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1 f internal Ca(2+) stores (i.e. they are 'non-capacitative').
2 family of cation channels are candidates for capacitative and non-capacitative Ca2+ entry channels.
3                     We conclude that the non-capacitative ARC channels share, with voltage-gated Ca(2
4 erous examples of label free impedimetric or capacitative assaying of biomolecules, these are rarely
5 ly-MTAPc enabled a high faradaic (signal) to capacitative (background) current during NO electro-oxid
6                 We studied the properties of capacitative Ca 2+ entry in astrocytes by means of singl
7                We found that, in astrocytes, capacitative Ca 2+ entry is not attributable to TRPC ope
8 novel form of Ca 2+ signaling, distinct from capacitative Ca 2+ entry, which suggests a specific sign
9 Sr2+ and Ba2+ do not enter astrocytes during capacitative Ca 2+ entry.
10 a 2+ stores depletion, a phenomenon known as capacitative Ca 2+ entry.
11 ced release of Ca from internal stores or by capacitative Ca entry.
12 he animal hemisphere of the oocyte, but that capacitative Ca influx occurs over the entire oocyte mem
13 eriments were performed to determine whether capacitative Ca(2+) entry (CCE) can be activated in cani
14           Although the molecular identity of capacitative Ca(2+) entry (CCE) channels remains elusive
15 -sensitive adenylyl cyclases (ACs) depend on capacitative Ca(2+) entry (CCE) for their regulation.
16     Store-operated cation (SOC) channels and capacitative Ca(2+) entry (CCE) play very important role
17                                              Capacitative Ca(2+) entry (CCE) was enhanced in PASMCs f
18 SMCs) showed that the TRPC1 channel mediates capacitative Ca(2+) entry (CCE), but the molecular signa
19 ed cardiomyocytes suggest the involvement of capacitative Ca(2+) entry (CCE), the influx of Ca(2+) th
20 ellular calcium stores, a mechanism known as capacitative Ca(2+) entry (CCE).
21 tage-gated Ca(2+) channels, a process termed capacitative Ca(2+) entry (CCE).
22 es sustained Ca(2+) signaling dependent upon capacitative Ca(2+) entry (CCE).
23 acellular Ca(2+) stores, hence activation of capacitative Ca(2+) entry (CCE).
24 ating from intracellular pools (MHA) or from capacitative Ca(2+) entry (EHA).
25  resting B cells with specific inhibitors of capacitative Ca(2+) entry (SK&F 96365) or PKC (Go6850).
26 easuring the cytosolic Ca(2+) response after capacitative Ca(2+) entry activation and Ca(2+) dynamics
27 I of C6-2B glioma cells is regulated only by capacitative Ca(2+) entry and not by a substantial eleva
28 on was completely prevented by inhibitors of capacitative Ca(2+) entry and only partially abrogated b
29 mate colocalization of adenylyl cyclase with capacitative Ca(2+) entry channels is an intrinsic prope
30           In these cells, a modest degree of capacitative Ca(2+) entry could be discerned in the face
31                         However, the role of capacitative Ca(2+) entry in EGF-mediated Ca(2+) mobiliz
32 ly, PI(3,4,5)P(3)-sensitive Ca(2+) entry and capacitative Ca(2+) entry represent major Ca(2+) influx
33                                              Capacitative Ca(2+) entry stimulates cAMP synthesis in m
34  EHA was more sensitive to Ca(2+) influx via capacitative Ca(2+) entry than intracellular release, wh
35 xcitable cells, overwhelms the effect of any capacitative Ca(2+) entry that may occur.
36 he Ca(2+) release process from the ER or the capacitative Ca(2+) entry through the plasma membrane.
37                                Inhibition of capacitative Ca(2+) entry with EGTA or LaCl(3) or low ex
38 constrictor-stimulated Ca(2+) store release, capacitative Ca(2+) entry, and noncapacitative Ca(2+) en
39 ological processes, including store-operated capacitative Ca(2+) entry, Ca(2+)-induced Ca(2+) release
40 h domains to be susceptible to regulation by capacitative Ca(2+) entry.
41 tored the sensitivity of adenylyl cyclase to capacitative Ca(2+) entry.
42 eterologously, were regulated exclusively by capacitative Ca(2+) entry.
43  a stage downstream of ER Ca(2+) release and capacitative Ca(2+) entry.
44 blated the regulation of adenylyl cyclase by capacitative Ca(2+) entry.
45 adenylyl cyclase activity and did not affect capacitative Ca(2+) entry.
46 nt of their plasma membranes and more robust capacitative Ca(2+) entry.
47 hol and thapsigargin (Tg)) known to activate capacitative Ca(2+) entry.
48 a membrane Ca(2+) channels, a process termed capacitative Ca(2+) entry.
49  Cbeta activation, Ca(2+) store release, and capacitative Ca(2+) entry.
50         DES effectively inhibited TG-induced capacitative Ca(2+) influx in a dose-dependent manner wi
51 mycin, a mitochondrial inhibitor that blocks capacitative Ca(2+) influx in other systems.
52 ore-operated cation channels can account for capacitative Ca(2+) influx in SMC and can play an import
53 ion of intracellular Ca(2+) stores activates capacitative Ca(2+) influx in smooth muscle cells, but t
54 or activation of store-operated channels and capacitative Ca(2+) influx in wide variety of cell types
55  Ca(2+) influx via a mechanism distinct from capacitative Ca(2+) influx induced by carbachol and Tg.
56                                              Capacitative Ca(2+) influx induced by thapsigargin was a
57 ull functions of eNOS and aequorin, and that capacitative Ca(2+) influx is the principle stimulus for
58 +)](i) to levels higher than those caused by capacitative Ca(2+) influx, the LAMP assay revealed that
59 effect of DES on store-operated channels and capacitative Ca(2+) influx, we used rat basophilic leuke
60 CRAC) currents and thapsigargin (TG)-induced capacitative Ca(2+) influx.
61 lease from internal stores does not activate capacitative Ca(2+) influx.
62 upport our previous proposal that TRPCs form capacitative Ca-entry channels.
63                 In intact platelets, maximal capacitative Ca2+ and Mn2+ influx developed rapidly (wit
64                  NO (1 micromol/L) inhibited capacitative Ca2+ and Mn2+ influx independently of the t
65  and caveolae, which contribute to increased capacitative Ca2+ entry (CCE) and DNA synthesis.
66 2 overexpression results in up-regulation of capacitative Ca2+ entry (CCE) and that SKF-96365, an inh
67                                              Capacitative Ca2+ entry (CCE) has been speculated to con
68                                              Capacitative Ca2+ entry (CCE) is Ca2+ entering after sti
69 R) Ca2+ stores activates Ca2+ influx via the capacitative Ca2+ entry (CCE) pathway.
70      Local Ca2+ release caused activation of capacitative Ca2+ entry (CCE).
71 irect activation of PKC, thus generating non-capacitative Ca2+ entry alongside that evoked following
72 s, but they were robustly stimulated only by capacitative Ca2+ entry and not al all by a substantial
73  undertaken to investigate the regulation of capacitative Ca2+ entry by phorbol ester-sensitive prote
74  rise generated by ionophore, Ca2+ entry via capacitative Ca2+ entry channels was solely responsible
75 to the suggestion that adenylyl cyclases and capacitative Ca2+ entry channels were localized in the s
76 nels are candidates for capacitative and non-capacitative Ca2+ entry channels.
77 in blunting the regulation of the cyclase by capacitative Ca2+ entry defined the intimacy between the
78 d conditions were devised that distinguished capacitative Ca2+ entry from both internal release and n
79 role in the regulation of SOCs by monitoring capacitative Ca2+ entry in 3T3-like embryonic fibroblast
80 a small G protein, is linked functionally to capacitative Ca2+ entry in human embryonic kidney 293 ce
81 gous channel proteins that appear to mediate capacitative Ca2+ entry in species from worms and files
82                                 The level of capacitative Ca2+ entry in Src- cells is restored to nea
83 s been suggested that this store-mediated or capacitative Ca2+ entry is brought about by a physical a
84                    Although the mechanism of capacitative Ca2+ entry is not known, evidence suggests
85 e we provide evidence for an additional, non-capacitative Ca2+ entry mechanism in human platelets.
86  data indicate that the inhibitory action on capacitative Ca2+ entry of glucosamine is distinct from
87 ited AVP-evoked Sr2+ entry without affecting capacitative Ca2+ entry or release of Ca2+ stores.
88 es but also provide a physiological role for capacitative Ca2+ entry other than store refilling.
89 bility of T cells to maintain a high rate of capacitative Ca2+ entry over prolonged periods of >10 mi
90                                          The capacitative Ca2+ entry pathway in J774 macrophages is r
91 bition of phosphatase type 1/2A inhibits the capacitative Ca2+ entry pathway in rat thymic lymphocyte
92                             Importantly, the capacitative Ca2+ entry pathway in rat thymic lymphocyte
93 tive calcium channels (VSCCs) as well as the capacitative Ca2+ entry pathway.
94 Ca2+ influx occurs predominantly through the capacitative Ca2+ entry pathway.
95 d, phase I appears to be mainly dependent on capacitative Ca2+ entry related to release of thapsigarg
96 e was also able to reverse the inhibition of capacitative Ca2+ entry seen following other treatments
97 essed Ca2+-inhibitable adenylyl cyclase with capacitative Ca2+ entry sites but also provide a physiol
98 n of Ca(2+)-sensitive adenylyl cyclases with capacitative Ca2+ entry sites, even when expressed heter
99 ntimacy between the adenylyl cyclase and the capacitative Ca2+ entry sites.
100 ses might display the strict requirement for capacitative Ca2+ entry that is shown by the Ca(2+)-inhi
101  [Ca2+]i inhibited the ability of subsequent capacitative Ca2+ entry to further increase [Ca2+]i.
102 The present study compared the regulation by capacitative Ca2+ entry versus ionophore-mediated Ca2+ e
103 to determine whether glucosamine's effect on capacitative Ca2+ entry was also due to ATP depletion, a
104                      Selective inhibition of capacitative Ca2+ entry with Gd3+ revealed that the non-
105  concentrations of Gd3+ irreversibly blocked capacitative Ca2+ entry without affecting AVP-evoked Sr2
106  activation of store-operated Ca2+ channels (capacitative Ca2+ entry).
107 ariously as store-operated Ca2+ entry (SOC), capacitative Ca2+ entry, and Ca2+ release-activated chan
108 -induced intracellular Ca2+ store depletion (capacitative Ca2+ entry, CCE) represents the preferentia
109 y expressed, are preferentially regulated by capacitative Ca2+ entry, compared with other means of el
110 poorly understood cellular mechanism, termed capacitative Ca2+ entry, is activated [3,4]; this permit
111  cells was inhibited by two drugs that block capacitative Ca2+ entry, La3+ and SK&F 96365.
112 rom internal stores followed by a sustained, capacitative Ca2+ entry, which is mediated by store-oper
113 clopiazonic acid or carbachol also activates capacitative Ca2+ entry.
114 luorescence by Mn2+ was used as a measure of capacitative Ca2+ entry.
115 rease in the rate of Mn2+ influx, suggesting capacitative Ca2+ entry.
116 cumulation, comparable with that elicited by capacitative Ca2+ entry.
117  by 1 microM Gd3+ which completely inhibited capacitative Ca2+ entry.
118 lay an active role in modulating the rate of capacitative Ca2+ entry.
119 2+ release from intracellular stores and for capacitative Ca2+ entry.
120 tracellular Ca2+ stores and thereby activate capacitative Ca2+ entry.
121 yed attenuation of the Ca2+ signal evoked by capacitative Ca2+ entry.
122 nzoyl-S-farnesyl-S-cysteine had no effect on capacitative Ca2+ entry.
123 inin-8 was observed only during the phase of capacitative Ca2+ influx and was blocked by zero Ca2+.
124                   However, the inhibition of capacitative Ca2+ influx in the presence of glucosamine
125       Additionally, our results suggest that capacitative Ca2+ influx may be mediated by both conform
126 tiate Ca2+ signaling through activation of a capacitative Ca2+ influx pathway.
127  stores while inhibiting their refilling via capacitative Ca2+ influx that results in partial emptyin
128 ic reticulum (ER) and the channels mediating capacitative Ca2+ influx through the plasma membrane.
129 n addition, the 2dGlc-mediated inhibition of capacitative Ca2+ influx was reversed by staurosporine,
130 d by depletion of intracellular Ca2+ stores (capacitative Ca2+ influx) was enhanced 3 h after injury.
131 lgernyl-L-cysteine blocked the activation of capacitative Ca2+ influx, whereas N-benzoyl-S-farnesyl-S
132                                              Capacitative Ca2+ influx, which occurs in response to mo
133 elease of Ca2+ from intracellular stores and capacitative Ca2+ influx.
134 id induced [Ca2+]i elevation consistent with capacitative Ca2+ influx.
135 rm expression (ET-1, ET-2, and ET-3) through capacitative Ca2+ influx.
136  the actions of farnesyl-cysteine analogs on capacitative Ca2+ influx.
137                        The amplitudes of the capacitative Ca2+ signals decreased at lower extracellul
138 se of intracellular Ca2+ stores followed by "capacitative" Ca2+ entry due to emptying of these stores
139  mitochondria to modulate store-operated or "capacitative" Ca2+ entry in Jurkat leukemic T cells and
140                                              Capacitative calcium entry (CCE) describes CA2+ influx i
141                                  We examined capacitative calcium entry (CCE) in Jurkat and in L6 ske
142 on the elucidation of the molecular basis of capacitative calcium entry (CCE) into cells.
143                             In animal cells, capacitative calcium entry (CCE) mechanisms become activ
144 standing extensive efforts, the mechanism of capacitative calcium entry (CCE) remains unclear.
145 f the presenilins (PS1 and PS2) in governing capacitative calcium entry (CCE), a refilling mechanism
146 l cells stimulates proliferation by inducing capacitative calcium entry (CCE).
147  global block in T cell receptor-independent capacitative calcium entry (CCE).
148 or by intracellular calcium store depletion [capacitative calcium entry (CCE)].
149 cells also showed significant impairments in capacitative calcium entry (CCE, also known as store-ope
150 dy, we have examined the interaction between capacitative calcium entry and arachidonic acid-activate
151  and inositol 1,4,5-trisphosphate (IP(3)) in capacitative calcium entry and calcium release-activated
152 , 2-aminoethoxydiphenyl borane, blocked both capacitative calcium entry and I(crac).
153 study, we examined the influence of 2-APB on capacitative calcium entry and intracellular Ca2+ concen
154 nduced calcium transients via enhancement of capacitative calcium entry and is associated with a spat
155 ol 12-myristate 13-acetate and inhibitors of capacitative calcium entry and most likely reflects the
156 esicular trafficking could lead to decreased capacitative calcium entry and subsequent apoptosis of c
157 ears to be due, at least in part, to reduced capacitative calcium entry at the plasma membrane.
158 annel openings are completely blocked by the capacitative calcium entry blocker, 2-aminoethoxydipheny
159 al of extracellular calcium or inhibition of capacitative calcium entry by 2-APB prevented ciglitazon
160 racellular calcium stores to plasma membrane capacitative calcium entry channels.
161 of Ca(2+) stores, or entry of Ca(2+) through capacitative calcium entry channels.
162                          The potentiation of capacitative calcium entry in astrocytes or muscle cells
163 in immature B cells and they exhibit greater capacitative calcium entry in response to Ag.
164                 Trpm5 may be responsible for capacitative calcium entry in taste receptor cells that
165 n, the S170F and DeltaE9 cells showed larger capacitative calcium entry indicating a direct effect on
166 hat a discrete step in the pathway signaling capacitative calcium entry interacts with and inhibits t
167                                     That is, capacitative calcium entry is potently inhibited by arac
168 ver, influx of extracellular calcium through capacitative calcium entry may be an unrecognized compon
169  originally thought, and may involve neither capacitative calcium entry nor a role for PLA2 and arach
170                                              Capacitative calcium entry or store-operated calcium ent
171 lations occurs through the store-operated or capacitative calcium entry pathway.
172   Thus we investigated whether inhibition of capacitative calcium entry per se could reduce endoplasm
173                                         When capacitative calcium entry was blocked with Gd3+, 2-APB
174                                              Capacitative calcium entry was not altered under these c
175                                 In addition, capacitative calcium entry was potentiated severalfold b
176 -dependent or UTP dose-dependent increase in capacitative calcium entry when calcium was added to the
177 on of vesicular transport results in reduced capacitative calcium entry which in turn results in apop
178  entry is inhibited by the pre-activation of capacitative calcium entry with thapsigargin.
179 re-operated Ca(2+) influx (SOCI; also called capacitative calcium entry) in glomerular mesangial cell
180 romoter in a Jurkat T-cell line defective in capacitative calcium entry, a signaling mechanism involv
181                   2-APB was found to inhibit capacitative calcium entry, but at concentrations greate
182 fect of two well characterized inhibitors of capacitative calcium entry, Gd3+ and 2-aminoethoxydiphen
183 affect agonist-induced calcium transients or capacitative calcium entry, indicating that 4-AP effects
184 and further understand the role of hTRPC3 in capacitative calcium entry, we examined the effect of tw
185 lar trafficking as a mechanism of regulating capacitative calcium entry, we investigated whether disr
186 t mechanism for regulated entry of Ca(2+) is capacitative calcium entry, whereby depletion of intrace
187 itivity to these inhibitors is indicative of capacitative calcium entry.
188 ms of intracellular calcium oscillations and capacitative calcium entry.
189 n calcium feedback regulation of I(crac) and capacitative calcium entry.
190 acellular calcium stores, a process known as capacitative calcium entry.
191 calcium stores with regard to the control of capacitative calcium entry.
192  pancreatic acinar cells, a process known as capacitative calcium entry.
193 e plasma membrane calcium influx channels or capacitative calcium entry.
194 TRPC) are involved in agonist-stimulated and capacitative calcium entry.
195 antly greater permeability to Ba2+ than does capacitative calcium entry.
196 imulation with neurotransmitters, and during capacitative calcium entry.
197  for polyphosphoinositides for activation of capacitative calcium entry.
198 increasing basal [Ca(2+)](i) to potentiating capacitative calcium entry.
199 store loading and abrogated the desensitized capacitative calcium influx associated with bortezomib t
200                                     In BCEC, capacitative calcium influx is involved in mediating a p
201 ibiting phosphoinositide 3-kinase, impairing capacitative calcium influx, and inhibiting cyclooxygena
202 tive adenylyl cyclases detect and respond to capacitative cation entry rather than global cytosolic c
203 icinity of these enzymes as a consequence of capacitative cation entry to partially regulate both of
204  application and completely disappeared when capacitative cation influx reached its maximum.
205 influx of Ca(2+) through the plasma membrane capacitative channels.
206 eripheral plasma membrane such that a single capacitative component can account for the biophysical p
207                                    Thus, the capacitative current in cultured skeletal muscle cells w
208       The development of the skeletal muscle capacitative current was inhibited by genistein, a tyros
209 ak channel and for a channel that mediates a capacitative current.
210          These results indicate that the non-capacitative divalent cation entry pathway is regulated
211 sustained elevation of cytosolic Ca2+ due to capacitative entry is not required for induction of apop
212 an that of sup- II cells, demonstrating that capacitative entry is reduced in sup+ I cells.
213 gesting that cytosolic Ca2+ elevation due to capacitative entry may be required for optimal ER pool f
214 ionophore ionomycin, we found evidence for a capacitative entry mechanism in mouse oocytes.
215 essential for stimulation of activity by the capacitative entry of Ca(2+) in the intact cell.
216 ut was specifically dependent on the induced capacitative entry of Ca(2+).
217 bitor thapsigargin (TG) but does not prevent capacitative entry of extracellular calcium.
218 more effectively attenuated by inhibitors of capacitative entry than of L-type channels.
219 duced an accumulation of vesicles, decreased capacitative entry, and induced apoptosis.
220 e [Ca2+]i originated from internal stores or capacitative entry.
221  factor MEK1 was unaffected by inhibitors of capacitative entry.
222 ntly reduces cytosolic Ca(2+) levels under a capacitative influx model and ER re-uptake of calcium, i
223 tion of Ca2+ from internal stores triggers a capacitative influx of extracellular Ca2+ across the pla
224                                              Capacitative influx of extracellular Ca2+ was inhibited
225 e to all stimuli examined is controlled by a capacitative mechanism and sets the frequency of spiking
226 n-excitable cells is generally ascribed to a capacitative mechanism in which the activation of the en
227 a2+ entry in nonexcitable cells focus on the capacitative mechanism where entry is activated as a dow
228 f activating Ca(2+) entry via the so-called "capacitative" mechanism, recent evidence suggests that C
229 re inconsistent with current versions of the capacitative model.
230 2+) does not conform to the widely accepted "capacitative" model and, instead, reflects the activity
231 Ca(2+) entry is usually thought to occur via capacitative or store-operated Ca(2+) channels.
232                               The process of capacitative or store-operated Ca(2+) entry has been ext
233 +) influx activated by store depletion (i.e. capacitative or store-operated Ca(2+) influx).
234 ar Ca2+ into the cytoplasm, a process termed capacitative or store-operated Ca2+ entry.
235 ross the plasma membrane, a process known as capacitative or store-operated Ca2+ entry.
236      We have recently questioned whether the capacitative or store-operated model for receptor-activa
237 reciprocal regulation of noncapacitative and capacitative (or store-operated) Ca2+ entry in nonexcita
238 suppress NFAT signaling by interfering with "capacitative" or "store-operated" calcium mobilization,
239                The cells therefore express a capacitative pathway activated by empty stores and a non
240  an increase in [Ca2+]i rapidly inhibits the capacitative pathway and more slowly activates mechanism
241 ient to maximally activate Ca2+ entry by the capacitative pathway and that products of phosphatidylin
242 in cytosolic [Ca2+], confirming that the non-capacitative pathway can evoke a significant increase in
243 trations of AVP is mediated largely by a non-capacitative pathway directly regulated by arachidonic a
244 s that distinguish it from the corresponding capacitative pathway in the same cells and therefore is
245 e Ca2+ entry with Gd3+ revealed that the non-capacitative pathway is the major route for the Ca2+ ent
246  pathway activated by empty stores and a non-capacitative pathway stimulated by receptors; only the f
247 l cyclase for Ca(2+) entry occurring via the capacitative pathway to attempt to discriminate between
248                      After inhibition of the capacitative pathway with Gd3+, AVP evoked a substantial
249 ptors are required for activation of the non-capacitative pathway, because microinjection of cells wi
250 id not mediate the effects of AVP on the non-capacitative pathway.
251 tore refilling nor of desensitization of the capacitative pathway.
252 strating a rapid partial inactivation of the capacitative pathway.
253 art, on formulating a suitable model for the capacitative response of the channel and double layer at

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