ライフサイエンスコーパス: pertussis toxin

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

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

3 and this activity was partially inhibited by pertussis toxin.

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

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

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

7 Ab treatment in combination with exposure to pertussis toxin.

8 urons, was abolished after pretreatment with pertussis toxin.

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

10 nulation via MRGPRX2, which was abolished by pertussis toxin.

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

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

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

14 effect that is blocked by preincubation with pertussis toxin.

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

16 activity was elevated expressed very little pertussis toxin.

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

18 rating pulmonary tumors by pretreatment with pertussis toxin.

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

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

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

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

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

24 oxidative burst, were likewise prevented by pertussis toxin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 Pertussis toxin, an inhibitor of G proteins, attenuated

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

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

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

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

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

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

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

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

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

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

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

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

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

55 The G(i/o) inhibitor pertussis toxin and inhibitors of PKA and PKC had no eff

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

57 Pertussis toxin and LY294002 inhibition demonstrated tha

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

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

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

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

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

63 preterm infants vs term infants, except for pertussis toxin and pneumococcal serotypes 4 and 19F aft

64 andidate containing non-adsorbed recombinant Pertussis Toxin and reduced the amount of antigen dose r

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

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

67 -1 and the IGF-2 responses were sensitive to pertussis toxin and the sphingosine kinase inhibitor, di

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

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

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

71 Inhibitors pertussis toxin and Y27632 reversed the inhibition of ne

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

91 was blocked by Cre-induced expression of the pertussis toxin catalytic subunit (PTXa).

92 s also applied for G(i)alpha GTP-loading and pertussis toxin-catalyzed ADP-ribosylation of G(i)alpha,

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

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

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

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

97 ieved protective IgG antibody levels against pertussis toxin, diphtheria, tetanus and 6 of 10 pneumoc

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

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

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

101 althy subjects aged 18-45 years with an anti-pertussis toxin IgG concentration of <20 IU/ml were inoc

102 Anti-pertussis toxin IgG seroconversion occurred in nine out

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

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

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

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

107 1 alpha), which can be completely blocked by pertussis toxin, indicating coupling to G(i/o).

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

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

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

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

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

113 Pertussis toxin inhibited both Lm entry into the PALS an

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

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

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

117 This signaling was pertussis toxin insensitive, suggesting that endothelial

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

136 9 protein was prevented by pretreatment with pertussis toxin or the opioid antagonist naloxone.

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

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

139 Pertussis toxin pretreatment reduced the amount of GRIN1

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

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

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

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

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

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

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

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

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

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

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

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

152 nant aP (r-aP) vaccine including recombinant pertussis toxin (PT) and filamentous hemagglutinin (FHA)

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

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

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

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

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

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

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

160 Pertussis toxin (PT) is secreted from Bordetella pertuss

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

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

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

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

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

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

167 Antibodies against pertussis toxin (PT), filamentous haemagglutinin (FHA) a

168 Antibodies against pertussis toxin (PT), filamentous hemagglutinin (FHA), a

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

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

171 aning immunity to 14 pneumococcal serotypes, pertussis toxin (PT), tetanus toxoid (TT) and varicella,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 was modestly inhibited by pretreatment with pertussis toxin (PTX), consistent with a minor role for

190 1143-induced AA contraction was sensitive to pertussis toxin (PTX), the LPA1&3 antagonist Ki16425, an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 12-h pretreatment of human islets with pertussis-toxin (PTX) improved GSIS and prevented the in

206 Both receptors induced pertussis-toxin (PTX) insensitive inhibition of cyclic A

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

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

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

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

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

212 atic ADP-ribosyltransferase PtxS1-subunit of pertussis toxin, respectively.

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

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

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

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

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

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

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

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

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

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

225 Icatibant caused MC degranulation via a pertussis toxin-sensitive G protein but did not activate

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

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

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

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

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

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

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

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

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

235 t TRPC4 channels are particularly coupled to pertussis toxin-sensitive G(i/o) proteins, with a co-dep

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

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

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

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

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

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

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

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

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

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

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

247 37L1 induced the phosphorylation of ERK in a pertussis toxin-sensitive manner, stimulated (35)S-GTPga

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

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

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

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

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

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

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

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

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

257 l-regulated kinases 1/2 pathways, along with pertussis toxin-sensitive signals.

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

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

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

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

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

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

264 MMP14 activation by GTPgammaS is pertussis toxin-sensitive.

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

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

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

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

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

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

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

272 1001, and an IS1001-like element, as well as pertussis toxin subunit S1 (ptxS1), for the detection of

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

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

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

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

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

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

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

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

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

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

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

284 Pertussis toxin treatment abolished morphine-induced rec

285 Pertussis toxin treatment of adoptively transferred mono

286 blockade of G-protein-coupled receptors with pertussis toxin treatment prior to transfer only partial

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

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

289 cement of the ASIC currents was resistant to pertussis toxin treatment, suggesting that Galpha (i)/Ga

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

291 though both these responses are sensitive to pertussis toxin treatment.

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

293 Pertussis toxin uncoupling-based studies have shown that

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

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

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

297 Pertussis toxin, which inhibits activation of G(i)/G(o),

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