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1  proteins or STIM2 overexpression results in store-operated activation of Imin channels, whereas STIM
2 terminal truncations than Orai1 in retaining store-operated activation.
3 itch the regulation of Imin channels between store-operated and store-independent modes.
4 Ca(2+) release, or SKF96365, an inhibitor of store-operated and TRPC channel-mediated Ca(2+) entry.
5      To assess the relative contributions of store-operated and voltage-gated Ca(2+) channels to this
6 ization with Orai1, the predominant membrane store operated Ca(2+) channel that cooperates with the e
7 tion in the expression of a component of the store operated Ca(2+) channel, TRPC1 blocks MTI-101 indu
8 small molecule inhibitor of Ca(2+) entry via store operated Ca(2+) entry (SOCE) channels formed by st
9                                              Store operated Ca(2+) entry (SOCE) via the Ca(2+) releas
10 IM1) and the Ca(2+) channel Orai1 as well as store operated Ca(2+) entry.
11                                              Store-operated Ca(2)(+) entry (SOCE) in skeletal muscle
12 blastoma cell line, we found that endogenous store-operated Ca(2)(+) entry (SOCE), which is critical
13 d in CD4(+) T cells, where it acted as a non-store-operated Ca(2+) channel and contributed to T cell
14  endoplasmic reticulum and activation of the store-operated Ca(2+) channel Orai1, enabling plasma-mem
15 4b closely associated with both POST and the store-operated Ca(2+) channel Orai1.
16                   Here we demonstrate that a store-operated Ca(2+) channel subunit, Orai1, is require
17                 Orai1 is a pore subunit of a store-operated Ca(2+) channel that is a major molecular
18        Here, we report that mice lacking the store-operated Ca(2+) channel, Orai1, in the brain show
19  our results demonstrate the pivotal role of store-operated Ca(2+) channel-mediated Ca(2+) influx in
20 r stromal interaction molecule 1 (STIM1) and store-operated Ca(2+) channels (e.g., the Orai1 channel)
21 es have also determined the relevant role of store-operated Ca(2+) channels (SOCC) in vascular tone r
22                                              Store-operated Ca(2+) channels (SOCs) are voltage-indepe
23                             Ca(2+) influx by store-operated Ca(2+) channels (SOCs) mediates all Ca(2+
24 Therefore, our data support the concept that store-operated Ca(2+) channels in hPECs and prostate can
25 mechanism for delivering Ca(2+) entering via store-operated Ca(2+) channels to specific target sites,
26 4P was suppressed when Ca(2+) influx through store-operated Ca(2+) channels was inhibited.
27 tive stores followed by Ca(2+) entry through store-operated Ca(2+) channels, and the latter selective
28 e acutely inhibited by YM58483, which blocks store-operated Ca(2+) channels.
29                     Both 4 and 10 elicited a store-operated Ca(2+) current I(CRAC) in patch-clamped c
30 c fluxes in SANCs, including activation of a store-operated Ca(2+) current, a reduction in L-type Ca(
31 (2+) leads to overactivation of the neuronal store-operated Ca(2+) entry (nSOC) pathway in YAC128 MSN
32 glandin D(2) increased Ca(2+) influx through store-operated Ca(2+) entry (SOCE) accompanied by the up
33                   STIM/ORAI proteins mediate store-operated Ca(2+) entry (SOCE) and drive fibro-proli
34  or deletion of both ESYT1 and ESYT2 reduced store-operated Ca(2+) entry (SOCE) and ORAI1-STIM1 clust
35 mal interaction molecule 1 (STIM1) regulates store-operated Ca(2+) entry (SOCE) and other ion channel
36 sis were dependent on TRPC4 channel-mediated store-operated Ca(2+) entry (SOCE) and sequential activa
37 ially regulates activation of STIM1-mediated store-operated Ca(2+) entry (SOCE) between cervical canc
38                                     Orai1, a store-operated Ca(2+) entry (SOCE) channel, was previous
39                                              Store-operated Ca(2+) entry (SOCE) channels are highly s
40                                              Store-operated Ca(2+) entry (SOCE) channels are importan
41  reticulum (ER) and subsequent activation of store-operated Ca(2+) entry (SOCE) channels in the plasm
42               Moreover, knockdown of two key store-operated Ca(2+) entry (SOCE) components, Orai1 and
43 1 inhibition or disease mutations potentiate store-operated Ca(2+) entry (SOCE) due to a presenilin 1
44                                              Store-operated Ca(2+) entry (SOCE) encoded by Orai1 prot
45                                              Store-operated Ca(2+) entry (SOCE) has emerged as an imp
46 el subunit, best recognized as a mediator of store-operated Ca(2+) entry (SOCE) in nonexcitable cells
47                                              Store-operated Ca(2+) entry (SOCE) into hCASMCs expressi
48                                              Store-operated Ca(2+) entry (SOCE) is a Ca(2+)-entry pro
49                                              Store-operated Ca(2+) entry (SOCE) is a major Ca(2+) inf
50                                              Store-operated Ca(2+) entry (SOCE) is a ubiquitous pathw
51                                              Store-operated Ca(2+) entry (SOCE) is a universal Ca(2+)
52 on depletion of intracellular Ca(2+) stores, store-operated Ca(2+) entry (SOCE) is activated.
53                                              Store-operated Ca(2+) entry (SOCE) is an essential proce
54 ra-2 and Mag-Fluo4) levels are decreased and store-operated Ca(2+) entry (SOCE) is inhibited, whereas
55                                              Store-operated Ca(2+) entry (SOCE) is the main Ca(2+) in
56                                              Store-operated Ca(2+) entry (SOCE) is the predominant Ca
57 on enhances extracellular Ca(2+) entry via a store-operated Ca(2+) entry (SOCE) mechanism in skeletal
58 i and fluid secretion and is mediated by the store-operated Ca(2+) entry (SOCE) mechanism.
59 al stem/progenitor cells (NSCs/NPCs) exhibit store-operated Ca(2+) entry (SOCE) mediated by Ca(2+) re
60 y been reported to play an important role in store-operated Ca(2+) entry (SOCE) mediated by ORAI and
61                                              Store-operated Ca(2+) entry (SOCE) mediates the increase
62  ER Ca(2+) level is in part monitored by the store-operated Ca(2+) entry (SOCE) system, an adaptive m
63 s, KO cells presented a notable reduction of store-operated Ca(2+) entry (SOCE) that was rescued by e
64                                              Store-operated Ca(2+) entry (SOCE) through Ca(2+) releas
65                                              Store-operated Ca(2+) entry (SOCE) through Ca(2+) releas
66                                              Store-operated Ca(2+) entry (SOCE) through Ca(2+) releas
67                                              Store-operated Ca(2+) entry (SOCE) through Ca(2+) releas
68                                              Store-operated Ca(2+) entry (SOCE) through sarcolemmal C
69 +) sensor STIM1 is crucial for activation of store-operated Ca(2+) entry (SOCE) through transient rec
70  fibrosis, 17beta-estradiol (E2) may inhibit store-operated Ca(2+) entry (SOCE) to impinge upon airwa
71 (ER) store, organizes as puncta that trigger store-operated Ca(2+) entry (SOCE) via plasmalemmal Ca(2
72                                              Store-operated Ca(2+) entry (SOCE) was blocked by the SO
73                                         This store-operated Ca(2+) entry (SOCE) was observed in appro
74   First, we discovered that RASSF4 regulates store-operated Ca(2+) entry (SOCE), a fundamental Ca(2+)
75                                              Store-operated Ca(2+) entry (SOCE), a major Ca(2+) signa
76                                              Store-operated Ca(2+) entry (SOCE), a ubiquitous mechani
77 +) levels, agonist-induced Ca(2+) increases, store-operated Ca(2+) entry (SOCE), and store-operated c
78                                              Store-operated Ca(2+) entry (SOCE), mediated by the endo
79 AT1) expression together with an increase in store-operated Ca(2+) entry (SOCE), SOCE-dependent nucle
80                                              Store-operated Ca(2+) entry (SOCE), the fundamental Ca(2
81 dulated intracellular Ca(2+) release but not store-operated Ca(2+) entry (SOCE), whereas neutrophil N
82        ORAI1 is an essential pore subunit of store-operated Ca(2+) entry (SOCE), which is a major Ca(
83 ate Orai channels at the plasma membrane for store-operated Ca(2+) entry (SOCE), while classical tran
84 ted Ca(2+) channel subunit, Orai1, underlies store-operated Ca(2+) entry (SOCE).
85 d CD95 into a cluster, eliciting a polarized store-operated Ca(2+) entry (SOCE).
86 mal interacting molecule 1 (STIM1) regulates store-operated Ca(2+) entry (SOCE).
87  Ca(2+) channel Orai1 at ER-PM junctions for store-operated Ca(2+) entry (SOCE).
88  showed decreased internal Ca(2+) stores and store-operated Ca(2+) entry (SOCE).
89  Ca(2+) entry across the plasma membrane via store-operated Ca(2+) entry (SOCE).
90 at [Ca(2+)]ER can regulate Ca(2+) influx via store-operated Ca(2+) entry (SOCE).
91 s able to activate Ca(2+) entry by enhancing store-operated Ca(2+) entry (SOCE).
92 ase co-localization of proteins required for store-operated Ca(2+) entry (SOCE).
93 lasma membrane (PM) Orai1 channels mediating store-operated Ca(2+) entry (SOCE).
94 M2 by siRNA or inhibition by G418 suppresses store-operated Ca(2+) entry and agonist-mediated Ca(2+)
95 et-derived growth factor activates canonical store-operated Ca(2+) entry and Ca(2+) release-activated
96           This activity relied on influx via store-operated Ca(2+) entry and Orai channels.
97  These dysfunctions stem from alterations in store-operated Ca(2+) entry and sarcoplasmic endoplasmic
98                 We show that hGAAP increased store-operated Ca(2+) entry and thereby the activity of
99 e with a SERCA inhibitor (thapsigargin) or a store-operated Ca(2+) entry blocker (GSK 7975 A) reverse
100 R-resident regulatory protein STIM1 triggers store-operated Ca(2+) entry by direct interaction with t
101 of the pore-forming subunit Orai1, the major store-operated Ca(2+) entry channel in platelets.
102 ently of Ca(2+) entry through the ubiquitous store-operated Ca(2+) entry channel Orai1, global Ca(2+)
103 l channel 4 (TRPC4) comprises an endothelial store-operated Ca(2+) entry channel, and TRPC4 inactivat
104                                Orai1-encoded store-operated Ca(2+) entry has recently emerged as an i
105 ped by GlaxoSmithKline, GSK-7975A, inhibited store-operated Ca(2+) entry in a concentration-dependent
106                    Additionally, we found no store-operated Ca(2+) entry in control or STIM1 overexpr
107 nflux from the extracellular medium, such as store-operated Ca(2+) entry in fibroblasts and membrane
108  suggest new therapies aiming at attenuating store-operated Ca(2+) entry in the treatment of patients
109 analysis that includes the potential role of store-operated Ca(2+) entry in these processes.
110                                              Store-operated Ca(2+) entry is a widely encountered mech
111                   The STIM1-ORAI1 pathway of store-operated Ca(2+) entry is an essential component of
112                                              Store-operated Ca(2+) entry is important for cell migrat
113 that with increasing agonist concentrations, store-operated Ca(2+) entry is mediated initially by end
114                       Our findings show that store-operated Ca(2+) entry is needed to sustain cytopla
115 tracellular stores, but depended strongly on store-operated Ca(2+) entry mechanisms.
116                                              Store-operated Ca(2+) entry mediated by STIM1 and ORAI1
117                                              Store-operated Ca(2+) entry occurs through the binding o
118 e 1 (STIM1) and Orai1, the components of the store-operated Ca(2+) entry pathway, to generate cells w
119   Intracellular Ca(2+) imaging revealed that store-operated Ca(2+) entry played a prominent role in S
120                   Our findings indicate that store-operated Ca(2+) entry regulates SGK1 expression in
121 -membrane cytosolic Ca(2+) abundances during store-operated Ca(2+) entry revealed that PMCA4 markedly
122 ated that CRF(2) expressed on MCs suppresses store-operated Ca(2+) entry signaling and MC degranulati
123 identified as a Ca(2+) sensor that regulates store-operated Ca(2+) entry through activation of the po
124                                              Store-operated Ca(2+) entry through Orai1 channels is a
125       Furthermore, Ca(2+) influx through the store-operated Ca(2+) entry triggered strong, whereas ER
126                                              Store-operated Ca(2+) entry was not detected in these ce
127                                              Store-operated Ca(2+) entry was similarly increased by o
128 ctivated calcium modulator (ORAI) 1-mediated store-operated Ca(2+) entry were found to regulate LPS-i
129 ak and that these actions are independent of store-operated Ca(2+) entry, a process that is absent in
130 brane junctions where STIM1, which regulates store-operated Ca(2+) entry, accumulates after depletion
131 STIM1) and Orai1 channels, key components of store-operated Ca(2+) entry, are selectively expressed i
132 s exploit host signaling pathways, including store-operated Ca(2+) entry, autophagy, and inflammasome
133                                              Store-operated Ca(2+) entry, essential for the adaptive
134                                              Store-operated Ca(2+) entry, involving endoplasmic retic
135 rnal Na(+) also had no significant effect on store-operated Ca(2+) entry, on cytosolic Ca(2+) oscilla
136 llular media, through a mechanism resembling store-operated Ca(2+) entry, typical of mammalian cells;
137 plasmic reticulum Ca(2+) load independent of store-operated Ca(2+) entry, we hypothesized that it con
138 erface with mitochondria; but also originate store-operated Ca(2+) entry-induced transcellular Ca(2+)
139                            Activation of the store-operated Ca(2+) entry-like Ca(2+) influx may be re
140 2+) uptake occurs through a process known as store-operated Ca(2+) entry.
141 oplasm but only transverse tubules supported store-operated Ca(2+) entry.
142 t type I fiber content but not through acute store-operated Ca(2+) entry.
143 ced ER Ca(2+) levels and, in turn, increased store-operated Ca(2+) entry.
144 ease from intracellular stores and driven by store-operated Ca(2+) entry.
145 dent contacts, however, are not required for store-operated Ca(2+) entry.
146 where it activates Orai1 channels, providing store-operated Ca(2+) entry.
147 ous septin proteins as crucial regulators of store-operated Ca(2+) entry.
148 signaling by a mechanism that is upstream of store-operated Ca(2+) entry.
149 ned by voltage-independent Ca(2+) influx via store-operated Ca(2+) entry.
150  regulates cardiac hypertrophy by triggering store-operated Ca(2+) entry.
151                  The molecular components of store-operated Ca(2+) influx channels (SOCs) in prolifer
152              Quercetin also rapidly inhibits store-operated Ca(2+) influx stimulated by thapsigargin.
153 ER-plasma membrane (PM) junctions to trigger store-operated Ca(2+) influx.
154 x, Ca(2+)-induced Ca(2+)-release (CICR), and store-operated Ca(2+) influx.
155                         Ca(2+) entry through store-operated Ca(2+) release-activated Ca(2+) (CRAC) ch
156 n immune cells, calcium entry occurs through store-operated Ca(2+) release-activated Ca(2+) (CRAC) ch
157                        Signaling through the store-operated Ca(2+) release-activated Ca(2+) (CRAC) ch
158 ated, highly calcium-selective channels: the store-operated Ca(2+) release-activated Ca(2+) (CRAC) ch
159                        ORAI1 constitutes the store-operated Ca(2+) release-activated Ca(2+) (CRAC) ch
160                          Here, we identified store-operated Ca(2+) release-activated Ca(2+) (CRAC) ch
161                                              Store-operated Ca(2+) release-activated Ca(2+) (CRAC) ch
162 o-exist endogenously in many cell types: the store-operated Ca(2+) release-activated CRAC channels an
163                                              Store-operated Ca(2+) signaling represents a major signa
164 PC) are involved in receptor-operated and/or store-operated Ca(2+) signaling.
165 d PARK14 disease locus (Pla2g6 gene) and the store-operated Ca(2+) signalling pathway.
166 chondrial, and lysosomal Ca(2+) pools and in store-operated Ca(2+) uptake in JNCL cells.
167 argin (TG), an ER Ca(2+)-ATPase blocker, and store-operated Ca(2+)-entry (SOCE).
168 sine kinases mobilizes Ca(2+) influx through store-operated Ca(2+)-release-activated Ca(2+) (CRAC) ch
169 equired entry of extracellular Ca(2+)through store-operated Ca(2+)channels.
170         We demonstrate that sigma1Rs inhibit store-operated Ca(2+)entry (SOCE), a major Ca(2+)influx
171 itates slow Ca(2+)-dependent inactivation of store-operated Ca(2+)entry (SOCE).
172                                          The store-operated Ca(2+)entry-associated regulatory factor
173 cking either Nox2 or Stim1 failed to trigger store-operated Ca2+ entry (SOCe) and NFAT nuclear accumu
174                           Application of the store-operated Ca2+ entry (SOCE) blockers BTP2 (10 mum)
175 c Ca2+ activity ([Ca2+](i)), accomplished by store-operated Ca2+ entry (SOCE) involving the pore-form
176                                              Store-operated Ca2+ entry (SOCE) is the major route of C
177 ellular Ca2+ concentrations are regulated by store-operated Ca2+ entry (SOCE) through Ca2+ release-ac
178 (CRAC) channel genes ORAI1 and STIM1 abolish store-operated Ca2+ entry (SOCE), and patients with thes
179 ed cytosolic signals is based on attenuating store-operated Ca2+ entry (SOCE).
180        A common mechanism for Ca2+ influx is store-operated Ca2+ entry (SOCE).
181 plays an essential role in the activation of store-operated Ca2+ entry (SOCE).
182       Although lowering Stim1 levels reduces store-operated Ca2+ entry and inhibits intestinal epithe
183                                              Store operated calcium entry (SOCE) is thought to primar
184  et al. present compelling evidence that the store-operated calcium (Ca2+) channel Orai1 sustains Th1
185 ied the interaction between calreticulin and store-operated calcium (Ca2+) entry (SOCE) machinery in
186 ude of currents similar to those ascribed to store-operated calcium (SOC) channels, particularly thos
187  synaptotoxic enhancement of STIM2-dependent store-operated calcium (SOC) entry.
188                               TRPM7 is not a store-operated calcium channel.
189                                              Store-operated calcium channels (SOCs) are calcium-selec
190 , the model shows that calcium entry through store-operated calcium channels is critical for calcium
191 ceptors (TCRs) followed by calcium entry via store-operated calcium channels.
192 e have previously demonstrated that neuronal store-operated calcium entry (nSOC) in hippocampal neuro
193 d in an increase in cell proliferation rate, store-operated calcium entry (SOCE) amplitude, cationic
194 um-dependent signaling pathways initiated by store-operated calcium entry (SOCE) are known to regulat
195              In the present study, we report store-operated calcium entry (SOCE) as a novel target of
196                 Our previous studies implied store-operated calcium entry (SOCE) as the major pathway
197                                              Store-operated calcium entry (SOCE) by calcium release a
198 ion of ATLs alters ER morphology and affects store-operated calcium entry (SOCE) by decreasing STIM1
199 elease and were attenuated by inhibiting the store-operated calcium entry (SOCE) channel Orai1.
200                     We hypothesized that the store-operated calcium entry (SOCE) channel, Orai1, part
201 e measured resting intracellular calcium and store-operated calcium entry (SOCE) in fast- and slow-tw
202 M1-deficient murine neutrophils show loss of store-operated calcium entry (SOCE) in response to both
203                                              Store-operated calcium entry (SOCE) is important in the
204                                              Store-operated calcium entry (SOCE) is involved in vario
205                                              Store-operated calcium entry (SOCE) is the mechanism by
206                                              Store-operated calcium entry (SOCE) is the predominant C
207                Transcriptional regulation by Store-operated Calcium Entry (SOCE) is well studied in n
208                                By inhibiting store-operated calcium entry (SOCE) or voltage-gated Ca(
209  relaxation required Ca(2+) flux through the store-operated calcium entry (SOCE) pathway and accompan
210                                          The store-operated calcium entry (SOCE) pathway is an import
211                                              Store-Operated Calcium Entry (SOCE) plays key roles in c
212     Despite recent advances in understanding store-operated calcium entry (SOCE) regulation, the fund
213 4-mediated depletion of ER calcium activates store-operated calcium entry (SOCE) through activation o
214 her major source of [Ca(2+)]cyt elevation is store-operated calcium entry (SOCE) through plasmalemmal
215 more, pharmacological studies suggested that store-operated calcium entry (SOCE), a calcium refilling
216 ic Ca(2+) concentrations in GC cells through store-operated calcium entry (SOCE), and then mediated C
217         Sustained Ca(2+) signaling, known as store-operated calcium entry (SOCE), occurs downstream o
218  initiated in immune cells by the process of store-operated calcium entry (SOCE), where receptor acti
219  such as excitation-contraction coupling and store-operated calcium entry (SOCE).
220 ly conserved Calcium influx pathway known as store-operated calcium entry (SOCE).
221 1) is a Ca(2+) sensor protein that initiates store-operated calcium entry (SOCE).
222                     This mechanism is called store-operated calcium entry (SOCE).
223 hannel that has been considered as a part of store-operated calcium entry (SOCE).
224 lar calcium and the subsequent activation of store-operated calcium entry (SOCE).
225 eptor potential melastatin 7 (TRPM7) reduces store-operated calcium entry (SOCE).
226                                       During store-operated calcium entry activation, calcium depleti
227                           Interestingly, the store-operated calcium entry channel inhibitor (SK&F9636
228 ndoplasmic reticulum calcium release-induced store-operated calcium entry contributes to intracellula
229 n vitro, TMEM16A is required for EGF-induced store-operated calcium entry essential for pancreatic ca
230 gated PPZ is based on activation of neuronal store-operated calcium entry in spines.
231                         Calcium flux through store-operated calcium entry is a central regulator of i
232  of an additional level in the regulation of store-operated calcium entry pathways.
233  identify the molecular mechanism underlying store-operated calcium entry that replenishes ER stores
234 ionally, the calcium-replenishing process of store-operated calcium entry was impaired in MFN2 knockd
235 represent the primary pathway for so-called "store-operated calcium entry" - the cellular entry of ca
236          We show that STIM1, an activator of store-operated calcium entry, regulates the dynamics of
237 ulum calcium activates STIM1/Orai1-dependent store-operated calcium entry.
238 e result of an acute loss of Orai1-dependent store-operated calcium entry.
239 ai proteins constitute the core machinery of store-operated calcium entry.
240 nd 2 (STIM1 and STIM2) are key modulators of store-operated calcium entry.
241 nctioning to sustain calcium signals through store-operated calcium entry.
242           Our results indicate that the P2Y6/store-operated calcium entry/IL-8 axis is involved in MS
243 om spines depends on STIM2-mediated neuronal store-operated calcium influx (nSOC) and continuous acti
244 ading to depletion of calcium ion stores and store-operated calcium influx.
245                The two key components of the store-operated calcium release-activated calcium channel
246 f a new immunomodulatory drug inhibiting the store-operated calcium release-activated calcium channel
247 d ER Ca(2+) store release, possibly engaging Store Operated cAMP Signaling (SOcAMPS) and activating C
248 STIM1 and STIM2 and their different roles in store-operated channel activation are indicative of an a
249  enhancement of SOCE activities sensitive to store-operated channel inhibitors (SKF-96365 and BTP2) a
250 sed diastolic [Ca(2+)]i, which is blunted by store-operated channel inhibitors.
251 linked to SOCE, without TRPM7 representing a store-operated channel itself.
252 , we show that pharmacological inhibition of store operated channels or reduction in the expression o
253                          In other cell types store-operated channels (SOC) have been shown to contrib
254 asmic reticulum (SR) Ca(2+) stores activates store-operated channels (SOCs) composed of canonical tra
255 lls (VSMCs), activation of Ca(2+) -permeable store-operated channels (SOCs) composed of canonical tra
256 or potential channel 1 (TRPC1) protein-based store-operated channels (SOCs) mediates Ca(2+) entry pat
257 t receptor potential channel 1 (TRPC1)-based store-operated channels (SOCs) mediates Ca(2+) entry pat
258 or potential channel 1 (TRPC1) protein-based store-operated channels (SOCs) mediates Ca(2+) entry pat
259 POINTS: Depletion of Ca(2+) stores activates store-operated channels (SOCs), which mediate Ca(2+) ent
260         Depletion of Ca(2+) stores activates store-operated channels (SOCs), which mediate Ca(2+) ent
261                                     Both the store-operated channels and the store-independent arachi
262 critically dependent on Ca(2+) entry through store-operated channels but do not depend strongly on Ca
263 ltage-gated channels are less important than store-operated channels in the control of airway smooth
264 alcium sensor that initiates the assembly of store-operated channels, and the calcium-independent pho
265 endoplasmic reticulum (ER) Ca(2+) sensor for store-operated channels.
266 TIM2 differ in the ability to activate these store-operated channels; Imin channels are regulated by
267 s signalling power; Ca(2+) microdomains near store-operated CRAC channels in the plasma membrane and
268 ur findings demonstrate that Ca2+ influx via store-operated CRAC channels is essential for CaCC activ
269 ent potassium channels (K(ATP)) or an inward store-operated current (SOC).
270 ses, store-operated Ca(2+) entry (SOCE), and store-operated currents (ISOC) are largely enhanced in t
271   On the other hand, many cell types display store-operated currents different from CRAC.
272 contribute to enhanced SOCE and differential store-operated currents in tumor cells, whereas ORAI2 an
273 e-activated Ca(2+) (CRAC) channel, mediating store-operated currents.
274 effect of NCLX activity on Ca(2+) influx via store-operated entry.
275 aracterized by exquisite Ca(2+) selectivity, store-operated gating, and distinct pore properties and
276                                        Last, store-operated influx, evoked by ER depletion, was remov
277                   Furthermore, generation of store-operated interactions between PIP(2) and TRPC1 and
278 clear whether STIM2 is capable of regulating store-operated non-CRAC channels.
279  hypothesis that pharmacological blockade of store-operated or Ca(2+) release-activated Ca(2+) channe
280 y, these structural requisites were found in store-operated Orai channels.
281 be activated by Ca(2+) nanodomains near open store-operated Orai1 and voltage-gated Ca(2+) channels i
282                                              Store-operated Orai1 channels are a major mechanism for
283 lular Ca(2+) that accompanies the opening of store-operated Orai1/CRAC channels.
284                                 In addition, store-operated PIP(2) and TRPC1 interactions were blocke
285  (shRNA) and absent in TRPC1(-/-) cells, and store-operated PKC phosphorylation of TRPC1 was inhibite
286                                              Store-operated PKC phosphorylation of TRPC1 was reduced
287 quires protein kinase C (PKC) activity, with store-operated PKC-dependent phosphorylation of TRPC1 es
288  SOCs, and U73122 and GF109203X also reduced store-operated PKC-dependent phosphorylation of TRPC1 pr
289 ation of TRPC1-based SOCs and highlight that store-operated PKCdelta activity is obligatory for chann
290 patients reveals a significant deficiency in store-operated PLA2g6-dependent Ca(2+) signalling, which
291 PLCbeta1 with small hairpin RNA reduced both store-operated PLC activity and stimulation of TRPC1 SOC
292                                    Moreover, store-operated PLCbeta1 activity measured with the fluor
293                       Here, we show that the store-operated response in Muller cells, radial glia tha
294          By characterizing the properties of store-operated signaling pathways in Muller cells, these
295  in VSMCs, and a novel role for STIM1, where store-operated STIM1-TRPC1 interactions stimulate Galpha
296  VSMCs, and a novel role for STIM1, in which store-operated STIM1-TRPC1 interactions stimulate PLCbet
297                                              Store-operated TRPC1 channel activity was inhibited by T
298                                              Store-operated TRPC1 channel and PLCbeta1 activities wer
299                                              Store-operated TRPC1 channels were identified by their e
300                                              Store-operated whole-cell cation currents were blocked b

 
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