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1 n mice and was associated with TRPC-mediated Ca2+ entry.
2 sm of activation of ICRAC and store-operated Ca2+ entry.
3 he store-operated mode of receptor-activated Ca2+ entry.
4  the plasma membrane to allow store-operated Ca2+ entry.
5 ellular calcium and on the driving force for Ca2+ entry.
6 uent stimuli eliciting action potentials and Ca2+ entry.
7 minant suppression of Tg- and OAG-stimulated Ca2+ entry.
8 on of IP3BPs had no effect on store-operated Ca2+ entry.
9 in HEK293 cells modestly enhanced TG-induced Ca2+ entry.
10 el paradigm for feedback control of cellular Ca2+ entry.
11  S2 cells significantly reduced TG-dependent Ca2+ entry.
12  DT40 B-cells, which expresses both forms of Ca2+ entry.
13 roepithelial cells are markedly dependent on Ca2+ entry.
14 , consistent with the coupling hypothesis of Ca2+ entry.
15 ation of L-type channels as the mediators of Ca2+ entry.
16 F96365 two antagonists of agonist-stimulated Ca2+ entry.
17 nt of the permeability response dependent on Ca2+ entry.
18 e GABA synapses, where DA acts by decreasing Ca2+ entry.
19  by regulating the process of store-operated Ca2+ entry.
20 ondary activation of L-type voltage-operated Ca2+ entry.
21 he antibody blocked thrombin- or IP3-induced Ca2+ entry.
22 g acidification that was highly dependent on Ca2+ entry.
23 sumably via the regulation of store-operated Ca2+ entry.
24 a2+ release, respectively, without affecting Ca2+ entry.
25 el Yvc1 and was independent of extracellular Ca2+ entry.
26 rization) prevented both the association and Ca2+ entry.
27 mportant pathway for synaptically controlled Ca2+ entry.
28 via a mechanism separate from store-operated Ca2+ entry.
29 e pathways exist for thapsigargin-stimulated Ca2+ entry.
30 cells exhibited Ca2+ concentration-dependent Ca2+ entry.
31  (Gd3+), partially inhibited hTRPM3-mediated Ca2+ entry.
32  carbachol further augmented hTRPM3-mediated Ca2+ entry.
33 e-sensitive Ca2+ channels and store-operated Ca2+ entry.
34  but this was not associated with subsequent Ca2+ entry.
35  through depolarization-induced increases in Ca2+ entry.
36 nduced TRPC6 knockdown significantly reduced Ca2+ entry.
37 gical inhibition of ICRAC and store-operated Ca2+ entry.
38 family of channels are involved in regulated Ca2+ entry.
39 e when O2 levels fall, causing voltage-gated Ca2+ entry.
40      We have examined whether store-operated Ca2+ entry, a common pathway for Ca2+ entry in non-excit
41 ecognition of IP3 determines agonist-induced Ca2+ entry (ACE), independent of its Ca2+ release activi
42 ma isoforms are required for agonist-induced Ca2+ entry (ACE).
43 Cs at the onset of beating (day 9) depend on Ca2+ entry across the plasma membrane (50%) whereas Ca2+
44         Phospholipase C signaling stimulates Ca2+ entry across the plasma membrane through multiple m
45                                              Ca2+ entry activates ERK indirectly, via recruitment of
46 d by mitochondria near plasmalemmal sites of Ca2+ entry acts as a modulator to upregulate the two kin
47 argin added to the external medium activated Ca2+ entry after Ca2+ store depletion, which we monitore
48  that Ca2+ release is the causal trigger for Ca2+ entry after receptor activation.
49 ased (i) Tg- and OAG-stimulated currents and Ca2+ entry and (ii) the level of endogenous TRPC1 but no
50             45Ca2+ was used to study passive Ca2+ entry and active Ca2+ efflux via the plasma membran
51 ding how G-protein-coupled receptors control Ca2+ entry and Ca2+-dependent events such as neurotransm
52 IM stoichiometry, resulting in inhibition of Ca2+ entry and Ca2+-dependent gene expression.
53 IM stoichiometry, resulting in inhibition of Ca2+ entry and Ca2+-dependent gene expression.
54 emporal isolation from those events, such as Ca2+ entry and consequent exocytosis, that are normally
55  BK channels or SR Ca2+ uptake, to promoting Ca2+ entry and contractility at term, and relate data on
56 ticotropin leads to depolarization-dependent Ca2+ entry and cortisol secretion.
57 hormonal signals to depolarization-dependent Ca2+ entry and cortisol secretion.
58 ID) syndrome are defective in store-operated Ca2+ entry and CRAC channel function.
59            Antisense TRPC3 similarly reduced Ca2+ entry and endogenous TRPC3.
60 evelopmental changes in the coupling between Ca2+ entry and exocytosis were studied in mouse inner ha
61 Sper1 is essential for depolarization-evoked Ca2+ entry and for hyperactivated movement, a key flagel
62 olarizations Ba2+ entry appeared larger than Ca2+ entry and generated similar but slower pH changes.
63  that in arterial smooth muscle steady-state Ca2+ entry and global [Ca2+]i are regulated by low-activ
64 lowering Stim1 levels reduces store-operated Ca2+ entry and inhibits intestinal epithelial repair aft
65 ther TRPV4 or AQP5 displayed greatly reduced Ca2+ entry and loss of RVD in response to hypotonicity,
66 c reticulum throughout the cell and coupling Ca2+ entry and mitochondrial Ca2+ uptake to Ca2+ release
67  channels are normally vital for presynaptic Ca2+ entry and neurotransmitter release at many central
68 ned to identify regulators of store-operated Ca2+ entry and NFAT nuclear import.
69 ed the involvement of TRPC1 in bFGF-mediated Ca2+ entry and proliferation of embryonic rat neural ste
70  leads to channel inactivation, which limits Ca2+ entry and protects against excitotoxicity.
71 tim as critical components of store-operated Ca2+ entry and showed that dOrai and its human homologue
72 ti-TRPC1 antibody inhibited the VEGF-induced Ca2+ entry and the increased endothelial permeability.
73           Here we show that thrombin-induced Ca2+ entry and the resultant AMP-activated protein kinas
74 fects on mechanisms of both Ca2+ release and Ca2+ entry and the resulting spatial and temporal aspect
75 ization, which reduces the driving force for Ca2+ entry and ultimately causes the potent suppression
76  agonist AR-R17779 while blocking the Na+ or Ca2+ entry and/or inhibiting signaling kinases.
77 endothelial cells augmented the VEGF-induced Ca2+ entry, and application of Ang1 opposed this effect.
78 tore-operated Ca2+ entry (SOC), capacitative Ca2+ entry, and Ca2+ release-activated channel opening (
79 propagation of [Ca2+]c waves, store-operated Ca2+ entry, and mitochondrial Ca2+ uptake, we used two I
80 res or 1-oleoyl-2-acetyl-sn-glycerol-induced Ca2+ entry, and significantly blocks an inward cation cu
81                        The cationic current, Ca2+ entry, and transendothelial electrical resistance d
82 ovide inotropic support through reverse-mode Ca2+ entry, and/or deplete intracellular Ca2+ stores.
83  cell size and limited to cells with similar Ca2+ entry (approximately 150 x 10(6) Ca2+ ions/pF cell
84 ellular stores, but their roles in mediating Ca2+ entry are unclear.
85  release from internal stores and persistent Ca2+ entry at the plasma membrane.
86 ns if they were briefly depolarized to allow Ca2+ entry before stimulation.
87  in NHK and M-1 cells that were treated with Ca2+ entry blockers allowed cAMP activation of the B-Raf
88                    Nevertheless, OAG-induced Ca2+ entry bore the hallmarks of TRPC6 function; it was
89 PM2 short variant (TRPM2-S) in mediating the Ca2+ entry burst required for induction of endothelial c
90  Inactivation of Ca-channels will also limit Ca2+ entry, but it remains unclear whether G-proteins ca
91  Neither phase of HPV requires voltage-gated Ca2+ entry, but SOCE contributes to phase 2.
92     However, activation of receptor-operated Ca2+ entry by oleoyl-2-acetyl-sn-glycerol, the membrane
93  membrane of stomatal guard cells, promoting Ca2+ entry by shifting the voltage-sensitivity of the ch
94 the full-length TRPM2 enhanced H2O2-mediated Ca2+ entry, cationic current, and the transendothelial e
95 , which contribute to increased capacitative Ca2+ entry (CCE) and DNA synthesis.
96                                 Capacitative Ca2+ entry (CCE) has been speculated to contribute to Ca
97 acellular Ca2+ store depletion (capacitative Ca2+ entry, CCE) represents the preferential Ca2+ source
98 lease and the activation of "store-operated" Ca2+ entry channels is an important but so far poorly un
99 elective (ARC) channels - receptor-activated Ca2+ entry channels whose activation is entirely indepen
100             The absence of voltage-dependent Ca2+ entry channels, which emerge later, indicates that
101 idates for capacitative and non-capacitative Ca2+ entry channels.
102 g hTRPC3 in stable form, TRPC3a gave rise to Ca2+-entry channels that are not only activated by the G
103 ed proliferation of NSC progeny, reduces the Ca2+ entry component of the Cai2+ response to bFGF witho
104 + entry (deltaF(Tot)) was separated into two Ca2+ entry components, LCC-mediated (deltaF(LCC)) and NC
105 ossess the calcium-selective, store-operated Ca2+ entry current, I(SOC).
106                                    The total Ca2+ entry (deltaF(Tot)) was separated into two Ca2+ ent
107 ation of Rho kinase was elicited due to both Ca2+ entry-dependent involvement of Ca2+/calmodulin-depe
108 urrent measured by patch-clamp recording and Ca2+ entry detected by intracellular fura-2 fluorescence
109                              TRPM2-dependent Ca2+ entry did not influence the extent or time course o
110 2A) as critical components of store-operated Ca2+ entry downstream of STIM.
111 (TRPC) channels are an important pathway for Ca2+ entry during PASMC proliferation.
112  produce CDF, and such facilitation augments Ca2+ entry during stimulation by repetitive action-poten
113 ry few IP3Rs contribute substantially to the Ca2+ entry evoked by the BCR.
114 m [Ca2+] ([Ca2+]t-sys) allowed estimation of Ca2+ entry flux from the rate of decay of [Ca2+]t-sys.
115 dothelial cells, which can trigger augmented Ca2+ entry following Ca2+ store depletion.
116  membrane of endothelial cells, and triggers Ca2+ entry following store depletion and the resultant i
117 -type Ca2+ channels, conduits of presynaptic Ca2+ entry for evoked neurotransmission.
118 nsient Ca2+ release from internal stores and Ca2+ entry from extracellular compartment.
119 of STIM on other modes of receptor-activated Ca2+ entry have not been examined.
120 r thapsigargin also activated La3+-sensitive Ca2+ entry in a PKCalpha-dependent manner.
121 as bursting electrical activity and periodic Ca2+ entry in beta-cells.
122 ay be an important contributor to pathogenic Ca2+ entry in dystrophic mouse muscle and may have impli
123 nd thereby activates store depletion-induced Ca2+ entry in endothelial cells.
124  proposed to be essential for store-operated Ca2+ entry in endothelial cells.
125                         Isotretinoin reduced Ca2+ entry in HaCaT cells and decreased survival of HaCa
126  of these channel proteins in store-operated Ca2+ entry in HEK293 cells.
127  of STIM1 inhibited TG- or agonist-dependent Ca2+ entry in HEK293 or SH-SY5Y cells.
128 ed similar non-selective cation currents and Ca2+ entry in HSY cells.
129 tion of TRPC1 is an important determinant of Ca2+ entry in human endothelial cells.
130 ired for the epidermal growth factor-induced Ca2+ entry in human glomerular mesangial cells.
131                         A chief mechanism of Ca2+ entry in lymphocytes is through store-operated calc
132 , can each mediate store-depletion-activated Ca2+ entry in mammalian cells, our findings with hTRC3a
133 de novel evidence that SAH leads to enhanced Ca2+ entry in myocytes of small diameter cerebral arteri
134 ns is a potentially important determinant of Ca2+ entry in neurotransmission.
135 re-operated Ca2+ entry, a common pathway for Ca2+ entry in non-excitable tissue, is apparent in the s
136 itative and capacitative (or store-operated) Ca2+ entry in nonexcitable cells represents a switching
137  particularly with respect to store-operated Ca2+ entry in nonexcitable cells.
138 ated Ca2+ (CRAC) channels and store-operated Ca2+ entry in rat basophilic leukemia (RBL-2H3) cells.
139 examine the potential role of store-operated Ca2+ entry in regulating cardiac calcineurin activation
140  (TRPC3)-expressing cells and did not affect Ca2+ entry in response to arachidonic acid.
141                               Store-operated Ca2+ entry in response to PLC-coupled receptor activatio
142 -trisphosphate receptors (IP3R), the lack of Ca2+ entry in response to receptor activation is attribu
143 c kidney (HEK) cells showed that it mediates Ca2+ entry in response to stimulation of the Gq-phosphol
144                      However, store-operated Ca2+ entry in response to the pump blocker, thapsigargin
145                      Such rhythmic dendritic Ca2+ entry in TC neurons during sleep-related firing pat
146                Thus, enhanced store-operated Ca2+ entry in the heart can regulate calcineurin-NFAT si
147  pathway in the activation of store-operated Ca2+ entry in the RBL-1 rat basophilic leukaemia cell-li
148 oA activation, indicating the requirement of Ca2+ entry in the response.
149 s work indicated that the non-store-operated Ca2+ entry in this cell type depends upon inositol trisp
150                               Store-operated Ca2+ entry induced by Ca2+ pump blockade or in response
151 ination was observed in nonneuronal cells on Ca2+ entry induced by ionomycin.
152 e taste bud and evoke depolarization-induced Ca2+ entry into a select subset of taste cells.
153  receptor- or phospholipase C (PLC)-mediated Ca2+ entry into animal cells.
154 ur previous work suggested that steady-state Ca2+ entry into arterial myocytes, and thus global [Ca2+
155 RPC3 channels, components of agonist-induced Ca2+ entry into cells.
156  poised to enhance the transduction of local Ca2+ entry into diverse signaling pathways.
157 the rapid release of neurotransmitters after Ca2+ entry into presynaptic terminals and also appears t
158 rve impulses or chemical stimulation promote Ca2+ entry into PSNTs, including nociceptors.
159  both STIM1 and STIM2 promote store-operated Ca2+ entry into T cells and fibroblasts and that STIM pr
160 versible cell depolarization and unregulated Ca2+ entry into the cell.
161                      Moreover, extracellular Ca2+ entry into the ER was evident even when intracellul
162  tube germination and elongation and blocked Ca2+ entry into the growing tip, suggesting that channel
163                    Our results indicate that Ca2+ entry into the presynaptic terminals during the act
164 otion of hyperactivated spermatozoa requires Ca2+ entry into the sperm tail by an alkalinization-acti
165 ted Ca2+ entry may be an important route for Ca2+ entry into the syncytiotrophoblast of term, but not
166 ulation of T-type Ca2+ currents and enhanced Ca2+ entry into these cells could contribute to the deve
167        One important mechanism that inhibits Ca2+ entry involves binding of G-protein betagamma subun
168                To maintain Ca2+ homeostasis, Ca2+ entry is balanced by efflux mediated by the sarcole
169           In many cell types, store-operated Ca2+ entry is manifest as a non-voltage-gated Ca2+ curre
170                               Store-operated Ca2+ entry is mediated by Ca2+ release-activated Ca2+ (C
171 tion potentials, suggesting that presynaptic Ca2+ entry is not primarily impaired.
172  to store-operated Ca2+ entry mechanism, the Ca2+ entry is preceded by activation of phospholipase C-
173 B activation, but the role of store-operated Ca2+ entry is unclear.
174               We propose that store-operated Ca2+ entry may be an important route for Ca2+ entry into
175                  Oscillating plasma membrane Ca2+ entry may play a role in generating intracellular C
176                                  As the sole Ca2+ entry mechanism in a variety of non-excitable cells
177 ossibility that Ang1 acts by inhibiting this Ca2+ entry mechanism in endothelial cells.
178                  According to store-operated Ca2+ entry mechanism, the Ca2+ entry is preceded by acti
179 2+ channels and by unknown receptor-operated Ca2+ entry mechanisms.
180 hippocampal neurons the relationship between Ca2+ entry, O2- production, and kinase activity.
181 ever, our results indicate that the elevated Ca2+ entry occurs through the reverse mode operation of
182                               Store-operated Ca2+ entry, partially attributed to transient receptor p
183 calcium (SOC) entry represents the principal Ca2+ entry pathway into nonexcitable cells.
184            In non-excitable cells, the major Ca2+ entry pathway is the store-operated pathway in whic
185 t with the hypothesis that hTRPM3 mediates a Ca2+ entry pathway that apparently is distinct from the
186                                     Multiple Ca2+ entry pathways may contribute to CREB activation in
187 t apparently is distinct from the endogenous Ca2+ entry pathways present in HEK 293 cells.
188 ays and molecular identity of the associated Ca2+ entry pathways remain unclear.
189  that STIM1 is a more universal regulator of Ca2+ entry pathways than previously thought, and appears
190             We conclude that the LCC and NCX Ca2+-entry pathways interact synergistically to trigger
191                            Agonist-activated Ca2+ entry plays a critical role in Ca2+ signalling in n
192         Initiation of this response required Ca2+ entry, primarily via TRPV1.
193 ctivation of local AMPA receptors suppresses Ca2+ entry (probably by silencing 20-40 P/Q-type channel
194 2+ signaling and reveal that LFA-1-dependent Ca2+ entry proceeds via a mechanism separate from store-
195 e roles of recently described store-operated Ca2+ entry proteins, Stim1 and Orai1.
196 h an HCV core (100 ng/mg) in vitro increased Ca2+ entry rate by approximately 2-fold.
197                               Store-operated Ca2+ entry reflects therefore a dynamic interplay betwee
198  Rho dominant-negative mutant or C3 dampened Ca2+ entry regardless of whether Ca2+ stores were emptie
199  important physiological targets to increase Ca2+ entry remain unresolved.
200                                    Sustained Ca2+ entry requires endoplasmic reticulum (ER) Ca2+ depl
201                            Receptor-operated Ca2+ entry (ROCE) and store-operated Ca2+ entry (SOCE) a
202                                The augmented Ca2+ entry secondary to TRPC1 expression may be an impor
203 of plasma membrane (PM) ion channels mediate Ca2+ entry signals triggered by the Ca2+ sensor Stromal
204 + channels are a central conduit of neuronal Ca2+ entry, so their Ca2+ feedback regulation promises w
205 been referred to variously as store-operated Ca2+ entry (SOC), capacitative Ca2+ entry, and Ca2+ rele
206 olecular components mediating store-operated Ca2+ entry (SOCE) and Ca2+ release-activated Ca2+ (CRAC)
207 x2 or Stim1 failed to trigger store-operated Ca2+ entry (SOCe) and NFAT nuclear accumulation.
208 perated Ca2+ entry (ROCE) and store-operated Ca2+ entry (SOCE) are known to be inhibited by tyrosine
209            Application of the store-operated Ca2+ entry (SOCE) blockers BTP2 (10 mum) or SKF96365 (50
210         TRPC1, a component of store-operated Ca2+ entry (SOCE) channels, is assembled in a complex wi
211  inhibitory activities toward store-operated Ca2+ entry (SOCE) in human embryonic kidney-293 cells.
212  ([Ca2+](i)), accomplished by store-operated Ca2+ entry (SOCE) involving the pore-forming ion channel
213                               Store-operated Ca2+ entry (SOCE) is activated following the depletion o
214                               Store-operated Ca2+ entry (SOCE) is likely the most common mode of regu
215                               Store-operated Ca2+ entry (SOCE) is the major route of Ca2+ influx in p
216 ncentrations are regulated by store-operated Ca2+ entry (SOCE) through Ca2+ release-activated Ca2+ (C
217 genes ORAI1 and STIM1 abolish store-operated Ca2+ entry (SOCE), and patients with these CRAC channel
218 d triad junctions and reduced store-operated Ca2+ entry (SOCE), which is likely due to uncoupled retr
219 P3-dependent Ca2+ release and store operated Ca2+ entry (SOCE).
220 ial role in the activation of store-operated Ca2+ entry (SOCE).
221 e-dependent Ca2+ channels and store-operated Ca2+ entry (SOCE).
222 ly in non-excitable cells, is store-operated Ca2+ entry (SOCE).
223 gnals is based on attenuating store-operated Ca2+ entry (SOCE).
224  mechanism for Ca2+ influx is store-operated Ca2+ entry (SOCE).
225 een calreticulin and store-operated calcium (Ca2+) entry (SOCE) machinery in megakaryocytes (Mks) fro
226                   Furthermore, the increased Ca2+ entry stimulates vigorous recruitment of convention
227             These findings indicate that the Ca2+ entry supporting [Ca2+]i oscillations in HEK293 cel
228       We have investigated the nature of the Ca2+ entry supporting [Ca2+]i oscillations in human embr
229 ansgenic mice showed abundant store-operated Ca2+ entry that was inhibited with SKF96365 but not vera
230 trical activity and depolarization-dependent Ca2+ entry, these compounds may have therapeutic potenti
231 chnique to investigate the interplay between Ca2+ entries through L-type Ca2+ channels (LCCs) and rev
232 in antagonist calmidazolium, suggesting that Ca2+ entry through alpha7 nAChRs specifically enhances s
233 re-mRNA editing at Q/R site-607, which gates Ca2+ entry through AMPA receptor channels.
234             Supralinear Ca2+ events required Ca2+ entry through AMPA receptors with a subsequent Ca2+
235 hat the transient BK current is activated by Ca2+ entry through both N- and L-type Ca2+ channels.
236 Antigen stimulation of immune cells triggers Ca2+ entry through Ca2+ release-activated Ca2+ (CRAC) ch
237                               Store-operated Ca2+ entry through calcium release-activated calcium cha
238  A fast transient BK current is activated by Ca2+ entry through high-threshold voltage-activated Ca2+
239    Mitochondrial trafficking is regulated by Ca2+ entry through ionotropic glutamate receptors, but t
240 rolonged AMPAR blockade acts through loss of Ca2+ entry through L-type Ca2+ channels to bring about a
241 ere dependent upon neural activity, external Ca2+ entry through L-type Ca2+ channels, and amplificati
242 als but requires membrane depolarization and Ca2+ entry through L-type Ca2+ channels.
243   Postsynaptic [Ca2+]i increases result from Ca2+ entry through ligand-gated channels, entry through
244 e, which permits some degree of reverse-mode Ca2+ entry through NCX1, as well as less efficient Ca2+
245                                              Ca2+ entry through NMDA receptor channels or voltage-gat
246 lso show that Reelin-induced augmentation of Ca2+ entry through NMDA receptors increases phosphorylat
247 otein kinase A (PKA)-dependent regulation of Ca2+ entry through NMDA-type glutamate receptors that wa
248 aptic plasticity--triggered, for example, by Ca2+ entry through NMDA-type glutamate receptors--only r
249 otential and, with it, the driving force for Ca2+ entry through other Ca2+-permeable pathways.
250 l, purinergic Ca2+ transients that represent Ca2+ entry through P2X receptors.
251 rom the endoplasmic reticulum (ER) activates Ca2+ entry through SOCs in the plasma membrane.
252                   Our findings indicate that Ca2+ entry through store-operated Ca2+ channels leads to
253 um (ER) stores, thereby triggering sustained Ca2+ entry through store-operated Ca2+ release-activated
254         Stimulation of immune cells triggers Ca2+ entry through store-operated Ca2+ release-activated
255 he nonselective cation channel that mediates Ca2+ entry through store-operated channels (SOCs) in hum
256                          Here we report that Ca2+ entry through store-operated CRAC (Ca2+ release-act
257 atory Ca2+ signals and specifically activate Ca2+ entry through the ARC channels fail to increase cal
258 ty, which would otherwise be overshadowed by Ca2+ entry through the host channel.
259 rthermore, we show that muscle APs depend on Ca2+ entry through the L-type Ca2+ channel EGL-19 with a
260 ardiac myocyte contractility is initiated by Ca2+ entry through the voltage-dependent L-type Ca2+ cha
261 ms controlling channel activity and coupling Ca2+ entry through these channels to cellular responses
262                      Priming the stores with Ca2+ entry through voltage dependent channels modulated
263                                  This causes Ca2+ entry through voltage-gated Ca2+ channels.
264 tracellular Ca2+ sensor to feedback-regulate Ca2+ entry through voltage-gated Ca2+ channels.
265 s downstream of the well known inhibition of Ca2+ entry through voltage-gated calcium channels.
266                                              Ca2+ entry through voltage-gated channels, activated by
267                                              Ca2+ entry through voltage-gated L-type Ca2+ channels tr
268                            We also show that Ca2+ entry through xCNGCs is required to mediate the rep
269 ction may be a general mechanism for linking Ca2+ entry to enhanced kinase activity and therefore to
270 s a voltage-gated Ca2+ channel that controls Ca2+ entry to mediate the hyperactivated motility needed
271 ciated with this induction in store-operated Ca2+ entry, TRPC3 transgenic mice showed increased calci
272 brane potential to negative potentials where Ca2+ entry via I(CatSper) is maximized.
273 endoplasmic reticulum stores, and subsequent Ca2+ entry via lanthanum-sensitive store-operated Ca2+ c
274                          To test the role of Ca2+ entry via NCX during ischemia and reperfusion, we s
275                              Consistent with Ca2+ entry via NCX during ischemia, we found that hearts
276 ischemia-reperfusion injury, suggesting that Ca2+ entry via reverse-mode NCX is a major cause of isch
277  borate, which suggests that they are due to Ca2+ entry via store-operated channels.
278 nel blockade and is essential for subsequent Ca2+ entry via the L-type Ca2+ channel.
279 LC)-IP3 pathway that activates extracellular Ca2+ entry via the plasmalemmal store-operated channel t
280         We further showed that Rho-activated Ca2+ entry via TRPC1 is important in the mechanism of th
281 elial permeability through the activation of Ca2+ entry via TRPM2.
282 len, as well as the absence of swelling when Ca2+ entry was abolished, indicate an essential role for
283                                              Ca2+ entry was associated with a distinct nonselective c
284                     Importantly, OAG-induced Ca2+ entry was blocked by the potent L-type Ca2+ channel
285 l, compared with the wild-type channel, when Ca2+ entry was normalized to cell size and limited to ce
286                               Although total Ca2+ entry was slightly larger for the synprint deletion
287                               Store-operated Ca2+ entry was stimulated using 1 microM thapsigargin in
288 TRPC6 knockdown, whereas vasopressin-induced Ca2+ entry was suppressed by more than 50%.
289 led that thapsigargin-induced store-operated Ca2+ entry was unaffected by TRPC6 knockdown, whereas va
290 els thought to be involved in store-operated Ca2+ entry, was also studied at the mRNA and protein lev
291 genes that alter thapsigargin (TG)-dependent Ca2+ entry, we discovered a required and conserved role
292          Although the total and NCX-mediated Ca2+ entries were increased again, deltaF(Tot) did not s
293                            Trans-sarcolemmal Ca2+ entries were measured fluorometrically in myocytes
294   Phosphorylation of TRPC1 and the resulting Ca2+ entry were essential for the increase in permeabili
295     Cell volume, pHi, ATP levels and passive Ca2+ entry were not affected by CDNB.
296 ndicate that caveolae are preferred sites of Ca2+ entry when Ca2+ stores in the endoplasmic reticulum
297 ectively blocked hormone secretion distal to Ca2+ entry, whereas the cross-coupling to G i/o proteins
298                  Hypotonicity also activated Ca2+ entry, which was required for subsequent RVD.
299 th muscle cells, BTP2 blocked store-operated Ca2+ entry within 10 min with an IC50 of 0.1-0.3 microM.
300 d with downstream IP3-dependent plasmalemmal Ca2+ entry without affecting the release of intracellula

 
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