AP-1 activity was blocked by the inhibition of nSMase2.

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

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

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

268 This effect was blocked by the PPARgamma antagonist GW9662.

269 shedding and increased AbetaO binding, which was blocked by the PrP(C)-specific antibody 6D11.

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 This effect was blocked by the Y1 receptor antagonist BIBO3304 trifl

274 "N neurons," whose NaCl responses were blocked by the amiloride analog benzamil, responded

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

276 ists suramin (150 mum) or PPADS (50 mum) but were blocked by the connexin channel blockers octanol (1

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

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

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

280 Abnormalities were blocked by the mTORC1 inhibitor sirolimus.

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

282 All BRET signals were blocked by the selective D2R antagonist haloperidol

283 These changes were blocked by the selective P2Y(11) inhibitor NF340.

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

285 All changes to ERK1/2 pathway intermediates were blocked by the TAAR1 antagonist, N-(3-ethoxyphenyl)

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

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

288 ally responsive neurons in the central brain was blocked by transient dFB activation, confirming an a

289 In resting cells, RIP of CREB3L1 is blocked by transmembrane 4 L6 family member 20 (TM4SF

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

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

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

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

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

295 of ICP elevation on outflow facility and IOP is blocked by TTX.

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

297 oduced enhanced levels of TGF-betaRII, which was blocked by U0126.

298 r hours, was quenched by 11-cis-retinal, and was blocked by uncoupling opsin from phototransduction,

299 al urine medium, while the control catheters are blocked by UPEC biofilms within 5 days.

300 ransformed growth of KPI, but not KP, tumors is blocked by Wnt pathway inhibition in vitro and in viv