ライフサイエンスコーパス: pertussis toxin

1 ade that was sensitive to ERK inhibitors and pertussis toxin.

2 activity was elevated expressed very little pertussis toxin.

3 cued by blocking G(i/o)alpha activation with pertussis toxin.

4 vented by inactivation of G(i/o) proteins by pertussis toxin.

5 by GPCRs, since the effects were blocked by pertussis toxin.

6 Ab treatment in combination with exposure to pertussis toxin.

7 urons, was abolished after pretreatment with pertussis toxin.

8 ist-induced reduction in BRET was blocked by pertussis toxin.

9 with the G inhibitory (Gi) pathway inhibitor pertussis toxin.

10 nist CP 105,696, and the G alpha i inhibitor pertussis toxin.

11 drocyte glycoprotein (MOG)-35-55 peptide/CFA/pertussis toxin.

12 effect that is blocked by preincubation with pertussis toxin.

13 by dopamine D2/D4 receptor antagonists or by pertussis toxin.

14 rating pulmonary tumors by pretreatment with pertussis toxin.

15 pon inhibition of Gi-mediated signaling with pertussis toxin.

16 r Syk(-/-) bone-marrow chimeras treated with pertussis toxin.

17 alpha-protein-coupled receptor activity with pertussis toxin.

18 h a BBB rendered permeable by treatment with pertussis toxin.

19 f sIPSCs in rats pretreated with intrathecal pertussis toxin.

20 sing hACVI even when G(i) was inactivated by pertussis toxin.

21 oxidative burst, were likewise prevented by pertussis toxin.

22 logical effects of MND could be abrogated by pertussis toxin.

23 nd CCL25 in the presence of the Gi inhibitor pertussis toxin.

24 lar signal-regulated kinases (ERK) 1/2 or by pertussis toxin.

25 GPR-Galpha(i1) BRET by Ric-8A was blocked by pertussis toxin.

26 fect is abrogated in a mouse model requiring pertussis toxin.

27 and this activity was partially inhibited by pertussis toxin.

28 Pretreatment with pertussis toxin (100 ng/ml, 4 h) or transfection of c-Ju

29 and follow-up levels for immunoglobulin G to pertussis toxin (21.48 [95% confidence interval, 12.51-3

30 with Boc2 (a specific peptide antagonist) or pertussis toxin (a G(i)-protein inhibitor) abolished com

31 lay has heretofore been masked by the use of pertussis toxin, a broad inhibitor of the G alpha(i/o) p

32 r of these effects nor did pretreatment with pertussis toxin, a G(i/o) protein inhibitor, suggesting

33 generated mice expressing the S1 subunit of pertussis toxin, a known inhibitor of G(i/o) signaling,

34 ype 1 secretion system (T1SS) substrate, and pertussis toxin, a type IV secretion system (T4SS) subst

35 Consistent with this result, pertussis toxin abrogated IBOP-induced dephosphorylation

36 We found that following EAE induction, pertussis toxin administration leads to IL-1 receptor ty

37 ntrast, inhibition of Galphai signaling with pertussis toxin affects speed but not the intermittent m

38 The fold increase in antibodies to pertussis toxin after original vaccination 10 years ago

39 tial for the host to overcome the effects of pertussis toxin, allowing both control of B. pertussis n

40 Pretreatment with pertussis toxin also reduced the EPI-mediated inhibition

41 modulation of OPC migration was abolished by pertussis toxin, although baseline migration was normal.

42 When treated with pertussis toxin, an inhibitor of G protein-coupled recep

43 Pertussis toxin, an inhibitor of G proteins, attenuated

44 Moreover, pretreatment of slices with pertussis toxin, an inhibitor of G(i/o)-proteins, did no

45 Treatment of fibroblasts with pertussis toxin, an inhibitor of Galphai-coupled recepto

46 n this process through findings showing that pertussis toxin, an inhibitor of Gi-coupled S1P receptor

47 Experiments with pertussis toxin, an RGS domain-deficient mutant of RGS7,

48 was also observed in neurons pretreated with pertussis toxin, an uncoupler of G proteins and MOR.

49 cs, and this reversal effect is inhibited by pertussis toxin and by genetic deletion of alpha-gustduc

50 Each of these responses was abolished by pertussis toxin and by knock-down of the expression of e

51 tion and cell migration were blocked both by pertussis toxin and by the mitogen-activated protein kin

52 AACOCF(3); 10 microm), inhibition of G(i) by pertussis toxin and chelation of intracellular Ca(2+) by

53 e agonist-mediated effects were inhibited by pertussis toxin and co-expression of RGS4, but were not

54 ytoskeletal rearrangement as demonstrated by Pertussis toxin and cytochalasin D inhibition.

55 Experiments with pertussis toxin and dominant-negative Galpha(i/o) protei

56 In these cells, treatment with pertussis toxin and expression of a Galpha(q/11)-(305-35

57 )]i, and this inhibition can be prevented by pertussis toxin and G-protein betagamma subunit inhibito

58 e enhancement of cAMP by S1P is resistant to pertussis toxin and independent of intracellular calcium

59 We also found that the addition of pertussis toxin and killed Mycobacterium tuberculosis to

60 Pertussis toxin and LY294002 inhibition demonstrated tha

61 Accordingly, the Galphai inhibitor pertussis toxin and MEK inhibitor U0126 blocked C5a inhi

62 erases (ADPRTs) such as Bordetella pertussis pertussis toxin and Mycoplasma pneumoniae community-acqu

63 ns, and Ca(2+) mobilization was inhibited by pertussis toxin and N-t-butoxycarbonyl-Phe-Leu-Phe-Leu-P

64 by G(i)/G(o)-proteins, and was attenuated by pertussis toxin and NF023, inconsistent with mediation b

65 propose that it is the systemic activity of pertussis toxin and not pulmonary pathology that promote

66 olar lymphoid sheath (PALS) was inhibited by pertussis toxin and required the presence of CD11c(+) ce

67 t activation and motility were suppressed by pertussis toxin and S1P1 antagonists.

68 -1 and the IGF-2 responses were sensitive to pertussis toxin and the sphingosine kinase inhibitor, di

69 However, Cav2.3 inhibition was sensitive to pertussis toxin and to intracellular application of guan

70 apparent relationship between the effects of pertussis toxin and tumor necrosis factor (TNF)- alpha.

71 Furthermore, inhibition by both pertussis toxin and U-73122 established signaling via th

72 Inhibitors pertussis toxin and Y27632 reversed the inhibition of ne

73 R-Gbetagamma interface, 3) were sensitive to pertussis toxin, and 4) were predictive of whether a lig

74 CB1R antagonist rimonabant and Gi uncoupler pertussis toxin, and absent in Cnr1(-/-) RGCs.

75 lpha observed in HEK cells, was sensitive to pertussis toxin, and involved the activation of mTOR sig

76 treatment with the G(i)(o)-protein inhibitor pertussis toxin, and pretreatment with lithium to deplet

77 tope for different antibodies targeting TNF, pertussis toxin, and the cancer target TROP2.

78 id not require CXCR1/2, was not inhibited by pertussis toxin, and was FcgammaRIIIb rather than Fcgamm

79 agnosis is confirmed by measuring serum anti-pertussis toxin (anti-PT) or anti-filamentous hemaggluti

80 ved Tdap during pregnancy vs postpartum (eg, pertussis toxin antibodies: 51.0 EU/mL [95% CI, 37.1-70.

81 Levels of antibody to pertussis toxin, antibody to filamentous hemagglutinin,

82 However, the increase was inhibited by pertussis toxin as well as by wortmannin but not by AG14

83 d by treating the vagal ganglia neurons with pertussis toxin, as well as phosphatidylinositol 3-kinas

84 d by treating the vagal ganglia neurons with pertussis toxin, as well as phosphatidylinositol 3-kinas

85 This reduction was fully corrected by pertussis toxin, atropine (a nonselective muscarinic ant

86 AR1 inhibited adenylyl cyclase activity, and pertussis toxin blocked PAR1 effects on both adenylyl cy

87 eta-methyl cyclodextrin or G alpha inhibitor pertussis toxin blocked resveratrol- and E(2)-induced eN

88 th similar kinetics; however, treatment with pertussis toxin blocked the migration of dermal DC and t

89 time points of inflammation was sensitive to pertussis toxin but was only partially affected by the d

90 ffects were insensitive to cholera toxin and pertussis toxin but were abolished by phorbol 12-myrista

91 Responses were insensitive to pertussis toxin, but increases in intracellular calcium

92 to S1P(1) small interfering RNA (siRNA) and pertussis toxin, demonstrating coupling of S1P(1) to G(i

93 nist-induced rosette formation is blocked by pertussis toxin, dependent on PI3K activity and accompan

94 Treatment of the cells with pertussis toxin did not alter the increase in affinity o

95 gly, an isogenic B. pertussis strain lacking pertussis toxin did not induce these effects in TNF- alp

96 obulin (Ig) G specific for diphtheria toxin, pertussis toxin, filamentous hemagglutinin and pertactin

97 at in primary cardiomyocytes (rat and human) pertussis toxin (Gi-coupled receptor inhibitor) substant

98 eceptor antagonists CV-3988 and WEB-2086 and pertussis toxin have no impact on PAF- or lysoPAF-mediat

99 s were tested for pertussis (oral fluid anti-pertussis toxin IgG) and randomly assigned (1:1) to mont

100 This signaling was blocked by pertussis toxin, implicating a Galphai-triggered signal

101 intracellular Ca(2+) and was insensitive to pertussis toxin, implicating opioid receptors that may c

102 Although the role of pertussis toxin in whooping cough is well-established, p

103 1 alpha), which can be completely blocked by pertussis toxin, indicating coupling to G(i/o).

104 ect was abolished in cells preincubated with pertussis toxin, indicating coupling to heterotrimeric G

105 ect of MQC was reversed by pretreatment with pertussis toxin, indicating that FFA3 acts via the Gi/o

106 ors blocked the chemotactic response, as did pertussis toxin, indicating that the response was mediat

107 cts were attenuated by both AEC wounding and pertussis toxin, indicating the involvement of a G(0)/G(

108 WF and/or Weibel-Palade bodies in Bordetella pertussis toxin-induced hypersensitivity to histamine, a

109 Pertussis toxin inhibited both Lm entry into the PALS an

110 of crawling but not directed motion, whereas pertussis toxin inhibited directed motion but not speed.

111 Rescue of pertussis toxin-inhibited activation of Gli by Sonic hed

112 Notably, dopamine stimulation or pertussis toxin inhibition of D2 receptor signaling did

113 because disruption of coupling to G(i) with pertussis toxin inhibits the activation of Gli by Sonic

114 coupled receptors, the effects of AAL-R were pertussis toxin insensitive in our model.

115 This signaling was pertussis toxin insensitive, suggesting that endothelial

116 The tethered Galphai2 was rendered pertussis toxin-insensitive by a C352I mutation, and rec

117 ) (and p66Shc-Ser(36) phosphorylation) via a pertussis toxin-insensitive epidermal growth factor rece

118 dering the interaction of this receptor with pertussis toxin-insensitive G proteins that transduce si

119 ouples to both pertussis toxin-sensitive and pertussis toxin-insensitive G proteins to activate leuko

120 G protein-coupled receptor (GPCR) coupled to pertussis toxin-insensitive G(q/11).

121 Reconstitution experiments with pertussis toxin-insensitive G-proteins revealed loss of

122 Endocytosis was inhibited by NA in a pertussis toxin-insensitive manner.

123 ease from thapsigargin-sensitive stores by a pertussis toxin-insensitive mechanism.

124 The pertussis toxin-insensitive uptake of chemokine by the r

125 The actions of the inactivating drugs were pertussis toxin-insensitive, indicating the lack of G(i)

126 This inhibition is slowly established, pertussis toxin-insensitive, partially reversed within t

127 ion, the sensitivity of TLQP-21 signaling to pertussis toxin is consistent with the known signaling p

128 d understanding of the glycans recognized by pertussis toxin is essential to understanding which cell

129 Just as pertussis toxin is used extensively to probe and inhibit

130 ts of mothers immunized during pregnancy had pertussis toxin levels estimated to be higher than the l

131 upled cannabinoid receptors, because neither pertussis toxin nor GDPbetaS treatments altered the WIN

132 f transgenic animals with the Gi/o inhibitor pertussis toxin normalized the phospholamban phosphoryla

133 s inhibited by pretreatment of the mice with pertussis toxin or a Rho kinase inhibitor.

134 bitors of cAMP/PKA signaling, insensitive to pertussis toxin or beta-arrestin knock-out, and mimicked

135 Treatment of cells with pertussis toxin or expression of dominant-negative Galph

136 ylcholine, after G-protein inactivation with pertussis toxin or in myocytes from M2- or M1/3-muscarin

137 Treatment with pertussis toxin or knock down of Galpha(q) or Galpha(o)

138 otein was prevented by the pretreatment with pertussis toxin or the opioid antagonist naloxone.

139 9 protein was prevented by pretreatment with pertussis toxin or the opioid antagonist naloxone.

140 ected by Clostridium botulinum C3 exoenzyme, pertussis toxin, or cholera toxin.

141 red with those without the polymorphism (for pertussis toxin, P = .028; for filamentous hemagglutinin

142 p115RhoGEFRGS-GFP (an RGS for G(12/13)) nor pertussis toxin pretreatment (inactivating G(i/o)), atte

143 Pertussis toxin pretreatment completely abolished the ab

144 the GA, and the translocation was blocked by pertussis toxin pretreatment or by the phospholipase Cbe

145 Pertussis toxin pretreatment reduced the amount of GRIN1

146 age of transferred eosinophils, sensitive to pertussis toxin pretreatment, peaked at approximately 24

147 RHGEF1, and DOCK2 is completely inhibited by pertussis toxin pretreatment, thus suggesting different

148 ane of these neurons, which was inhibited by pertussis toxin pretreatment.

149 d vascular leak, and systemic treatment with pertussis toxin prevented rescue by Par2 agonist and sen

150 th blood CD4 T cells; neither anti-CD62L nor pertussis toxin prevents entry of naive CD4 T cells into

151 Pretreatment of myocytes with pertussis toxin prevents the internalization of VDCCs, s

152 Incubation of monocytes with pertussis toxin prior to use in flow experiments signifi

153 In contrast, pertussis toxin produces strong blockade, indicating inv

154 Pertussis toxin proved to be a useful tool in these stud

155 IV transporter responsible for secretion of pertussis toxin (PT) across the outer membrane of Bordet

156 B. pertussis uses pertussis toxin (PT) and adenylate cyclase toxin (ACT) t

157 pertussis releases several toxins, including pertussis toxin (PT) and adenylate cyclase toxin (ACT),

158 MCs) of cord blood antibodies to recombinant pertussis toxin (PT) and filamentous hemagglutinin (FHA)

159 We tested sera from 14 patients for anti-pertussis toxin (PT) antibodies and used species-specifi

160 The five subunits of pertussis toxin (PT) have a combined molecular weight of

161 by polymerase chain reaction (PCR) and anti-pertussis toxin (PT) immunoglobulin G, respectively.

162 ssis, the causative agent of whooping cough, pertussis toxin (PT) is a key virulence factor that prom

163 Pertussis toxin (PT) is an important virulence factor pr

164 sis is characterized, and a central role for pertussis toxin (PT) is described.

165 Pertussis toxin (PT) is secreted from Bordetella pertuss

166 Pertussis toxin (PT) moves from the host cell surface to

167 dritic cell-activating adjuvants [Bordetella pertussis toxin (PT) or CpG ODN or a squalene-based oil-

168 Pertussis toxin (PT) plays a major role in the virulence

169 een used to measure the molecular weights of pertussis toxin (PT) subunits.

170 Pertussis toxin (PT), a secreted virulence factor of Bor

171 We previously studied the role of pertussis toxin (PT), an important Bordetella pertussis

172 Antibody responses to pertussis toxin (PT), filamentous hemagglutinin (FHA), f

173 Immunoglobulin G (IgG) antibodies against pertussis toxin (PT), filamentous hemagglutinin (FHA), p

174 bsequently eliminated by cell treatment with pertussis toxin (PT).

175 e acids has been reported to be sensitive to pertussis toxin (PTX) and dominant-negative Galpha(i) in

176 vo by the mycobacterial component of CFA and pertussis toxin (PTX) and in vitro by the ligation of To

177 ese effects persist in cells pretreated with pertussis toxin (PTX) and, like dopamine, may work to re

178 Similar to plant lectins, pertussis toxin (PTx) can activate the TCR and bind to a

179 Pertussis toxin (PTx) had no effect on hBD-induced Ca(2+

180 Pertussis toxin (PTx) has been shown to exert a variety

181 Pertussis toxin (PTx) is an AB(5) toxin produced by the

182 Pertussis toxin (PTX) is an AB5-type exotoxin produced b

183 Bordetella pertussis toxin (PTX) promotes insulin secretion, sugges

184 have reported that in vivo administration of pertussis toxin (PTx) reduces the number and function of

185 ng and ADP-ribosylating activity, similar to pertussis toxin (PTX) S1 subunit (PTX-S1).

186 f the numerous monoclonal antibodies binding pertussis toxin (PTx) that have been produced and charac

187 Binding of pertussis toxin (PTx) was examined by a glycan microarra

188 Pertussis toxin (Ptx) was used to decrease integrin-beta

189 in B10.D1-H2(q)/SgJ mice was overridden when pertussis toxin (PTX) was used to mimic the effects of e

190 ric G(o) signaling through the expression of pertussis toxin (PTX) within either the alpha/beta or ga

191 Pertussis toxin (PTX), a classical co-adjuvant for activ

192 1143-induced AA contraction was sensitive to pertussis toxin (PTX), the LPA1&3 antagonist Ki16425, an

193 n implicated in PC migration, treatment with Pertussis toxin (Ptx), which ablates these signals, did

194 Inhibition was reversed by pertussis toxin (PTX), which blocks Galphai/o activation

195 t the extreme requirement for IL-1R involves pertussis toxin (Ptx), which is expressed only by B. per

196 resence or absence of the ancillary adjuvant pertussis toxin (PTX), which models the effects of infec

197 Only the beta(3b)-AR promotes pertussis toxin (PTX)-sensitive cAMP accumulation.

198 Galpha(i/o) subunits with a mutation at the pertussis toxin (PTX)-sensitive cysteine (C351I) and wit

199 t data to elucidate that the presence of the pertussis toxin (PTX)-sensitive D2S receptor is critical

200 protection and ERK activation were linked to pertussis toxin (PTX)-sensitive G-protein-coupled effect

201 brain activate Kir3 channels by stimulating pertussis toxin (PTX)-sensitive G-protein-coupled recept

202 egress-promoting chemoattractants sensed by pertussis toxin (PTX)-sensitive Galphai protein-coupled

203 G protein-coupled receptor (GPCR) GPR18 in a pertussis toxin (PTX)-sensitive manner and produces anti

204 ot LTD(4) reduced cAMP levels in rat AM by a pertussis toxin (PTX)-sensitive mechanism.

205 rded after arresting G(alphai) activity with pertussis toxin (PTX).

206 displayed sensitivity to the G(i) inhibitor pertussis toxin (PTX).

207 ays targeting insertion sequence IS481 (IS), pertussis toxin ptxA promoter region (PT), and outer mem

208 repeat analysis (MLVA), pertactin (prnA) and pertussis toxin (ptxA) genotyping, and serotyping.

209 Treatment of WT cells with pertussis toxin recapitulated the P2Y14 phenotype, sugge

210 ction in locomotion, systemic treatment with pertussis toxin reduced naive T lymphocyte speed by 59%,

211 nduced AMPK phosphorylation was prevented by pertussis toxin, reduced by protein kinase A (PKA) activ

212 alian cell division, treatment of cells with pertussis toxin, reduction of Ric-8A expression, or decr

213 rthermore, inhibition of G(i) signaling with pertussis toxin restores cardiac function in heart failu

214 at injection of PS/2 mAb in combination with pertussis toxin resulted in anaphylaxis and mortality.

215 Activation of NF-kappaB by C-peptide was pertussis toxin sensitive and dependent on activation of

216 As chemotaxis was pertussis toxin sensitive in both WT and CB2(-/-) macrop

217 GS cells because of enhanced signaling via a pertussis toxin sensitive mechanism.

218 The MCH effect was dose dependent, pertussis toxin sensitive, and was abolished in MCHR1 KO

219 uman polymorphonuclear leukocytes (PMNs) are pertussis toxin sensitive, decrease actin polymerization

220 n human microvascular endothelial cells were Pertussis toxin sensitive, indicating a G-protein couple

221 Silencing was, however, pertussis toxin sensitive, which suggests that inhibitor

222 SP cells towards medulla, whereas a distinct pertussis-toxin sensitive pathway was required for medul

223 n adult mouse ventricular myocytes through a pertussis toxin-sensitive (G(i/o)-mediated) pathway.

224 PAFR couples to both pertussis toxin-sensitive and pertussis toxin-insensitiv

225 , formylmethionylleucylphenylalanine induced pertussis toxin-sensitive Ca(2+) flux in FHL 124 cells,

226 R(hi) T cells homed to the T cell zone using pertussis toxin-sensitive chemokine receptors and appear

227 CXCL9 and -16 in vitro and to the liver in a pertussis toxin-sensitive fashion.

228 ion of COX-2 appeared to be mediated via the pertussis toxin-sensitive G protein-coupled CB1 receptor

229 We also identified a role for pertussis toxin-sensitive G protein-coupled receptors an

230 Despite the fact that S1PRs are pertussis toxin-sensitive G protein-coupled receptors, t

231 neurons, sex peptide appears to act through Pertussis toxin-sensitive G proteins and suppression of

232 ERK1/2 phosphorylation through activation of pertussis toxin-sensitive G proteins as well as G(q) pro

233 This inhibition was mediated by one or more pertussis toxin-sensitive G proteins of the G(i/o) subfa

234 bition was voltage-dependent and mediated by pertussis toxin-sensitive G proteins, consistent with a

235 d inhibition of adenylyl cyclase activity by pertussis toxin-sensitive G proteins.

236 ing pathway through coupling of PAR-1 to the pertussis toxin-sensitive G(i)-protein.

237 by medium-chain FFAs couples primarily to a pertussis toxin-sensitive G(i/o) pathway.

238 ax and Bak and downregulation of Bcl-2 via a pertussis toxin-sensitive G-protein-coupled receptor (GP

239 only Gbetagamma subunits associated with the pertussis toxin-sensitive Galpha(i/o) subunits signal to

240 enom, inhibits Cav2.2 channels by activating pertussis toxin-sensitive Gi/o proteins via the GABAB re

241 phospholipase C, LSD responses also involve pertussis toxin-sensitive heterotrimeric G(i/o) proteins

242 SCFAs induced a dose-dependent and pertussis toxin-sensitive IL-8 response in bronchial epi

243 induced a rapid, concentration-dependent and pertussis toxin-sensitive increase in ASP(+) accumulatio

244 oduced a rapid, concentration-dependent, and pertussis toxin-sensitive increase of ASP(+) uptake.

245 Gs and promotes Gi binding, with concomitant pertussis toxin-sensitive inhibition of adenylyl cyclase

246 In contrast, S1P induces pertussis toxin-sensitive inhibition of isoproterenol-st

247 agonist stimulation primarily activates the pertussis toxin-sensitive inhibitory G protein (G(i)).

248 ing assay, nicotinic acid stimulation led to pertussis toxin-sensitive lowering of cAMP, recruitment

249 nd glucose-stimulated ERK1/2 activation in a pertussis toxin-sensitive manner, implicating the alpha

250 37L1 induced the phosphorylation of ERK in a pertussis toxin-sensitive manner, stimulated (35)S-GTPga

251 ble for triggering the Ca(2+) response, in a pertussis toxin-sensitive manner, suggesting the involve

252 ate phospholipase C activity via a partially pertussis toxin-sensitive mechanism, and that 8-pCPT-2'-

253 d further by determining the GRIN1-dependent pertussis toxin-sensitive neurite outgrowth.

254 rom IL-17-activated PCs, but not ECs, induce pertussis toxin-sensitive neutrophil polarization, likel

255 ecursors at the subgranular zone relies on a pertussis toxin-sensitive pathway independent of Cxcl12-

256 epidermal growth factor receptor-dependent, pertussis toxin-sensitive pathway requiring activation o

257 AH1 transcription through a GPR30-dependent, pertussis toxin-sensitive pathway that requires the acti

258 gD inhibited M-currents, but primarily via a pertussis toxin-sensitive pathway.

259 We reveal a role for pertussis toxin-sensitive signaling for TRM cell dendrit

260 ction of macrophage TNF-alpha production was pertussis toxin-sensitive, and analysis of the cellular

261 We determine in hDAT A559V a pertussis toxin-sensitive, CaMKII-dependent phosphorylat

262 Wnt6-induced signal transduction revealed a pertussis toxin-sensitive, ERK-mediated, but beta-cateni

263 )-N-methylpyridinium (ASP+), to illuminate a pertussis toxin-sensitive, extracellular signal-regulate

264 ntiation by PregS occurs via a noncanonical, pertussis toxin-sensitive, G protein-coupled, and Ca(2+)

265 rred splenic NK cells to the draining LN was pertussis toxin-sensitive, suggesting involvement of che

266 MMP14 activation by GTPgammaS is pertussis toxin-sensitive.

267 oring PV+ basket cells couple to an unusual, pertussis-toxin-sensitive pathway.

268 essary for IFN-gamma production and required pertussis-toxin-sensitive recruitment, in part mediated

269 and G(i) proteins as evidenced by the robust pertussis toxin sensitivities of their effects on cardio

270 w here that pretreatment of neutrophils with pertussis toxin significantly inhibits neutrophil cleara

271 or the G-protein-coupled receptor inhibitor pertussis toxin strongly suppressed BMP2 induction of os

272 fluence (Sst(-/-) mice or pretreatement with pertussis toxin) strongly increased glucagon release, di

273 tion sequences (ISs) in combination with the pertussis toxin subunit S1 (ptxS1) singleplex assay.

274 1001, and an IS1001-like element, as well as pertussis toxin subunit S1 (ptxS1), for the detection of

275 t was observed when migration was blocked by pertussis toxin, suggesting that migration of pulmonary

276 dulation of OPC migration was insensitive to pertussis toxin, suggesting that S1P5-initiated signalin

277 oth a formyl peptide receptor antagonist and pertussis toxin, suggesting that secreted annexin-1 acts

278 Surprisingly, although pertussis toxin targets a cysteine residue within the al

279 n of G protein alpha-subunits by cholera and pertussis toxins, the fundamentally different BepA-media

280 nal vaccination results in higher birth anti-pertussis toxin titers in preterm neonates.

281 is effect was abolished by pretreatment with pertussis toxin to inactivate G(i) proteins.

282 Moreover, treatment with pertussis toxin to inactivate signaling via G alpha i-pr

283 Treatment with pertussis toxin to overcome Galphai-mediated retention s

284 Treating CD4(+) T cells with pertussis toxin to uncouple the Galphai subunit from CCR

285 lated p38 activation was rapid, sensitive to pertussis toxin, to siRNA against either G alpha t2 or p

286 ol plus atenolol) of I(Ca,L) was examined in pertussis toxin-treated neonatal mouse ventricular myocy

287 Pertussis toxin treatment abolished morphine-induced rec

288 This activation is sensitive to pertussis toxin treatment but independent of phosphoinos

289 Pertussis toxin treatment of adoptively transferred mono

290 ced ERK phosphorylation persisted even after pertussis toxin treatment to abrogate G(i) and occurs in

291 -AG-induced Rac1 activation was sensitive to pertussis toxin treatment, hence involving G(i) proteins

292 ndered G(i)-protein signaling incompetent by pertussis toxin treatment, supporting an active stromal-

293 bserved with Ric-8A was further augmented by pertussis toxin treatment.

294 Pertussis toxin uncoupling-based studies have shown that

295 Estimated GMC of IgG to pertussis toxin was <5 ELISA units (EU)/mL at infant age

296 as not the case for endothelial CD47 because pertussis toxin, which inactivates G(alphai), had no inh

297 beta(2) agonists on retrieval are blocked by pertussis toxin, which inactivates signaling by G(i/o)-c

298 cross-sectional serosurvey of antibodies to pertussis toxin, which peak soon after infection and the

299 Cells treated with pertussis toxin, with reduced expression of G(ialpha1),

300 are also required for A-P guidance, because pertussis toxin, wortmannin, and expression of a p110gam