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1 beta2-talin1 interaction, and intracellular Ca2+ mobilization.
2 e-gated Ca2+ influx into receptor-controlled Ca2+ mobilization.
3 ich the cAMP signaling pathway can influence Ca2+ mobilization.
4 uires cooperation with other signals such as Ca2+ mobilization.
5 n with InsP3 under conditions that prevented Ca2+ mobilization.
6 es (MAPK) ERK1/2 and p38, but did not affect Ca2+ mobilization.
7 gene expression, and a late requirement for Ca2+ mobilization.
8 (NK3), displayed distinct modes of action in Ca2+ mobilization.
9 rates, including p62, p110, and Shc, and for Ca2+ mobilization.
10 s the inhibitory effect of PKC activators on Ca2+ mobilization.
11 hrough co-activation of adenylyl cyclase and Ca2+ mobilization.
12 pression of Fas appears to be independent of Ca2+ mobilization.
13 ol phospholipid hydrolysis and intracellular Ca2+ mobilization.
14 phospholipase C activation and intracellular Ca2+ mobilization.
15 nses and uncover, in some cells, oscillatory Ca2+ mobilization.
16 es C, D, and A2, in protein kinase C, and in Ca2+ mobilization.
17 400 microM at rest, and 1 to 50 microM after Ca2+ mobilization.
18 gation, secretion, arachidonate release, and Ca2+ mobilization.
19 otaxin binding and CCR3-mediated cytoplasmic Ca2+ mobilization.
20 s to respond to diverse signals that lead to Ca2+ mobilization.
21 imulated cAMP accumulation and intracellular Ca2+ mobilization.
22 ficantly different patterns of intracellular Ca2+ mobilization.
23 k regulation of the pathways responsible for Ca2+ mobilization.
24 n inositol 1,4,5-triphosphate (IP3)-mediated Ca2+ mobilization.
25 pH influenced the magnitude of intracellular Ca2+ mobilization.
26 positive role for PKC-theta in TCR-mediated Ca2+ mobilization.
27 ike domain of SP-A are necessary to optimize Ca2+ mobilization.
28 via phosphoinositide 3-kinase, PKCzeta, and Ca2+ mobilization.
29 th a profound influence on receptor-mediated Ca2+ mobilization.
30 Ang II caused Ca2+ mobilization.
31 of IgG capable of stimulating intracellular Ca2+ mobilization.
32 er total protein tyrosine phosphorylation or Ca2+ mobilization.
33 axis but not for CXCL1-induced intracellular Ca2+ mobilization.
34 2+, ryanodine (0.1 mM) inhibited AVP-induced Ca2+ mobilization.
35 n-induced expression of RANKL is mediated by Ca2+ mobilization.
36 no effect on PAFR-mediated PI hydrolysis and Ca2+ mobilization.
37 t attenuated muscarinic M3 receptor-mediated Ca2+ mobilization.
38 more modestly, Fc gamma RIIB1 inhibition of Ca2+ mobilization.
39 istribution by an inhibitor of intracellular Ca2+ mobilization, 8-(diethylamino)-octyl-3,4,5-trimetho
40 l 1,4,5-trisphosphate (InsP3) evoked quantal Ca2+ mobilization: a rapid acceleration in the rate of 4
41 nhibit (a) initial contraction by inhibiting Ca2+ mobilization and (b) sustained contraction by inhib
42 MP levels, would both inhibit human platelet Ca2+ mobilization and adhesion molecule expression ex vi
43 e coupling between AVP-induced intracellular Ca2+ mobilization and apical exocytosis was investigated
45 ed by injection of IP3 through intracellular Ca2+ mobilization and Ca2+ influx through voltage-gated
48 teins and respond to AGAs with intracellular Ca2+ mobilization and extracellular regulated protein ki
49 ar level, amrinone inhibited agonist-induced Ca2+ mobilization and had modest inhibitory effects on a
50 and NF-kappa B via SP-induced intracellular Ca2+ mobilization and indicate a crucial role for neurop
52 Ca2+ channels, (iii) have minimal effects on Ca2+ mobilization and InsP3 formation in intact cells, (
53 , activation of muscarinic receptors induced Ca2+ mobilization and inward currents in SNc dopamine ne
54 sary to achieve a rapid biological response (Ca2+ mobilization and IP3 formation), both SH2 domains o
55 oth protein kinase C (PKC) translocation and Ca2+ mobilization and is inhibited by cyclosporin A, and
56 t with FTY720 or FTY-P prevented S1P-induced Ca2+ mobilization and migration in vascular endothelial
57 we demonstrate that SAA selectively induced Ca2+ mobilization and migration of HEK cells expressing
58 Golgi-translocated PKCalpha upstream of both Ca2+ mobilization and PLD activation in a complex with P
60 inhibits G protein turnover, PLC activation, Ca2+ mobilization and secretion, it is required for norm
61 -enhanced BCR signaling causes intracellular Ca2+ mobilization and total pTyr phosphorylation of an i
62 purinergic receptor-activated intracellular Ca2+ mobilization and was inhibited by Cl- channel block
63 coincided with resensitization of SP-induced Ca2+ mobilization and with the return of surface SP bind
64 er cascades leading to cGMP accumulation and Ca2+ mobilization and/or influx and that both pathways a
66 ed for ligand binding, cAMP accumulation, or Ca2+ mobilization, and 3) phosphorylation of the COOH-te
67 horylation of TCR-zeta and ZAP-70, defective Ca2+ mobilization, and a approximately 90% reduction in
68 iple receptors, including GPVI, which causes Ca2+ mobilization, and alpha2beta1, which stimulates a s
70 ptide inhibited phosphoinositide hydrolysis, Ca2+ mobilization, and degranulation stimulated by PAF.
71 ,5-triphosphate [I(1,4,5)P3], which mediates Ca2+ mobilization, and diacylglycerol (DG), which activa
72 olipase C (PLC)-gamma2, leading to prolonged Ca2+ mobilization, and increases in extracellular signal
73 tein tyrosine phosphorylation, intracellular Ca2+ mobilization, and interleukin-2 promoter-driven tra
74 acid metabolites, tyrosine phosphorylation, Ca2+ mobilization, and only inositol trisphosphate produ
77 sphate production, tyrosine phosphorylation, Ca2+ mobilization, and secretion of histamine and arachi
78 1,4,5-triphosphate production, intracellular Ca2+ mobilization, and the up-regulation of Ca2+/calmodu
79 , BAPTA, prevented AVP-induced intracellular Ca2+ mobilization, apical exocytosis, and increase of os
80 mal, indicating that both PKC activation and Ca2+ mobilization are essential for normal secretion.
81 shown to activate protein kinase G, to block Ca2+ mobilization, as well as to markedly attenuate acti
83 ecific agonist and antagonist activity using Ca2+-mobilization assays in RH7777 cells expressing the
84 ulates both Src family kinase activation and Ca2+ mobilization associated with class II- and BCR-medi
85 permeabilized cells, (1,3,4,5)IP4 inhibited Ca2+ mobilization at concentrations exceeding those like
86 ion, MAPK phosphorylation, and intracellular Ca2+ mobilization but has no effect on KDR phosphorylati
90 K was insensitive to selective inhibitors of Ca2+ mobilization, but it was blocked upon phospholipase
94 toxin almost completely blocked LPA-induced Ca2+ mobilization by Edg2 but only partially blocked tha
95 ylation but not cross-desensitization of its Ca2+ mobilization by fMLP or C5a, indicating an inhibito
97 tes could function as a negative feedback on Ca2+ mobilization by inhibiting inositol 1,4,5-trisphosp
98 has recently been shown that NAADP mediates Ca2+ mobilization by insulin in human pancreatic beta-ce
103 of inositol phosphates and the inhibition of Ca2+ mobilization by the phospholipase C inhibitor U7312
106 1,4,5-triphosphate production, intracellular Ca2+ mobilization, CaMKII activity, filamin phosphorylat
107 alone and in all pairwise combinations, for Ca2+ mobilization, cAMP synthesis, phosphorylation of ma
110 appear to act upstream of phospholipase C in Ca2+ mobilization, decreased the SP-A-induced rise in MR
111 lpha-induced extracellular acidification and Ca2+ mobilization demonstrating functional antagonism.
113 phospholipase C-gamma (PLC-gamma), internal Ca2+ mobilization does not play a significant role in th
114 03 cells was unable to alter TRAP-stimulated Ca2+ mobilization either before or after suppression of
115 how that the Gbeta5-RGS7 complex can inhibit Ca2+ mobilization elicited by muscarinic acetylcholine r
116 vations that followed the quantal pattern of Ca2+ mobilization, even at the level of individual mitoc
118 ls expressing SHP-1 (C453S) showed increased Ca2+ mobilization, extracellular signal-regulated kinase
120 ndins act directly to impair agonist-induced Ca2+ mobilization following endotoxin exposure; however,
121 s in [Ca2+]i were shown to be the product of Ca2+ mobilization from caffeine/ryanodine-sensitive intr
123 ication of pharmacological agents that alter Ca2+ mobilization from intracellular stores and experime
124 single PAC1 receptor variant responsible for Ca2+ mobilization from intracellular stores and influx t
125 in in the presence of 2.5 mmol/l Ca2+, while Ca2+ mobilization from intracellular stores was partiall
126 fter an initial hyperpolarization induced by Ca2+ mobilization from the endoplasmic reticulum (ER), t
127 ell type, namely cyclic ADP-ribose-dependent Ca2+ mobilization from the sarcoplasmic reticulum via ry
129 ine vasopressin 10(7) mol/L; and studied for Ca2+ mobilization, glycoprotein IIb/IIIa activation, and
130 These distinct receptor-specific patterns of Ca2+ mobilization imply significantly different roles fo
133 e have examined Mg2+ mobilization as well as Ca2+ mobilization in B cells undergoing Fas-initiated ap
134 In conclusion, muscarinic receptor-mediated Ca2+ mobilization in cultured hippocampal neurones shows
135 ed GTPase activity in platelet membranes and Ca2+ mobilization in cultured human smooth muscle cells
136 e (fMLP), was able to specifically attenuate Ca2+ mobilization in human phagocytes induced by SAA, bu
137 y the fact that GA was incapable of inducing Ca2+ mobilization in insect cells transfected with the t
138 me plasma membrane patch can be activated by Ca2+ mobilization in intact cells and by InsP3 in excise
140 al mechanism of cAMP-dependent inhibition of Ca2+ mobilization in megakaryocytes appears to be by inh
142 examined the role of mu-opioid receptors and Ca2+ mobilization in morphine-induced astrocyte developm
143 , the peptide SFLLRN and trypsin, stimulated Ca2+ mobilization in RBL-2H3 cells but did not cause pri
144 igher G protein activation and a more robust Ca2+ mobilization in RBL-2H3 cells expressing carboxyl t
145 nd thrombin receptor and caused little or no Ca2+ mobilization in RBL-2H3 cells, effectively primed t
146 Interestingly, mPAFR mediated a sustained Ca2+ mobilization in response to PAF and was more active
147 cant fraction of the Plcg1(-/-) cells showed Ca2+ mobilization in response to PDGF, suggesting that t
149 ovoke increased NF-AT gene transcription and Ca2+ mobilization in the absence of Wnt stimulation.
150 c agonist phenylephrine was unable to induce Ca2+ mobilization in the isolated NPE and failed to do s
154 l images were used to simultaneously monitor Ca2+ mobilization in the two distinct, apically joined c
156 otoxin would impair agonist-induced calcium (Ca2+) mobilization in rat mesangial cells, owing to the
157 sequences for HASMCs, such as inhibition of [Ca2+] mobilization in response to thrombin stimulation.
158 to various signaling mechanisms involved in Ca2+ mobilization, including inhibition or activation of
159 centration of TR agonist was increased, peak Ca2+ mobilization increased, but influx of extracellular
160 resulted in mouse DAP12 phosphorylation and Ca2+ mobilization, indicating that Ly49P is a competent
162 tudinal layer, however, the initial steps in Ca2+ mobilization involve activation of cytosolic PLA2 (
163 system, we now show that P2Y receptor-evoked Ca2+ mobilization is controlled by membrane voltage in a
164 Tyrosine phosphorylation of PLC-gamma2 and Ca2+ mobilization is markedly attenuated in SLP-76-defic
165 jection of the Ca2+ chelator BAPTA show that Ca2+ mobilization is necessary and sufficient for LTS in
166 illations in the IMCD and that intracellular Ca2+ mobilization is required for exocytotic insertion o
167 ble cells, in which the primary mechanism of Ca2+ mobilization is through (1,4,5)IP3-dependent Ca2+ r
168 by Edg4, which suggests that Edg2 transduces Ca2+ mobilization largely through pertussis toxin-sensit
171 receptors for LPA allowed examination of the Ca2+ mobilization mediated specifically by each subtype.
172 h phorbol ester, which reduced the extent of Ca2+ mobilization occurring in response to the hormone.
175 and for FPRL1, it was not reported to induce Ca2+ mobilization or chemotaxis in FPRL1-transfected cel
176 able to mediate growth factor activation of Ca2+ mobilization or inositol 1,4,5-trisphosphate (IP3)
177 ontrast, P2UR function, as assayed by either Ca2+ mobilization or inositol trisphosphate generation,
178 horylation events correlates with a distinct Ca2+ mobilization pattern that characterizes APL-stimula
179 mediate G-protein activation, intracellular Ca2+ mobilization, phosphoinositide (PI) hydrolysis, and
180 d G(12/13) proteins leading to intracellular Ca2+ mobilization, PKC activation and regulation of the
182 eptor-mediated uncoupling of Ca2+ entry from Ca2+ mobilization provides an effective control mechanis
183 mutant failed to reconstitute TCR-dependent Ca2+ mobilization, Ras activation, CD69 expression and N
184 mediate KDR signaling such as intracellular Ca2+ mobilization rather than Flt-1-induced CDC42 activa
185 M4b is activated following receptor-mediated Ca2+ mobilization, representing a regulatory mechanism t
186 dless of this, CD45-negative cells exhibited Ca2+ mobilization responses that were greatly diminished
188 bits rectificatory behaviour with respect to Ca2+ mobilization; responses originating within the NPE
189 in SHR VSMCs showed a greater dependence on Ca2+ mobilization, since chelation of intracellular Ca2+
193 ospholipase C (Plc)gamma2 but independent of Ca2+ mobilization, suggesting that the target of BCR sti
194 requires the presence of rapid intracellular Ca2+ mobilization that might also explain the selective
195 e proteins may account for the disruption of Ca2+ mobilization that occurs in models of acute pancrea
196 gin produced relatively stringent degrees of Ca2+ mobilization that produced an endoplasmic reticulum
197 he first time, that independent of cytosolic Ca2+ mobilization, there is augmentation of eNOS activit
198 l-dependent alterations in the ability of SR Ca2+ mobilization to contribute to contractile activatio
200 with CXCR1, IL-8 (CXCL8) cross-desensitized Ca2+ mobilization to PAF by all the receptors but only P
202 precursors, CD19 ligation does not activate Ca2+ mobilization until the pre-B cell stage of developm
203 oncentration required to induce half-maximal Ca2+ mobilization was 0.14 microM for Ins(1,4,5)P3, 1.8
207 entation of tert-butyl hydroperoxide-induced Ca2+ mobilization was inhibited by pretreatment with the
208 ct of uPAR cross-linking, and uPAR-triggered Ca2+ mobilization was not blocked by anti-CR3 mAbs.
210 a2+, while a distinct level of intracellular Ca2+ mobilization was readily detected under the conditi
211 roduction and proliferation, and the peak of Ca2+ mobilization was reduced although of normal duratio
213 tol phosphate accumulation and intracellular Ca2+ mobilization were determined for both receptors.
214 Rho-family GTP-GDP exchange factor Vav, and Ca2+ mobilization were enhanced, whereas tyrosine phosph
215 e properties of muscarinic receptor-mediated Ca2+ mobilization were investigated in hippocampal cultu
216 ctivated kinases, phospholipase Cgamma-1 and Ca2+ mobilization, were not affected in Cbl-b(-/-) T cel
217 and phospholipase C-dependent intracellular Ca2+ mobilization when it is expressed in HEK 293 cells.
218 A levels, BCR down-regulation occurs through Ca2+ mobilization, whereas IL-4R down-regulation occurs
219 fMLP and C5a as determined by chemotaxis and Ca2+ mobilization, whereas mature DCs (mDCs) respond to
220 scarinic agonists elevate cGMP by triggering Ca2+ mobilization, which activates NO synthase to produc
221 receptor (Ki = 0.78 nM), blocks LTB4-induced Ca2+ mobilization with an IC50 of 6.6 +/- 1.5 nM, and de
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