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1  protein of the SOCE machinery that leads to 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 rates, including p62, p110, and Shc, and for Ca2+ mobilization.
9 (NK3), displayed distinct modes of action in 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  beta2-talin1 interaction, and intracellular Ca2+ mobilization.
22 imulated cAMP accumulation and intracellular Ca2+ mobilization.
23 ficantly different patterns of intracellular Ca2+ mobilization.
24 k regulation of the pathways responsible for Ca2+ mobilization.
25 n inositol 1,4,5-triphosphate (IP3)-mediated Ca2+ mobilization.
26 pH influenced the magnitude of intracellular Ca2+ mobilization.
27  positive role for PKC-theta in TCR-mediated Ca2+ mobilization.
28 ike domain of SP-A are necessary to optimize Ca2+ mobilization.
29  via phosphoinositide 3-kinase, PKCzeta, and Ca2+ mobilization.
30 th a profound influence on receptor-mediated Ca2+ mobilization.
31                                Ang II caused Ca2+ mobilization.
32  of IgG capable of stimulating intracellular Ca2+ mobilization.
33 er total protein tyrosine phosphorylation or Ca2+ mobilization.
34 axis but not for CXCL1-induced intracellular Ca2+ mobilization.
35 2+, ryanodine (0.1 mM) inhibited AVP-induced Ca2+ mobilization.
36 n-induced expression of RANKL is mediated by Ca2+ mobilization.
37 no effect on PAFR-mediated PI hydrolysis and Ca2+ mobilization.
38  more modestly, Fc gamma RIIB1 inhibition of Ca2+ mobilization.
39 t attenuated muscarinic M3 receptor-mediated Ca2+ mobilization.
40 istribution by an inhibitor of intracellular Ca2+ mobilization, 8-(diethylamino)-octyl-3,4,5-trimetho
41 l 1,4,5-trisphosphate (InsP3) evoked quantal Ca2+ mobilization: a rapid acceleration in the rate of 4
42 nhibit (a) initial contraction by inhibiting Ca2+ mobilization and (b) sustained contraction by inhib
43 MP levels, would both inhibit human platelet Ca2+ mobilization and adhesion molecule expression ex vi
44 e coupling between AVP-induced intracellular Ca2+ mobilization and apical exocytosis was investigated
45  ((2,4,5)IP3), stimulated both intracellular Ca2+ mobilization and Ca2+ entry.
46 ed by injection of IP3 through intracellular Ca2+ mobilization and Ca2+ influx through voltage-gated
47  and (iii) the BR cell A2BAR couples to both Ca2+ mobilization and cAMP accumulation.
48                           We observed strong Ca2+ mobilization and enhancement of chemotaxis followin
49 teins and respond to AGAs with intracellular Ca2+ mobilization and extracellular regulated protein ki
50 ar level, amrinone inhibited agonist-induced Ca2+ mobilization and had modest inhibitory effects on a
51  and NF-kappa B via SP-induced intracellular Ca2+ mobilization and indicate a crucial role for neurop
52 rmination of phosphoinositide hydrolysis and Ca2+ mobilization and inhibits proliferation.
53 Ca2+ channels, (iii) have minimal effects on Ca2+ mobilization and InsP3 formation in intact cells, (
54 , activation of muscarinic receptors induced Ca2+ mobilization and inward currents in SNc dopamine ne
55 sary to achieve a rapid biological response (Ca2+ mobilization and IP3 formation), both SH2 domains o
56 oth protein kinase C (PKC) translocation and Ca2+ mobilization and is inhibited by cyclosporin A, and
57 t with FTY720 or FTY-P prevented S1P-induced Ca2+ mobilization and migration in vascular endothelial
58  we demonstrate that SAA selectively induced Ca2+ mobilization and migration of HEK cells expressing
59 Golgi-translocated PKCalpha upstream of both Ca2+ mobilization and PLD activation in a complex with P
60  as a costimulatory receptor for TCR induced Ca2+ mobilization and proliferation.
61 inhibits G protein turnover, PLC activation, Ca2+ mobilization and secretion, it is required for norm
62 -enhanced BCR signaling causes intracellular Ca2+ mobilization and total pTyr phosphorylation of an i
63  purinergic receptor-activated intracellular Ca2+ mobilization and was inhibited by Cl- channel block
64 coincided with resensitization of SP-induced Ca2+ mobilization and with the return of surface SP bind
65 er cascades leading to cGMP accumulation and Ca2+ mobilization and/or influx and that both pathways a
66                           EGF did not induce Ca2+ mobilization, and 2-aminobiphenyl borate did not in
67 ed for ligand binding, cAMP accumulation, or Ca2+ mobilization, and 3) phosphorylation of the COOH-te
68 horylation of TCR-zeta and ZAP-70, defective Ca2+ mobilization, and a approximately 90% reduction in
69 iple receptors, including GPVI, which causes Ca2+ mobilization, and alpha2beta1, which stimulates a s
70                   In cellular proliferation, Ca2+ mobilization, and bioluminescence resonance energy
71 ptide inhibited phosphoinositide hydrolysis, Ca2+ mobilization, and degranulation stimulated by PAF.
72 ,5-triphosphate [I(1,4,5)P3], which mediates Ca2+ mobilization, and diacylglycerol (DG), which activa
73 olipase C (PLC)-gamma2, leading to prolonged Ca2+ mobilization, and increases in extracellular signal
74 tein tyrosine phosphorylation, intracellular Ca2+ mobilization, and interleukin-2 promoter-driven tra
75  acid metabolites, tyrosine phosphorylation, Ca2+ mobilization, and only inositol trisphosphate produ
76 mplicating src-tyrosine kinases, PI3-kinase, Ca2+ mobilization, and p12-LOX translocation.
77 ls, leading to Src-family kinase activation, Ca2+ mobilization, and proliferation.
78 sphate production, tyrosine phosphorylation, Ca2+ mobilization, and secretion of histamine and arachi
79 1,4,5-triphosphate production, intracellular Ca2+ mobilization, and the up-regulation of Ca2+/calmodu
80 , BAPTA, prevented AVP-induced intracellular Ca2+ mobilization, apical exocytosis, and increase of os
81 mal, indicating that both PKC activation and Ca2+ mobilization are essential for normal secretion.
82 shown to activate protein kinase G, to block Ca2+ mobilization, as well as to markedly attenuate acti
83 riphosphate, GTPase, cAMP, and intracellular Ca2+ mobilization assays of function.
84 ecific agonist and antagonist activity using Ca2+-mobilization assays in RH7777 cells expressing the
85 ulates both Src family kinase activation and Ca2+ mobilization associated with class II- and BCR-medi
86  permeabilized cells, (1,3,4,5)IP4 inhibited Ca2+ mobilization at concentrations exceeding those like
87 ion, MAPK phosphorylation, and intracellular Ca2+ mobilization but has no effect on KDR phosphorylati
88 eptide FLLRN both inhibited thrombin-induced Ca2+ mobilization but not priming.
89  of cells with heparin prevented PDGF-evoked Ca2+ mobilization but not Sr2+ entry.
90 AFR (i.e., phosphoinositide (PI) hydrolysis, Ca2+ mobilization) but not by FR or CXCR1.
91 K was insensitive to selective inhibitors of Ca2+ mobilization, but it was blocked upon phospholipase
92                       Blocking intracellular Ca2+ mobilization by BAPTA-AM or thapsigargin did not in
93 XCR2, stimulation of 331T cross-desensitized Ca2+ mobilization by both FR and C5aR.
94                                          The Ca2+ mobilization by Edg2 and Edg4 was further character
95  toxin almost completely blocked LPA-induced Ca2+ mobilization by Edg2 but only partially blocked tha
96 ylation but not cross-desensitization of its Ca2+ mobilization by fMLP or C5a, indicating an inhibito
97 phosphorylation and cross-desensitization of Ca2+ mobilization by FR, C5aR, and PAFR.
98 tes could function as a negative feedback on Ca2+ mobilization by inhibiting inositol 1,4,5-trisphosp
99  has recently been shown that NAADP mediates Ca2+ mobilization by insulin in human pancreatic beta-ce
100 t of membrane ion channels and intracellular Ca2+ mobilization by internal stores.
101           In contrast, little is known about Ca2+ mobilization by nicotinic acid adenine dinucleotide
102                          In sea urchin eggs, Ca2+ mobilization by nicotinic acid adenine dinucleotide
103                              In neutrophils, Ca2+ mobilization by the CXCR2-specific chemokine, growt
104 of inositol phosphates and the inhibition of Ca2+ mobilization by the phospholipase C inhibitor U7312
105                                Inhibitors of Ca2+ mobilization (Ca(2+)-free medium, thapsigargin [inh
106 C), inhibiting agonist-induced intracellular Ca2+ mobilization ([Ca2+]i).
107 1,4,5-triphosphate production, intracellular Ca2+ mobilization, CaMKII activity, filamin phosphorylat
108  alone and in all pairwise combinations, for Ca2+ mobilization, cAMP synthesis, phosphorylation of ma
109 ls and mediated phosphoinositide hydrolysis, Ca2+ mobilization, chemotaxis, and secretion.
110                                IP3R-mediated Ca2+ mobilization control hCPC growth and their regenera
111 appear to act upstream of phospholipase C in Ca2+ mobilization, decreased the SP-A-induced rise in MR
112 lpha-induced extracellular acidification and Ca2+ mobilization demonstrating functional antagonism.
113                         Thus, PAR-2-mediated Ca2+ mobilization desensitizes by irreversible receptor
114  phospholipase C-gamma (PLC-gamma), internal Ca2+ mobilization does not play a significant role in th
115 03 cells was unable to alter TRAP-stimulated Ca2+ mobilization either before or after suppression of
116 how that the Gbeta5-RGS7 complex can inhibit Ca2+ mobilization elicited by muscarinic acetylcholine r
117 vations that followed the quantal pattern of Ca2+ mobilization, even at the level of individual mitoc
118                 Examination of intracellular Ca2+ mobilization events revealed that the ability to tr
119 ls expressing SHP-1 (C453S) showed increased Ca2+ mobilization, extracellular signal-regulated kinase
120 , Ly-49D(R54L) transfectants fail to mediate Ca2+ mobilization following Ab cross-linking.
121 ndins act directly to impair agonist-induced Ca2+ mobilization following endotoxin exposure; however,
122 s in [Ca2+]i were shown to be the product of Ca2+ mobilization from caffeine/ryanodine-sensitive intr
123 ion of Gq-protein coupled receptors triggers Ca2+ mobilization from internal stores.
124 ication of pharmacological agents that alter Ca2+ mobilization from intracellular stores and experime
125 single PAC1 receptor variant responsible for Ca2+ mobilization from intracellular stores and influx t
126 in in the presence of 2.5 mmol/l Ca2+, while Ca2+ mobilization from intracellular stores was partiall
127 fter an initial hyperpolarization induced by Ca2+ mobilization from the endoplasmic reticulum (ER), t
128 ell type, namely cyclic ADP-ribose-dependent Ca2+ mobilization from the sarcoplasmic reticulum via ry
129 ncoupler or ionophore applied after complete Ca2+ mobilization from the SR/ER.
130 ine vasopressin 10(7) mol/L; and studied for Ca2+ mobilization, glycoprotein IIb/IIIa activation, and
131 These distinct receptor-specific patterns of Ca2+ mobilization imply significantly different roles fo
132          Finally, PKA enhanced InsP3-induced Ca2+ mobilization in a range of permeabilized cell types
133                               STCP-1 induces Ca2+ mobilization in a small percentage of primary activ
134 e have examined Mg2+ mobilization as well as Ca2+ mobilization in B cells undergoing Fas-initiated ap
135  In conclusion, muscarinic receptor-mediated Ca2+ mobilization in cultured hippocampal neurones shows
136 ed GTPase activity in platelet membranes and Ca2+ mobilization in cultured human smooth muscle cells
137 e (fMLP), was able to specifically attenuate Ca2+ mobilization in human phagocytes induced by SAA, bu
138 y the fact that GA was incapable of inducing Ca2+ mobilization in insect cells transfected with the t
139 me plasma membrane patch can be activated by Ca2+ mobilization in intact cells and by InsP3 in excise
140 complex down-regulated the TCR-CD3-increased Ca2+ mobilization in Jurkat cells.
141 al mechanism of cAMP-dependent inhibition of Ca2+ mobilization in megakaryocytes appears to be by inh
142         The chemokine STCP-1 does not induce Ca2+ mobilization in monocytes, dendritic cells, neutrop
143 examined the role of mu-opioid receptors and Ca2+ mobilization in morphine-induced astrocyte developm
144 , the peptide SFLLRN and trypsin, stimulated Ca2+ mobilization in RBL-2H3 cells but did not cause pri
145 igher G protein activation and a more robust Ca2+ mobilization in RBL-2H3 cells expressing carboxyl t
146 nd thrombin receptor and caused little or no Ca2+ mobilization in RBL-2H3 cells, effectively primed t
147    Interestingly, mPAFR mediated a sustained Ca2+ mobilization in response to PAF and was more active
148 cant fraction of the Plcg1(-/-) cells showed Ca2+ mobilization in response to PDGF, suggesting that t
149 otonin secretion, and impaired intracellular Ca2+ mobilization in response to several agonists.
150 ovoke increased NF-AT gene transcription and Ca2+ mobilization in the absence of Wnt stimulation.
151 c agonist phenylephrine was unable to induce Ca2+ mobilization in the isolated NPE and failed to do s
152                                          The Ca2+ mobilization in the NPE, in contrast, remained unch
153                            Subsequently, the Ca2+ mobilization in the Pe in response to the brimonidi
154 7FD, we examined TCR-triggered intracellular Ca2+ mobilization in the two clones.
155 l images were used to simultaneously monitor Ca2+ mobilization in the two distinct, apically joined c
156 kinase, mitogen-activated protein kinase, or Ca2+ mobilization in this response.
157 otoxin would impair agonist-induced calcium (Ca2+) mobilization in rat mesangial cells, owing to the
158 sequences for HASMCs, such as inhibition of [Ca2+] mobilization in response to thrombin stimulation.
159  to various signaling mechanisms involved in Ca2+ mobilization, including inhibition or activation of
160 centration of TR agonist was increased, peak Ca2+ mobilization increased, but influx of extracellular
161  resulted in mouse DAP12 phosphorylation and Ca2+ mobilization, indicating that Ly49P is a competent
162                                              Ca2+ mobilization induced by guanosine triphosphate (GTP
163 tudinal layer, however, the initial steps in Ca2+ mobilization involve activation of cytosolic PLA2 (
164 system, we now show that P2Y receptor-evoked Ca2+ mobilization is controlled by membrane voltage in a
165   Tyrosine phosphorylation of PLC-gamma2 and Ca2+ mobilization is markedly attenuated in SLP-76-defic
166 jection of the Ca2+ chelator BAPTA show that Ca2+ mobilization is necessary and sufficient for LTS in
167 illations in the IMCD and that intracellular Ca2+ mobilization is required for exocytotic insertion o
168 ble cells, in which the primary mechanism of Ca2+ mobilization is through (1,4,5)IP3-dependent Ca2+ r
169 by Edg4, which suggests that Edg2 transduces Ca2+ mobilization largely through pertussis toxin-sensit
170                  These findings suggest that Ca2+ mobilization may be one of the first signaling even
171                                              Ca2+ mobilization mediated by neurotensin receptors is a
172 receptors for LPA allowed examination of the Ca2+ mobilization mediated specifically by each subtype.
173 h phorbol ester, which reduced the extent of Ca2+ mobilization occurring in response to the hormone.
174 n desensitization of delta-receptor-mediated Ca2+ mobilization, one of which includes PKC.
175 s, ligand activation of CXCR7 does not cause Ca2+ mobilization or cell migration.
176 and for FPRL1, it was not reported to induce Ca2+ mobilization or chemotaxis in FPRL1-transfected cel
177  able to mediate growth factor activation of Ca2+ mobilization or inositol 1,4,5-trisphosphate (IP3)
178 ontrast, P2UR function, as assayed by either Ca2+ mobilization or inositol trisphosphate generation,
179 horylation events correlates with a distinct Ca2+ mobilization pattern that characterizes APL-stimula
180  mediate G-protein activation, intracellular Ca2+ mobilization, phosphoinositide (PI) hydrolysis, and
181 d G(12/13) proteins leading to intracellular Ca2+ mobilization, PKC activation and regulation of the
182              Importantly, the O2*--triggered Ca2+ mobilization preceded a loss in mitochondrial membr
183 eptor-mediated uncoupling of Ca2+ entry from Ca2+ mobilization provides an effective control mechanis
184  mutant failed to reconstitute TCR-dependent Ca2+ mobilization, Ras activation, CD69 expression and N
185  mediate KDR signaling such as intracellular Ca2+ mobilization rather than Flt-1-induced CDC42 activa
186 M4b is activated following receptor-mediated Ca2+ mobilization, representing a regulatory mechanism t
187 dless of this, CD45-negative cells exhibited Ca2+ mobilization responses that were greatly diminished
188 d for normal phosphoinositide hydrolysis and Ca2+ mobilization responses.
189 bits rectificatory behaviour with respect to Ca2+ mobilization; responses originating within the NPE
190  in SHR VSMCs showed a greater dependence on Ca2+ mobilization, since chelation of intracellular Ca2+
191 PKA) by cAMP did not result in inhibition of Ca2+ mobilization stimulated by PAF.
192                                     Finally, Ca2+ mobilization studies reveal a difference between tr
193  observed in extracellular and intracellular Ca2+ mobilization studies.
194 ospholipase C (Plc)gamma2 but independent of Ca2+ mobilization, suggesting that the target of BCR sti
195 requires the presence of rapid intracellular Ca2+ mobilization that might also explain the selective
196 e proteins may account for the disruption of Ca2+ mobilization that occurs in models of acute pancrea
197 gin produced relatively stringent degrees of Ca2+ mobilization that produced an endoplasmic reticulum
198 he first time, that independent of cytosolic Ca2+ mobilization, there is augmentation of eNOS activit
199 l-dependent alterations in the ability of SR Ca2+ mobilization to contribute to contractile activatio
200 tein-independent signal that synergizes with Ca2+ mobilization to induce CCL2 production.
201  with CXCR1, IL-8 (CXCL8) cross-desensitized Ca2+ mobilization to PAF by all the receptors but only P
202                          Despite the reduced Ca2+ mobilization, translocation of cytoplasmic NF-ATc t
203  precursors, CD19 ligation does not activate Ca2+ mobilization until the pre-B cell stage of developm
204 oncentration required to induce half-maximal Ca2+ mobilization was 0.14 microM for Ins(1,4,5)P3, 1.8
205                     Blocking either phase of Ca2+ mobilization was cytoprotective, highlighting PLC-g
206                          Thus, intracellular Ca2+ mobilization was hardly detected under the conditio
207            Rapid and transient intracellular Ca2+ mobilization was induced in monocytes by IL-12-indu
208 entation of tert-butyl hydroperoxide-induced Ca2+ mobilization was inhibited by pretreatment with the
209 ct of uPAR cross-linking, and uPAR-triggered Ca2+ mobilization was not blocked by anti-CR3 mAbs.
210         However, unlike TRH and AII actions, Ca2+ mobilization was not coupled to Ca2+ influx during
211 a2+, while a distinct level of intracellular Ca2+ mobilization was readily detected under the conditi
212 roduction and proliferation, and the peak of Ca2+ mobilization was reduced although of normal duratio
213 f the uniporter during IP3 receptor-mediated Ca2+ mobilization, we established novel methods.
214 tol phosphate accumulation and intracellular Ca2+ mobilization were determined for both receptors.
215  Rho-family GTP-GDP exchange factor Vav, and Ca2+ mobilization were enhanced, whereas tyrosine phosph
216 e properties of muscarinic receptor-mediated Ca2+ mobilization were investigated in hippocampal cultu
217 ctivated kinases, phospholipase Cgamma-1 and Ca2+ mobilization, were not affected in Cbl-b(-/-) T cel
218  and phospholipase C-dependent intracellular Ca2+ mobilization when it is expressed in HEK 293 cells.
219 A levels, BCR down-regulation occurs through Ca2+ mobilization, whereas IL-4R down-regulation occurs
220 fMLP and C5a as determined by chemotaxis and Ca2+ mobilization, whereas mature DCs (mDCs) respond to
221 scarinic agonists elevate cGMP by triggering Ca2+ mobilization, which activates NO synthase to produc
222 receptor (Ki = 0.78 nM), blocks LTB4-induced Ca2+ mobilization with an IC50 of 6.6 +/- 1.5 nM, and de
223  direct comparison of relative intracellular Ca2+ mobilization with respect to agonist dose.

 
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