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1 cytokine production in response to Toll-like receptor stimulation.
2 d to reduced E-selectin expression after EP4 receptor stimulation.
3 MAPK signaling in response to formyl peptide receptor stimulation.
4 he responsiveness of the cells to subsequent receptor stimulation.
5 P accumulation in response to formyl peptide receptor stimulation.
6 and its downstream pathways following B cell receptor stimulation.
7 tein kinases in immune cells after toll-like receptor stimulation.
8 s switch was independent from glucocorticoid receptor stimulation.
9 tivity of C3d in enhancing suboptimal B-cell receptor stimulation.
10 ers to a state of unresponsiveness to B cell receptor stimulation.
11 ivated in response to calcium-permeable AMPA receptor stimulation.
12 (mPFC) and (3) the dependence of these on D2-receptor stimulation.
13 s and was maintained for at least 24 h after receptor stimulation.
14 d other pathogenic stimuli along with T cell receptor stimulation.
15  in FIGIRKO mice but was responsive to beta3-receptor stimulation.
16 3-hydroxy-5-methylisoxazole-4-propionic acid receptor stimulation.
17 s in response to toll-like receptor 2 (TLR2) receptor stimulation.
18 etagogues to induce secretion via muscarinic receptor stimulation.
19 erbated release of cytokines after toll-like receptor stimulation.
20 R-driven activation yet responsive to innate receptor stimulation.
21 observed experimentally with beta-adrenergic receptor stimulation.
22 on NO generation and/or muscarinic/nicotinic receptor stimulation.
23 amin did not block the effects of apical P2Y receptor stimulation.
24 re transiently dephosphorylated upon antigen receptor stimulation.
25 antigen-specific CD8(+) T cells after T cell receptor stimulation.
26 ncreased proliferation in response to T-cell receptor stimulation.
27 ant TRPC channels were robustly activated by receptor stimulation.
28 ing after growth factor or G protein-coupled receptor stimulation.
29 evated coincident with injury/pronociceptive receptor stimulation.
30 exogenous VEGF-B(167) exerted a compensatory receptor stimulation.
31  peritoneal macrophages show evidence of IgG receptor stimulation.
32  activation in response to TNF and Toll-like receptor stimulation.
33 ted in the absence of ongoing pronociceptive receptor stimulation.
34 ell surface receptor density after sustained receptor stimulation.
35 l activation by synergistic LFA-1 and T-cell receptor stimulation.
36 tivity, and IFN-gamma secretion after T cell receptor stimulation.
37  naive and memory CD4(+) T cells upon T cell receptor stimulation.
38 activation following epidermal growth factor receptor stimulation.
39 ack inhibition of Jak2 kinase activity after receptor stimulation.
40  response to PDGF receptor and insulin/IGF-1 receptor stimulation.
41 sion was not altered by acute or repeated DA receptor stimulation.
42 reticulum (ER) decouples GCK activation from receptor stimulation.
43 and ERKs, but not Itk, in response to T cell receptor stimulation.
44 eases in proliferation in response to B cell receptor stimulation.
45 s T cell proliferation in response to T cell receptor stimulation.
46 e both dependent on extracellular ATP and P2 receptor stimulation.
47 and cell proliferation in response to B-cell receptor stimulation.
48 e-8 and FADD as an induced response to death receptor stimulation.
49 and enhanced NF-kappaB activity upon antigen receptor stimulation.
50 c since both are activated following antigen receptor stimulation.
51 ukin (IL) 4 upon in vivo and in vitro T cell receptor stimulation.
52 actin cytoskeleton inefficiently upon T cell receptor stimulation.
53 excess Ca2+ influx and acute beta-adrenergic receptor stimulation.
54 -15 eliminated the metabolic requirement for receptor stimulation.
55 ly modifies responses to pattern-recognition receptor stimulation.
56 APK, NF-kappaB and NFAT activity upon T cell receptor stimulation.
57 on of Lck and downstream signaling after Fas receptor stimulation.
58  in reactivated CD4(+)Tm cells during T-cell receptor stimulation.
59 lpha-amylase secretion after beta-adrenergic receptor stimulation.
60 acrophages in the absence of prior Toll-like receptor stimulation.
61 tory priming with phorbol ester or Toll-like receptor stimulation.
62 nflammatory cytokine production after T cell receptor stimulation.
63 e in the glycolytic activity after toll-like receptor stimulation.
64 amma subunit enrichment or G-protein-coupled receptor stimulation.
65 nd were defective in activation after T-cell receptor stimulation.
66 ckade on cellular proliferation after T-cell receptor stimulation.
67 and reestablished BTK activation upon B cell receptor stimulation.
68 e fear-enhancing effects of repeated ghrelin receptor stimulation.
69 ages and dendritic cells following Toll-like receptor stimulation.
70 pable of blocking the effects of cholinergic receptor stimulation.
71 tain signaling depending on the magnitude of receptor stimulation.
72 duce LFA-1 binding activity after activating receptor stimulation.
73 rom amygdala neurons was enhanced by ghrelin receptor stimulation.
74 nd enhanced T-cell function following T-cell receptor stimulation.
75 of PP1 activity in response to synaptic NMDA 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                 In contrast, basolateral P2Y receptor stimulation activated basolateral K+ channels a
80                   Similarly to direct opioid receptor stimulation, activation of the NPFF(2) receptor
81 y be activated after Galphaq-protein-coupled receptor stimulation, affecting Ca(2+) cycling, enhancin
82               The overall response to T-cell receptor stimulation alone or in combination with IL-7,
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  Abs, faster off-rates may permit continuous receptor stimulation and more efficient erythropoiesis.
99 rs in regulating chronic pattern recognition receptor stimulation and NOD2-induced outcomes has not b
100 y, activated downstream of G-protein-coupled receptor stimulation and RhoA, in glioblastoma cell prol
101 ed to induce miR-29 upon pattern recognition receptor stimulation and showed enhanced release of IL-1
102      Dissipation of ATP by CD39 reduced P2X7 receptor stimulation and thereby suppressed baseline leu
103 to transforming growth factor-beta (TGFbeta) receptor stimulation and transport of Smad2 by kinesin-1
104  including the quality/quantity of Toll-like receptor stimulation and/or type of Ag-presenting cells.
105 nuclear factor kappaB induction after B-cell receptor stimulation, and B-cell activating factor-induc
106 cells was found to involve purinergic P2Y(2) receptor stimulation, and both ligand-dependent mechanis
107 nt mechanisms through adrenergic or dopamine receptor stimulation, and by several cAMP-independent me
108 ve an attenuated cytokine response to T-cell receptor stimulation, and can suppress the proliferation
109 oviruses to external stimuli, such as T-cell receptor stimulation, and slowed the reversion of reacti
110 F2K occurs in response to A2A-type adenosine receptor stimulation, and that activation of protein kin
111           One key brainstem site in which AT receptor stimulation appears to contribute to the elevat
112 ) CD57(+) T lymphocytes upon in vitro T-cell receptor stimulation are increased in PBC.
113 reby SFKs are activated by G protein-coupled receptor stimulation are not fully understood.
114 S) generated within cytotoxic lymphocytes by receptor stimulation are required for lyososomal permeab
115          Thus, our findings pointed to IGF-I receptor stimulation as a rational strategy to successfu
116 sside was ultimately dependent on muscarinic receptor stimulation as all effects were blocked by atro
117 M contractile responses to G-protein-coupled receptor stimulation, as well as hypoxia in pulmonary ar
118                                      Antigen receptor stimulation assembles an NF-kappaB activating p
119 g stresses, including IFNgamma and Toll-like receptor stimulation, bacterial infection, starvation an
120 ficient B cells were hyperreactive to B cell receptor stimulation (BCR stimulation).
121 lecular analyses implicate aberrant androgen receptor stimulation, biliary acid disturbances, and alt
122 P was up-regulated in lymphocytes by antigen receptor stimulation but not by inflammatory stimuli.
123 d to induce hyporesponsiveness to activating receptor stimulation, but did induce tolerance to MHC I-
124 ibit impaired proliferation following T cell receptor stimulation, but the contribution of these dist
125                                  Thus, A(2A) receptor stimulation by adenosine, a breakdown product o
126        Here, we show that beta(3)-adrenergic receptor stimulation by CL 316,243 promotes adipose tiss
127                           beta(2)-adrenergic receptor stimulation by epinephrine can enhance ERK1/2 a
128                                         NMDA receptor stimulation by homocysteine was determined by p
129 ntigen-like protein 3 (SSL3), which prevents receptor stimulation by pathogen-associated lipopeptides
130                                           FP receptor stimulation by PGF(2alpha) induced the phosphor
131 This interaction is markedly disrupted after receptor stimulation by the specific agonist UK14304, su
132                          In response to NMDA receptor stimulation, CaMKIIalpha moves rapidly from a d
133  the view that NOP receptor blockade and DOP receptor stimulation caused synergistic overinhibition o
134                      In rodents, dopamine D1 receptor stimulation causes a complex behavioral super-s
135                                   Similarly, receptor stimulation causes exit of the alpha(1a)AR from
136                                  Upon T cell receptor stimulation, CD4(+) T helper (Th) lymphocytes r
137 re, we report that PYK2 is activated by NMDA receptor stimulation (chemical LTD) in cultured neurons.
138 ures in the absence of any G protein-coupled receptor stimulation, colocalizes with beta2-YFP and cla
139 ter shifted in the gradient following T-cell receptor stimulation, consistent with a change in struct
140                                      5-HT(4) receptor stimulation could represent an innovative and r
141 s modified for optimal HLA binding or T-cell receptor stimulation) covering five TAAs and the univers
142 CD4(+) T cells proliferated poorly to T-cell receptor stimulation, despite normal responses to phorbo
143                                          Fas receptor stimulation does not activate canonical downstr
144 n method and tonography indicated that EP(4) receptor stimulation facilitated aqueous humor outflow f
145    In the olfactory epithelium (OE), odorant receptor stimulation generates cAMP signals that functio
146 y cellular functions, and its hydrolysis via receptor stimulation governs cell signaling.
147 agy induction during starvation, hypoxia, or receptor stimulation has been widely studied, the key ep
148 ceptor-tyrosine kinase and G-protein-coupled receptor stimulations have been shown to lead to PLD act
149 s involved in an initial increase in PA upon receptor stimulation; however, when PLD is blocked, the
150  activation is digital in response to T-cell-receptor stimulation; however, whether other receptors o
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 grows of the role of inappropriate Toll-like receptor stimulation in inflammation and autoimmunity, s
155    In this study, we examined the role of Ag receptor stimulation in iNKT cells during several bacter
156 nd that synaptic N-methyl-D-aspartate (NMDA) receptor stimulation in neurons leads to activation of P
157 ransient Mg(2+) influx is induced by antigen receptor stimulation in normal T cells and by growth fac
158 ere, we assessed whether endogenous dopamine receptor stimulation in nucleus accumbens contributes to
159            2-AG was also released upon OX(1) receptor stimulation in recombinant HEK-293 and neuro-2a
160 sults demonstrate a novel role for sustained receptor stimulation in regulation of intracellular traf
161  that hyperphagia can be driven by mu-opioid receptor stimulation in restricted regions of ventral me
162 e the deleterious effects of beta-adrenergic receptor stimulation in septic shock.
163 norphin-B expression mediated by dopamine D1 receptor stimulation in the development of 3,4-dihydroxy
164 or-deficient macrophages is mediated by IL-1 receptor stimulation in the kidney.
165 ther evidence for the importance of 5-HT(1A) receptor stimulation in the NOR deficit produced by subc
166  manipulations to show that dopamine D1-like receptor stimulation in the OFC is required for drug con
167 gic input from the VTA, via dopamine D1-like receptor stimulation in the OFC, is required for OFC-BLA
168 ntiate into IL-17 producer cells upon T-cell receptor stimulation in the presence of IL-1beta, IL-2,
169          By counteracting the effects of AT1 receptor stimulation in the target organ, exogenous admi
170 phine exposure requires a decrease in opiate receptor stimulation in the VTA and can be relieved by a
171 he rapid induction of glycolysis upon T-cell receptor stimulation in TM cells.
172 n-12, respectively, in response to Toll-like receptor stimulation in vitro.
173 ely, but not IFN-gamma in response to T-cell receptor stimulation in vitro.
174 oxy-5-methylisoxazole-4-propionate glutamate receptor) stimulation in the nucleus accumbens (NAc) is
175                                   Purinergic receptor stimulation, including P2X(7)Rs, of endotoxin-p
176  cells lost the ability to respond to T cell receptor stimulation, including reduced expression of ce
177                          alpha(1)-Adrenergic receptor stimulation increased the apoptosis of astrocyt
178 ult normal neurospheres, alpha(1)-adrenergic receptor stimulation increased the expression of glial m
179 rimental studies showed that beta-adrenergic receptor stimulation increases the rate of Ca(2)(+) rele
180 phorylated and activated by beta1-adrenergic receptor stimulation-induced EGF receptor (EGFR) transac
181 longed, whereas in more mature neurons, NMDA receptor stimulation induces a protein phosphatase 1-dep
182                                      Antigen receptor stimulation induces HS1 phosphorylation, and HS
183             We revealed that altering T-cell receptor stimulation influenced recruitment of mRNAs to
184 clamp analysis demonstrated that alpha(2)-NA receptor stimulation inhibited a caesium and ZD7288-sens
185                            G protein-coupled receptor stimulation inhibits TRPM3 channel activity thr
186 Il4, translates analog differences in T cell receptor stimulation into a digital decision for Il4 ree
187  SFK phosphorylation in response to thrombin receptor stimulation is downstream from G(q)/Ca(2+) sign
188  activity in the VTA and associated dopamine receptor stimulation is necessary for the synaptic poten
189  role of STIM1 in TRPC channel activation by receptor stimulation is not fully understood.
190 holine levels and/or nicotinic acetylcholine receptor stimulation is sufficient to attenuate nicotine
191  a critical period during which repeated CB1 receptor stimulation is sufficient to elicit an enduring
192 ignals activate BA, besides beta3-adrenergic receptor stimulation, is limited.
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 gagement of CD4 by HIV gp120 prior to T-cell receptor stimulation leads to dysregulation of early sig
197  T cells were activated by suboptimal T cell receptor stimulation, LFA-1 played an indispensable role
198                                        A(2B) receptor stimulation limits endothelial cell inflammator
199              Our results indicate that 5-HT6 receptor stimulation may be a mechanism initiating some
200 the decrease of cAMP elicited by dopamine D4 receptor stimulation may be secondary to decreased [Ca(2
201 thway in the CeA that is activated by CRF(1) receptor stimulation, mediates GABA release at nerve ter
202            These dual effects of alpha(2)-NA receptor stimulation - membrane hyperpolarization and en
203 ed PGIS nitration and associated thromboxane receptor stimulation might be important in the initiatio
204 g of negative stimuli, but whether 5-HT2A/1A receptor stimulation modulates the processing of negativ
205                                  Upon immune receptor stimulation, Nfatc1/Egfp expression is elevated
206                             Interestingly on receptor stimulation NHERF1 no longer interacts directly
207            We show that, after TLR/adenosine receptor stimulation, NR4A2 depletion promotes significa
208         Cyclin E expression following T cell receptor stimulation of ADAP-deficient T cells is transi
209 sive effects of stress were mediated by CRF2 receptor stimulation of dynorphin release and subsequent
210 ressing 293 cells selectively increased D(2) receptor stimulation of extracellular signal-regulated k
211                                       T-cell receptor stimulation of LTR-Tax CD4(+) T cells induced T
212 d after chronic NOD2 and pattern recognition receptor stimulation of macrophages; similar attenuation
213                                           Ag receptor stimulation of preactivated T cells causes rapi
214 content in EVs released upon in vitro T cell receptor stimulation of Th1, Th17, and T regulatory (Tre
215                                         AMPA receptor stimulation of wild-type OPCs caused decreased
216 etermine the effect of acute and repeated DA receptor stimulation on AMPA receptor (AMPAR) synaptic t
217 the enhancing action of purine or bradykinin receptor stimulation on eNOS Ser-635/633 phosphorylation
218 to examine the pharmacology of S1P and EP(4) receptor stimulation on IOP regulation as occurs within
219                                  Sweet taste receptor stimulation only increased GLP-1 secretion.
220  Adult anxiety was evoked by either 5-HT2A/C receptor stimulation or 5-HT1A receptor blockade of naiv
221 mechanistic activity extending beyond simple receptor stimulation or blockade.
222 t ganglion neurons, independent of mu opioid receptor stimulation or G protein activation.
223  currents activated through either mu-opioid receptor stimulation or intracellular dialysis of guanos
224 rocess that does not require beta-adrenergic receptor stimulation or protein kinase A activation.
225 s from these mice are hyperactive to antigen-receptor stimulation owing to a loss of inhibitory signa
226  TNF-alpha protein production following TLR2 receptor stimulation (p < 0.001).
227 s increased in RA T cells 2 min after T-cell receptor stimulation (P < 0.001).
228 s in response to death receptor or Toll-like receptor stimulation, pathogen infection, or sterile cel
229                                 Following Ag receptor stimulation, peripheral B cells in the double m
230 ho-S657 peaked and declined rapidly after Ag receptor stimulation, phospho-S649 occurred later and wa
231  phosphorylation produced by beta-adrenergic receptor stimulation, phosphodiesterase or protein kinas
232 intermediates (ROI) generated in response to receptor stimulation play an important role in cellular
233 intermediates (ROI) generated in response to receptor stimulation play an important role in mediating
234       We showed previously that OX(1) orexin receptor stimulation produced a strong (3)H overflow res
235 demonstration that localized beta-adrenergic receptor stimulation produces spatiotemporal synchroniza
236 tead, viral persistence and prolonged T cell receptor stimulation progressively redirects CD4 T cell
237 t in vivo GPCR visualization enables mapping receptor stimulation promoted by a behavioral challenge
238                            In addition, PDGF receptor stimulation promoted epicardial cell migration,
239 /11-coupled GPCR, or epidermal growth factor receptor stimulation promotes beta-arrestin2 recruitment
240  the contribution of cholangiocyte toll-like receptor stimulation promoting the ongoing inflammatory
241 show that BAT activation by beta3-adrenergic receptor stimulation protects from atherosclerosis in hy
242 m and leads to an altered response to B cell receptor stimulation, reduced BAFF-R surface expression,
243  together, these findings suggest that A(2A) receptor stimulation reduces, while A(2A) blockade ampli
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 ts of IL-13 in response to polyclonal T-cell receptor stimulation, suggesting they may play different
252 alphaA whose generation is induced by immune receptor stimulation supports the proliferation and inhi
253                                        A(2A)-receptor stimulation suppressed the development of T-cel
254 bition of signaling events triggered by VEGF-receptor stimulation that are upstream of c-kit activati
255                                         NMDA receptor stimulation that induces LTD transiently activa
256 f MZ B cells, it had no influence on antigen receptor stimulation that is blunted in peritoneal cavit
257                            Importantly, NMDA receptor stimulation that triggered CaMKII activation pr
258 biological effects of dopamine D(1) and D(2) receptor stimulation, the alterations of the transcripti
259  is induced by immune receptor and chemokine receptor stimulation, the molecular regulation of RGS13
260           We also found that, following P2X7 receptor stimulation, the phosphorylation of ERK1/2 was
261                                  Upon T cell receptor stimulation, these T cells also produced large
262 ctivated by extracellular ATP and purinergic receptor stimulation, this study demonstrates that airwa
263 c leukotrieneC4 produced downstream thrombin receptor stimulation through the catalytic activity of l
264 ecreases in phosphorylation through a T cell receptor stimulation time course on tyrosine residues fo
265 romone response because it couples pheromone receptor stimulation to activation of the appropriate mi
266 P1-P5) each play a specific role in coupling receptor stimulation to CheA activity.
267 nalling complex that links G-protein-coupled receptor stimulation to K(+) channel activity.
268 LIN restricts Met1-Ub formation after immune receptor stimulation to prevent unwarranted proinflammat
269 ses by palmitoylation, where it couples NMDA receptor stimulation to production of nitric oxide (NO)
270          To isolate the actions of B2 or P2Y receptor stimulation to the neurons, we prepared cardiom
271           It involves a chain of events from receptor stimulation to the sequential modulation of two
272 neurotransmitters, through G-protein-coupled receptor stimulation, to control cellular electrical exc
273 80)/B7-2 (CD86) molecules, along with T-cell receptor stimulation, together facilitate T-cell activat
274                                              Receptor stimulation triggered signal transduction, secr
275                              Thus, glutamate receptor stimulation triggers Ca(2+)- and mitochondrial
276 idase activity whereas concurrent purinergic receptor stimulation triggers protein denitroyslation, l
277                             Following T cell receptor stimulation, Vav1 facilitates formation of sign
278 nd Th2 CD4(+) effector lymphocytes by T cell receptor stimulation was blocked in lal(-/-) mice.
279                    The response to adenosine receptor stimulation was impaired in eKO mice in single
280    We decided to investigate whether 5-HT(4) receptor stimulation was necessary for the effects of SS
281     In slices obtained from control rats, DA receptor stimulation was observed to exert complex actio
282 lls, and concomitant TLR4 and cognate B-cell receptor stimulation was required on a single-cell level
283                           Postnatal 5-HT2A/C receptor stimulation was sufficient to evoke anxiety in
284 ograft models with demonstrations that IGF-I receptor stimulation was sufficient to generate a 45% in
285 vasoconstrictor responses to direct alpha(1)-receptor stimulation were blunted during exercise versus
286 larly, vasoconstrictor responses to alpha(2)-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 re-operated Ca2+ channels after B lymphocyte receptor stimulation, which was reversed by the provisio
291                                       M3-ACh receptor stimulation with 10 microM acetylcholine result
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 sponse was reversed by concurrent muscarinic receptor stimulation with the addition of carbachol, dem
300 , occurred normally in response to Toll-like receptor stimulation, yet ERK phosphorylation and NF-kap

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