ライフサイエンスコーパス: receptor stimulation

1 ages and dendritic cells following Toll-like receptor stimulation.

2 pable of blocking the effects of cholinergic receptor stimulation.

3 tain signaling depending on the magnitude of receptor stimulation.

4 rom amygdala neurons was enhanced by ghrelin receptor stimulation.

5 nd enhanced T-cell function following T-cell receptor stimulation.

6 of PP1 activity in response to synaptic NMDA receptor stimulation.

7 cytokine production in response to Toll-like receptor stimulation.

8 d to reduced E-selectin expression after EP4 receptor stimulation.

9 MAPK signaling in response to formyl peptide receptor stimulation.

10 P accumulation in response to formyl peptide receptor stimulation.

11 tein kinases in immune cells after toll-like receptor stimulation.

12 s switch was independent from glucocorticoid receptor stimulation.

13 tivity of C3d in enhancing suboptimal B-cell receptor stimulation.

14 ivated in response to calcium-permeable AMPA receptor stimulation.

15 (mPFC) and (3) the dependence of these on D2-receptor stimulation.

16 s and was maintained for at least 24 h after receptor stimulation.

17 d other pathogenic stimuli along with T cell receptor stimulation.

18 in FIGIRKO mice but was responsive to beta3-receptor stimulation.

19 3-hydroxy-5-methylisoxazole-4-propionic acid receptor stimulation.

20 s in response to toll-like receptor 2 (TLR2) receptor stimulation.

21 s that are rapidly induced by B cell antigen receptor stimulation.

22 etagogues to induce secretion via muscarinic receptor stimulation.

23 erbated release of cytokines after toll-like receptor stimulation.

24 in fractional cell killing at low levels of receptor stimulation.

25 R-driven activation yet responsive to innate receptor stimulation.

26 observed experimentally with beta-adrenergic receptor stimulation.

27 amin did not block the effects of apical P2Y receptor stimulation.

28 re transiently dephosphorylated upon antigen receptor stimulation.

29 5H is induced by ZIKV infection or Toll-like receptor stimulation.

30 antigen-specific CD8(+) T cells after T cell receptor stimulation.

31 ncreased proliferation in response to T-cell receptor stimulation.

32 ant TRPC channels were robustly activated by receptor stimulation.

33 ing after growth factor or G protein-coupled receptor stimulation.

34 evated coincident with injury/pronociceptive receptor stimulation.

35 exogenous VEGF-B(167) exerted a compensatory receptor stimulation.

36 peritoneal macrophages show evidence of IgG receptor stimulation.

37 ted in the absence of ongoing pronociceptive receptor stimulation.

38 ell surface receptor density after sustained receptor stimulation.

39 l activation by synergistic LFA-1 and T-cell receptor stimulation.

40 ic interneuron activation through neurokinin receptor stimulation.

41 tivity, and IFN-gamma secretion after T cell receptor stimulation.

42 naive and memory CD4(+) T cells upon T cell receptor stimulation.

43 activation following epidermal growth factor receptor stimulation.

44 ack inhibition of Jak2 kinase activity after receptor stimulation.

45 response to PDGF receptor and insulin/IGF-1 receptor stimulation.

46 sion was not altered by acute or repeated DA receptor stimulation.

47 and ERKs, but not Itk, in response to T cell receptor stimulation.

48 eases in proliferation in response to B cell receptor stimulation.

49 s T cell proliferation in response to T cell receptor stimulation.

50 e both dependent on extracellular ATP and P2 receptor stimulation.

51 eukemogenic growth advantage in scenarios of receptor stimulation.

52 tory priming with phorbol ester or Toll-like receptor stimulation.

53 duce LFA-1 binding activity after activating receptor stimulation.

54 he responsiveness of the cells to subsequent receptor stimulation.

55 and its downstream pathways following B cell receptor stimulation.

56 ers to a state of unresponsiveness to B cell receptor stimulation.

57 on NO generation and/or muscarinic/nicotinic receptor stimulation.

58 egative regulator of cardiac beta-adrenergic receptor stimulation.

59 activation in response to TNF and Toll-like receptor stimulation.

60 reticulum (ER) decouples GCK activation from receptor stimulation.

61 -15 eliminated the metabolic requirement for receptor stimulation.

62 ly modifies responses to pattern-recognition receptor stimulation.

63 APK, NF-kappaB and NFAT activity upon T cell receptor stimulation.

64 on of Lck and downstream signaling after Fas receptor stimulation.

65 in reactivated CD4(+)Tm cells during T-cell receptor stimulation.

66 lpha-amylase secretion after beta-adrenergic receptor stimulation.

67 acrophages in the absence of prior Toll-like receptor stimulation.

68 s increased T-cell reactivity upon Toll-like-receptor stimulation.

69 nflammatory cytokine production after T cell receptor stimulation.

70 e in the glycolytic activity after toll-like receptor stimulation.

71 amma subunit enrichment or G-protein-coupled receptor stimulation.

72 nd were defective in activation after T-cell receptor stimulation.

73 ckade on cellular proliferation after T-cell receptor stimulation.

74 and reestablished BTK activation upon B cell receptor stimulation.

75 e fear-enhancing effects of repeated ghrelin receptor stimulation.

76 triction combined with daily beta-adrenergic receptor stimulation (ACi) and show that chronic CGP tre

77 rgic alpha1-adrenoceptor and dopaminergic D1 receptor stimulation activate feedforward calcium-protei

78 olished indicating that both ET(A) and ET(B) receptor stimulation activate this conductance.

79 Both cell swelling and receptor stimulation activated astrocytic VRAC, which re

80 In contrast, basolateral P2Y receptor stimulation activated basolateral K+ channels a

81 Similarly to direct opioid receptor stimulation, activation of the NPFF(2) receptor

82 y be activated after Galphaq-protein-coupled receptor stimulation, affecting Ca(2+) cycling, enhancin

83 Receptor stimulation also elevated cytoplasmic Ca(2+); C

84 A(2B) receptor stimulation also promotes the production of ang

85 evelopment, they fail to proliferate upon Ag-receptor stimulation although NF-kappaB, MAP kinase and

86 annabinoid-sensitive synapses to cannabinoid receptor stimulation, although it altered some intrinsic

87 mpartmentalization of the Fas receptor after receptor stimulation, an important process for apoptotic

88 5-HT(1A) receptor stimulation and 5-HT(6) and 5-HT(7) receptor an

89 uration, supersensitivity to beta-adrenergic receptor stimulation and Ca(2+) mishandling following MI

90 Inhibition of PANX1 blocked A2A receptor stimulation and cAMP accumulation in response t

91 l ganglion cell toxicity through direct NMDA receptor stimulation and implicate, for the first time,

92 se hearts undergoing chronic beta-adrenergic receptor stimulation and in a rat model of postischemic

93 ate PIP2 homeostasis in cells during intense receptor stimulation and in the resting state, respectiv

94 +) current in the absence of beta-adrenergic receptor stimulation and in voltage-dependent facilitati

95 ritic cells were less sensitive to Toll-like receptor stimulation and induced significantly lower lev

96 y genetic reduction of Cdk5 activity or NMDA receptor stimulation and is dependent on Mdm2.

97 matically sensitizes GIRK responses to GABAB receptor stimulation and markedly slows channel deactiva

98 g T cell proliferation in response to T cell receptor stimulation and mediating fibroblast cell migra

99 xpression of TOX is driven by chronic T cell receptor stimulation and NFAT activation.

100 rs in regulating chronic pattern recognition receptor stimulation and NOD2-induced outcomes has not b

101 y, activated downstream of G-protein-coupled receptor stimulation and RhoA, in glioblastoma cell prol

102 ed to induce miR-29 upon pattern recognition receptor stimulation and showed enhanced release of IL-1

103 Dissipation of ATP by CD39 reduced P2X7 receptor stimulation and thereby suppressed baseline leu

104 to transforming growth factor-beta (TGFbeta) receptor stimulation and transport of Smad2 by kinesin-1

105 including the quality/quantity of Toll-like receptor stimulation and/or type of Ag-presenting cells.

106 influences of beta(1)-AR (beta(1)-adrenergic receptor) stimulation and peripheral O(2) saturation (Sp

107 nuclear factor kappaB induction after B-cell receptor stimulation, and B-cell activating factor-induc

108 cells was found to involve purinergic P2Y(2) receptor stimulation, and both ligand-dependent mechanis

109 nt mechanisms through adrenergic or dopamine receptor stimulation, and by several cAMP-independent me

110 oviruses to external stimuli, such as T-cell receptor stimulation, and slowed the reversion of reacti

111 F2K occurs in response to A2A-type adenosine receptor stimulation, and that activation of protein kin

112 One key brainstem site in which AT receptor stimulation appears to contribute to the elevat

113 x in mammalian lymphocytes following antigen receptor stimulation are Ca(2+) release-activated Ca(2+)

114 ) CD57(+) T lymphocytes upon in vitro T-cell receptor stimulation are increased in PBC.

115 reby SFKs are activated by G protein-coupled receptor stimulation are not fully understood.

116 S) generated within cytotoxic lymphocytes by receptor stimulation are required for lyososomal permeab

117 Thus, our findings pointed to IGF-I receptor stimulation as a rational strategy to successfu

118 sside was ultimately dependent on muscarinic receptor stimulation as all effects were blocked by atro

119 M contractile responses to G-protein-coupled receptor stimulation, as well as hypoxia in pulmonary ar

120 Antigen receptor stimulation assembles an NF-kappaB activating p

121 g stresses, including IFNgamma and Toll-like receptor stimulation, bacterial infection, starvation an

122 ficient B cells were hyperreactive to B cell receptor stimulation (BCR stimulation).

123 lecular analyses implicate aberrant androgen receptor stimulation, biliary acid disturbances, and alt

124 P was up-regulated in lymphocytes by antigen receptor stimulation but not by inflammatory stimuli.

125 d to induce hyporesponsiveness to activating receptor stimulation, but did induce tolerance to MHC I-

126 ibit impaired proliferation following T cell receptor stimulation, but the contribution of these dist

127 Thus, A(2A) receptor stimulation by adenosine, a breakdown product o

128 Here, we show that beta(3)-adrenergic receptor stimulation by CL 316,243 promotes adipose tiss

129 beta(2)-adrenergic receptor stimulation by epinephrine can enhance ERK1/2 a

130 NMDA receptor stimulation by homocysteine was determined by p

131 ntigen-like protein 3 (SSL3), which prevents receptor stimulation by pathogen-associated lipopeptides

132 This interaction is markedly disrupted after receptor stimulation by the specific agonist UK14304, su

133 Upon Ag receptor stimulation, Ca(2+) can enter the lymphocyte vi

134 In response to NMDA receptor stimulation, CaMKIIalpha moves rapidly from a d

135 e current results provide evidence that D(1) receptor stimulation causally affects core aspects of co

136 the view that NOP receptor blockade and DOP receptor stimulation caused synergistic overinhibition o

137 In rodents, dopamine D1 receptor stimulation causes a complex behavioral super-s

138 Upon T cell receptor stimulation, CD4(+) T helper (Th) lymphocytes r

139 re, we report that PYK2 is activated by NMDA receptor stimulation (chemical LTD) in cultured neurons.

140 ter shifted in the gradient following T-cell receptor stimulation, consistent with a change in struct

141 5-HT(4) receptor stimulation could represent an innovative and r

142 Fas receptor stimulation does not activate canonical downstr

143 n method and tonography indicated that EP(4) receptor stimulation facilitated aqueous humor outflow f

144 In the olfactory epithelium (OE), odorant receptor stimulation generates cAMP signals that functio

145 y cellular functions, and its hydrolysis via receptor stimulation governs cell signaling.

146 agy induction during starvation, hypoxia, or receptor stimulation has been widely studied, the key ep

147 ceptor-tyrosine kinase and G-protein-coupled receptor stimulations have been shown to lead to PLD act

148 s involved in an initial increase in PA upon receptor stimulation; however, when PLD is blocked, the

149 activation is digital in response to T-cell-receptor stimulation; however, whether other receptors o

150 outcomes of the first human trial of liver X receptor stimulation (i.e., a dramatic increase of chole

151 Our findings reveal a novel link between EGF receptor stimulation, ILK-containing complexes, and acti

152 mediated vasodilatation is independent of P1-receptor stimulation in both young and older adults.

153 and ALDH2 were both activated by A(2b)/A(3) receptor stimulation in HMC-1, and PKCepsilon inhibition

154 In this study, we examined the role of Ag receptor stimulation in iNKT cells during several bacter

155 nd that synaptic N-methyl-D-aspartate (NMDA) receptor stimulation in neurons leads to activation of P

156 ransient Mg(2+) influx is induced by antigen receptor stimulation in normal T cells and by growth fac

157 ere, we assessed whether endogenous dopamine receptor stimulation in nucleus accumbens contributes to

158 2-AG was also released upon OX(1) receptor stimulation in recombinant HEK-293 and neuro-2a

159 sults demonstrate a novel role for sustained receptor stimulation in regulation of intracellular traf

160 that hyperphagia can be driven by mu-opioid receptor stimulation in restricted regions of ventral me

161 e the deleterious effects of beta-adrenergic receptor stimulation in septic shock.

162 norphin-B expression mediated by dopamine D1 receptor stimulation in the development of 3,4-dihydroxy

163 or-deficient macrophages is mediated by IL-1 receptor stimulation in the kidney.

164 ther evidence for the importance of 5-HT(1A) receptor stimulation in the NOR deficit produced by subc

165 manipulations to show that dopamine D1-like receptor stimulation in the OFC is required for drug con

166 gic input from the VTA, via dopamine D1-like receptor stimulation in the OFC, is required for OFC-BLA

167 ntiate into IL-17 producer cells upon T-cell receptor stimulation in the presence of IL-1beta, IL-2,

168 By counteracting the effects of AT1 receptor stimulation in the target organ, exogenous admi

169 phine exposure requires a decrease in opiate receptor stimulation in the VTA and can be relieved by a

170 he rapid induction of glycolysis upon T-cell receptor stimulation in TM cells.

171 n-12, respectively, in response to Toll-like receptor stimulation in vitro.

172 ely, but not IFN-gamma in response to T-cell receptor stimulation in vitro.

173 oxy-5-methylisoxazole-4-propionate glutamate receptor) stimulation in the nucleus accumbens (NAc) is

174 cells lost the ability to respond to T cell receptor stimulation, including reduced expression of ce

175 In vivo studies revealed that 5-HT(2A) receptor stimulation increased cortical mtDNA and ATP le

176 alpha(1)-Adrenergic receptor stimulation increased the apoptosis of astrocyt

177 ult normal neurospheres, alpha(1)-adrenergic receptor stimulation increased the expression of glial m

178 rimental studies showed that beta-adrenergic receptor stimulation increases the rate of Ca(2)(+) rele

179 phorylated and activated by beta1-adrenergic receptor stimulation-induced EGF receptor (EGFR) transac

180 longed, whereas in more mature neurons, NMDA receptor stimulation induces a protein phosphatase 1-dep

181 T cell receptor stimulation induces depletion of the endoplasmi

182 Antigen receptor stimulation induces HS1 phosphorylation, and HS

183 We revealed that altering T-cell receptor stimulation influenced recruitment of mRNAs to

184 G protein-coupled receptor stimulation inhibits TRPM3 channel activity thr

185 Il4, translates analog differences in T cell receptor stimulation into a digital decision for Il4 ree

186 SFK phosphorylation in response to thrombin receptor stimulation is downstream from G(q)/Ca(2+) sign

187 activity in the VTA and associated dopamine receptor stimulation is necessary for the synaptic poten

188 role of STIM1 in TRPC channel activation by receptor stimulation is not fully understood.

189 holine levels and/or nicotinic acetylcholine receptor stimulation is sufficient to attenuate nicotine

190 a critical period during which repeated CB1 receptor stimulation is sufficient to elicit an enduring

191 ignals activate BA, besides beta3-adrenergic receptor stimulation, is limited.

192 are altered to promote sustained cholinergic receptor stimulation, it becomes evident that alpha5 als

193 calcium influx (G protein activation) after receptor stimulation, it does cause ERK activation, alth

194 TP receptor stimulation lead to loss of K(Ca)2.3 mediated h

195 Receptor stimulation leads to concerted activation of tw

196 T cells were activated by suboptimal T cell receptor stimulation, LFA-1 played an indispensable role

197 A(2B) receptor stimulation limits endothelial cell inflammator

198 thway in the CeA that is activated by CRF(1) receptor stimulation, mediates GABA release at nerve ter

199 Ls was induced by the coordination of T cell receptor stimulation, microenvironmental stressors and P

200 ed PGIS nitration and associated thromboxane receptor stimulation might be important in the initiatio

201 g of negative stimuli, but whether 5-HT2A/1A receptor stimulation modulates the processing of negativ

202 Upon immune receptor stimulation, Nfatc1/Egfp expression is elevated

203 Interestingly on receptor stimulation NHERF1 no longer interacts directly

204 We show that, after TLR/adenosine receptor stimulation, NR4A2 depletion promotes significa

205 Cyclin E expression following T cell receptor stimulation of ADAP-deficient T cells is transi

206 function was unchanged, but beta-adrenergic receptor stimulation of cardiac inotropy, cAMP, PKA, L-t

207 sive effects of stress were mediated by CRF2 receptor stimulation of dynorphin release and subsequent

208 ressing 293 cells selectively increased D(2) receptor stimulation of extracellular signal-regulated k

209 Designer receptor stimulation of G(q) signaling, but not G(s) sig

210 T-cell receptor stimulation of LTR-Tax CD4(+) T cells induced T

211 d after chronic NOD2 and pattern recognition receptor stimulation of macrophages; similar attenuation

212 Ag receptor stimulation of preactivated T cells causes rapi

213 content in EVs released upon in vitro T cell receptor stimulation of Th1, Th17, and T regulatory (Tre

214 AMPA receptor stimulation of wild-type OPCs caused decreased

215 etermine the effect of acute and repeated DA receptor stimulation on AMPA receptor (AMPAR) synaptic t

216 the enhancing action of purine or bradykinin receptor stimulation on eNOS Ser-635/633 phosphorylation

217 to examine the pharmacology of S1P and EP(4) receptor stimulation on IOP regulation as occurs within

218 Sweet taste receptor stimulation only increased GLP-1 secretion.

219 Adult anxiety was evoked by either 5-HT2A/C receptor stimulation or 5-HT1A receptor blockade of naiv

220 mechanistic activity extending beyond simple receptor stimulation or blockade.

221 t ganglion neurons, independent of mu opioid receptor stimulation or G protein activation.

222 currents activated through either mu-opioid receptor stimulation or intracellular dialysis of guanos

223 n cytosolic Ca(2+) oscillations generated by receptor stimulation or on CRAC channel-driven gene expr

224 s from these mice are hyperactive to antigen-receptor stimulation owing to a loss of inhibitory signa

225 s increased in RA T cells 2 min after T-cell receptor stimulation (P < 0.001).

226 TNF-alpha protein production following TLR2 receptor stimulation (p < 0.001).

227 s in response to death receptor or Toll-like receptor stimulation, pathogen infection, or sterile cel

228 Following Ag receptor stimulation, peripheral B cells in the double m

229 ho-S657 peaked and declined rapidly after Ag receptor stimulation, phospho-S649 occurred later and wa

230 phosphorylation produced by beta-adrenergic receptor stimulation, phosphodiesterase or protein kinas

231 intermediates (ROI) generated in response to receptor stimulation play an important role in cellular

232 We showed previously that OX(1) orexin receptor stimulation produced a strong (3)H overflow res

233 IP(3)R (Inositol-trisphosphate receptor) stimulation produced larger [Ca(2+)](Nuc) incr

234 demonstration that localized beta-adrenergic receptor stimulation produces spatiotemporal synchroniza

235 tead, viral persistence and prolonged T cell receptor stimulation progressively redirects CD4 T cell

236 t in vivo GPCR visualization enables mapping receptor stimulation promoted by a behavioral challenge

237 /11-coupled GPCR, or epidermal growth factor receptor stimulation promotes beta-arrestin2 recruitment

238 the contribution of cholangiocyte toll-like receptor stimulation promoting the ongoing inflammatory

239 After M2 receptor stimulation, proNGF-B (25 kDa), which is involv

240 show that BAT activation by beta3-adrenergic receptor stimulation protects from atherosclerosis in hy

241 m and leads to an altered response to B cell receptor stimulation, reduced BAFF-R surface expression,

242 together, these findings suggest that A(2A) receptor stimulation reduces, while A(2A) blockade ampli

243 These lasting and marked effects of M(1) receptor stimulation reinforce our interest in this targ

244 enotype, particularly during beta-adrenergic receptor stimulation, remain unclear.

245 nflux in response to ER stress or purinergic receptor stimulation resulting in AA liberation for PGE(

246 In animal experiments, dopamine D2-like receptor stimulation revealed partially antagonistic eff

247 tform to show that, in response to Toll-like receptor stimulation, short-term HSCs and multipotent pr

248 Most importantly, EP4 receptor stimulation showed potent anti-inflammatory act

249 presented paradoxical responses to dopamine receptor stimulation, showing hypoactivity following inj

250 Upon store depletion after T-cell receptor stimulation, STIM1 translocates and coclusters

251 Specifically, increasing D1 receptor stimulation strengthened Pavlovian-to-instrumen

252 ts of IL-13 in response to polyclonal T-cell receptor stimulation, suggesting they may play different

253 alphaA whose generation is induced by immune receptor stimulation supports the proliferation and inhi

254 A(2A)-receptor stimulation suppressed the development of T-cel

255 bition of signaling events triggered by VEGF-receptor stimulation that are upstream of c-kit activati

256 ses T cells by promoting inappropriate P2Y11 receptor stimulation that impairs T cell metabolism and

257 NMDA receptor stimulation that induces LTD transiently activa

258 f MZ B cells, it had no influence on antigen receptor stimulation that is blunted in peritoneal cavit

259 Importantly, NMDA receptor stimulation that triggered CaMKII activation pr

260 biological effects of dopamine D(1) and D(2) receptor stimulation, the alterations of the transcripti

261 is induced by immune receptor and chemokine receptor stimulation, the molecular regulation of RGS13

262 We also found that, following P2X7 receptor stimulation, the phosphorylation of ERK1/2 was

263 Upon T cell receptor stimulation, these T cells also produced large

264 ctivated by extracellular ATP and purinergic receptor stimulation, this study demonstrates that airwa

265 c leukotrieneC4 produced downstream thrombin receptor stimulation through the catalytic activity of l

266 o study the effects of acute beta-adrenergic receptor stimulation (through isoproterenol (ISO) treatm

267 ecreases in phosphorylation through a T cell receptor stimulation time course on tyrosine residues fo

268 P1-P5) each play a specific role in coupling receptor stimulation to CheA activity.

269 nalling complex that links G-protein-coupled receptor stimulation to K(+) channel activity.

270 LIN restricts Met1-Ub formation after immune receptor stimulation to prevent unwarranted proinflammat

271 ses by palmitoylation, where it couples NMDA receptor stimulation to production of nitric oxide (NO)

272 To isolate the actions of B2 or P2Y receptor stimulation to the neurons, we prepared cardiom

273 It involves a chain of events from receptor stimulation to the sequential modulation of two

274 neurotransmitters, through G-protein-coupled receptor stimulation, to control cellular electrical exc

275 80)/B7-2 (CD86) molecules, along with T-cell receptor stimulation, together facilitate T-cell activat

276 Receptor stimulation triggered signal transduction, secr

277 Thus, glutamate receptor stimulation triggers Ca(2+)- and mitochondrial

278 Following T cell receptor stimulation, Vav1 facilitates formation of sign

279 nd Th2 CD4(+) effector lymphocytes by T cell receptor stimulation was blocked in lal(-/-) mice.

280 The response to adenosine receptor stimulation was impaired in eKO mice in single

281 We decided to investigate whether 5-HT(4) receptor stimulation was necessary for the effects of SS

282 In slices obtained from control rats, DA receptor stimulation was observed to exert complex actio

283 lls, and concomitant TLR4 and cognate B-cell receptor stimulation was required on a single-cell level

284 Postnatal 5-HT2A/C receptor stimulation was sufficient to evoke anxiety in

285 ograft models with demonstrations that IGF-I receptor stimulation was sufficient to generate a 45% in

286 vasoconstrictor responses to direct alpha(1)-receptor stimulation were blunted during exercise versus

287 t depends upon both muscarinic and nicotinic receptor stimulation, where the generation of NO is like

288 t depends upon both muscarinic and nicotinic receptor stimulation, where the generation of NO is like

289 cient T cells were hyperresponsive to T-cell receptor stimulation, which resulted in increased secret

290 M3-ACh receptor stimulation with 10 microM acetylcholine result

291 ction following T cell receptor (TCR) and co-receptor stimulation with a combination of anti-CD3 and

292 aive CD4 T cells (CD25(-)Foxp3(-)) by T-cell receptor stimulation with additional transforming growth

293 inhibits B cell responses induced by B cell receptor stimulation with antigen.

294 Further, RAW 264.7 A(3) receptor stimulation with Cl-IB-MECA reduces IFN-gamma-i

295 eous SR Ca(2+) releases upon beta-adrenergic receptor stimulation with isoproterenol in Trdn(-/-) myo

296 Local beta-adrenergic receptor stimulation with noradrenaline (norepinephrine;

297 In conclusion, 5-HT2A/1A receptor stimulation with psilocybin seems to reduce soc

298 eptide receptor 1 (RXFP1), to cAMP following receptor stimulation with sub-picomolar concentrations o

299 conomic choice and investigated whether D(1) receptor stimulation would bias preferences toward optio

300 , occurred normally in response to Toll-like receptor stimulation, yet ERK phosphorylation and NF-kap