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1 tic calcium release mediated by enhanced RyR calcium release.
2 es to phospholipase C-mediated intracellular calcium release.
3 lation and enhanced 5-HT2A receptor-mediated calcium release.
4 f IP3 at concentrations sufficient to induce calcium release.
5 bout the mechanism coupling NAADP binding to calcium release.
6 ontent and its more pronounced decline after calcium release.
7 (3)RII levels and therefore pro-hypertrophic calcium release.
8 ryanodine receptor by way of calcium-induced calcium release.
9 ion of PLCgamma1 and increased intracellular calcium release.
10 sitol 1,4,5-trisphosphate receptor-dependent calcium release.
11 ation, or by ionomycin-induced intracellular calcium release.
12 ven in the presence of direct stimulators of calcium release.
13 release profile and the rate of spontaneous calcium release.
14 ex is required specifically for Fas-mediated calcium release.
15 estospongin C, an inhibitor of IP3R-mediated calcium release.
16 signaling, blocked T-cell receptor-mediated calcium release.
17 hanced M3R-mediated augmentation of GSIS and calcium release.
18 acidic organelles to mediate NAADP-dependent calcium release.
19 with mutant htt and normalized intracellular calcium release.
20 as an agonist with regard to US28-stimulated calcium release.
21 large concentrations of IP3 are required for calcium release.
22 tokine-mediated suppression of functional ER calcium release.
23 is mediated by ryanodine receptor-dependent calcium release.
24 -RyRs increases the incidence of spontaneous calcium release.
25 loma cells accompanied by apoptosis-inducing calcium release.
26 found that the H2R induces Galphaq-mediated calcium release.
27 s released by the process of calcium-induced calcium release.
28 but no effect on intracellular RyR2-mediated calcium release.
29 ge changes and then triggering intracellular calcium release.
30 n, which in turn results in another abnormal calcium release.
31 to the nucleus specifically after lysosomal calcium release.
32 ,4,5-trisphosphate-dependent intra-acrosomal calcium release.
33 n of TMTC1 or TMTC2 increased the stimulated calcium released.
34 endothelial NO synthase is activated 1), via calcium release, 2), via phosphorylation reactions, and
35 nship between abnormal TATS and asynchronous calcium release, a major determinant of cardiac contract
37 ed to wild-type cells as a result of reduced calcium release activated calcium currents, and independ
38 interaction molecule 1) clustering and CRAC (calcium release activated calcium) channel activation.
39 forms a highly calcium-selective pore of the calcium release activated channel, and alpha-SNAP is nec
41 roposed as core components of store-operated calcium release-activated calcium (CRAC) and store-opera
42 membrane protein Orai forms the pore of the calcium release-activated calcium (CRAC) channel and gen
44 ORAI1 is the pore-forming subunit of the calcium release-activated calcium (CRAC) channel, a stor
45 rystal structure of Orai, the pore unit of a calcium release-activated calcium (CRAC) channel, is use
46 require long-lasting calcium influx through calcium release-activated calcium (CRAC) channels and th
48 illatory to a sustained elevated pattern via calcium release-activated calcium (CRAC)-mediated capaci
49 traps Orai1 in the PM through binding of its calcium release-activated calcium activation domain.
50 The two key components of the store-operated calcium release-activated calcium channel are the Ca(2+)
52 hich are known to be essential components of calcium release-activated calcium channel, allows entry
53 ignal mediator, ORAI1, a pore subunit of the calcium release-activated calcium channel, was identifie
57 tromal interaction molecule (STIM) 1 and the calcium release-activated calcium modulator (ORAI) 1-med
58 The stromal interaction molecule (STIM)-ORAI calcium release-activated calcium modulator (ORAI) pathw
59 phocytes express not only cell membrane ORAI calcium release-activated calcium modulator 1 but also v
60 nts, such as stromal interaction molecule 1, calcium release-activated calcium modulator 1, and trans
64 y LFA-1 facilitates the cooperation with the calcium release-activated channel Orai1 in directing loc
68 nation of specially developed cell lines and calcium release analysis hardware, has created a new and
69 e- or inositol 1,4,5-trisphosphate-dependent calcium release and abolished when both lysosomal and en
70 lacement of CGB decreases InsP(3)R-dependent calcium release and alters normal signaling patterns.
71 ulations based on a model of calcium-induced calcium release and cell-to-cell diffusion through gap j
72 ent T cells exhibited severe defects in both calcium release and dephosphorylation of nuclear factor
73 s provide insight into regulation of cardiac calcium release and how alterations to this process may
74 tment of HSG cells resulted in intracellular calcium release and induction of endocytosis at levels s
78 race that can drive temporal order-dependent calcium release and LTD induction in Purkinje cells and
79 mutation decreases sensitivity to activated calcium release and myoplasmic calcium levels, subsequen
81 evoke redistribution, even though it caused calcium release and Orai1-mediated calcium entry in the
82 n cysteine residues on intralumenal loops of calcium release and reuptake channels have been implicat
84 fects and acting to promote effects, such as calcium release and stress signaling, via intracellular
87 ent cytosolic and mitochondrial pH decrease, calcium release, and phosphorylation of stress signaling
89 eractions between synaptically and ER-evoked calcium release at glutamatergic synapses in young AD tr
90 tive enhancement of bradykinin (BDK)-induced calcium release, because of a decrease in BDK ED50 value
92 e reduction of ryanodine receptor 1 mediated calcium release but, since knocking out genes in animal
93 7,8-diol (SKF83959), found no stimulation of calcium release, but it did find a broad range of cross-
94 osed role of calsequestrin in termination of calcium release by conformationally inducing closure of
98 lts, polymer treatment reduced the amount of calcium released by 27% to 30% in comparison with the un
100 F-TrkA-dependent signaling events, including calcium release, calcineurin activation and phosphorylat
101 alcium levels upon addition to cell culture, calcium release can be determined in these cell lines up
102 in the SR lumen after depolarization-induced calcium release cause the dissociation of JP45 from CASQ
103 e mammalian ryanodine receptor intracellular calcium release channel (RyR) with high (fM) potency and
104 er-S-nitrosylation of the ryanodine receptor calcium release channel (RyR1) in skeletal muscle disrup
105 um channel directly activates opening of the calcium release channel (RyR1) in the sarcoplasmic retic
106 Ca2+ leak via the cardiac ryanodine receptor/calcium release channel (RyR2) is thought to play a role
107 le, including the cardiac ryanodine receptor/calcium release channel (RyR2) required for muscle contr
114 of the major cardiac sarcoplasmic reticulum calcium release channel/ryanodine receptor (RyR2), at Se
115 antial reduction in the expression levels of calcium release channels (ryanodine receptors, RyR2) in
116 f calcium cycling that luminal gating of the calcium release channels (RyRs) mediated by the luminal
117 d as a regulator of Ryanodine receptor (RyR) calcium release channels by serving as a SR luminal sens
118 receptors (RyRs), a family of intracellular calcium release channels essential for many cellular pro
119 d as a novel family of endolysosome-targeted calcium release channels gated by nicotinic acid adenine
120 ble progress has been made in characterizing calcium release channels in the nuclear membrane, very l
121 rons by stabilizing ryanodine receptor (RyR) calcium release channels in the open configuration, whic
122 ceptors (RyRs) form a class of intracellular calcium release channels in various excitable tissues an
127 ine receptor types 1 (RyR1) and 2 (RyR2) are calcium release channels that are highly enriched in ske
128 P2XRs regulate vacuole activity by acting as calcium release channels, activated by translocation of
129 protein that stabilizes the closed state of calcium release channels, i.e. the ryanodine receptors.
134 and functions (phagocytosis, degranulation, calcium release, chemotaxis, and reactive oxygen species
135 essed for receptor function, using assays of calcium release, chemotaxis, receptor endocytosis, and l
136 ellular calcium, implicating calcium-induced calcium release (CICR) as the novel source of the Ca(i)(
137 e regulation of regenerative calcium-induced calcium release (CICR) during Ca(2+) spark evolution rem
138 ains, suggesting an aberrant calcium-induced calcium release (CICR) effect within spines and dendrite
143 k-Y130E were deficient in antigen-stimulated calcium release, degranulation, and production of some c
144 cific for either MAPK/ERK phosphorylation or calcium release demonstrated that the two pathways conve
146 nd on a beat-to-beat basis and mitochondrial calcium release depends on mNCE activity and mitochondri
150 amic copper redistributions are dependent on calcium release, establishing a link between mobile copp
151 ayed Ca(2+) transients, frequent spontaneous calcium release events and increased susceptibility to p
154 that sphingosine is a positive regulator of calcium release from acidic stores and that understandin
155 er hypothesis for NAADP action proposes that calcium release from acidic stores subsequently acts to
156 ne Dinucleotide Phosphate (NAADP) stimulates calcium release from acidic stores such as lysosomes and
157 ged Sph leads to a significant and transient calcium release from acidic stores that is independent o
158 provide further evidence that NAADP mediates calcium release from acidic stores through activation of
159 ium storage, 1,25(OH)(2)D not only increases calcium release from bone, but also inhibits calcium inc
160 inositol 1,4,5-trisphosphate (IP3)-dependent calcium release from endoplasmic reticulum by inducing d
161 lation activates ryanodine receptor-mediated calcium release from endoplasmic reticulum stores, leadi
162 showed that the potentiation of RyR-mediated calcium release from internal stores by caffeine was abs
163 ibition of voltage-gated calcium channels or calcium release from internal stores reduces regenerativ
166 Cholinergic inhibitory responses depend on calcium release from intracellular calcium stores, and r
167 o block or enhance CICR to determine whether calcium release from intracellular stores affected actio
169 ular communication through gap junctions and calcium release from intracellular stores as mediators o
170 lso produces vasomotor responses by inducing calcium release from intracellular stores through its pr
171 protein coupled receptors (GPCRs) that cause calcium release from intracellular stores while other st
172 ) activates signaling cascades, resulting in calcium release from intracellular stores, ERK1/2 activa
173 ults demonstrate that, in addition to gating calcium release from intracellular stores, mAChR activat
178 ificantly, a specific inhibitor of apoptotic calcium release from IP3R strongly blocked lymphocyte ap
180 1a-mediated inositol phosphate formation and calcium release from mouse neurons in a PKC-dependent ma
183 aled a unique receptor-mediated mechanism of calcium release from SGs that involves SG store-operated
184 ening on SG membranes as a potential mode of calcium release from SGs that may serve to raise local c
185 r, whereas increased axon outgrowth involves calcium release from stores through IP3 receptors as wel
187 helial hyperplasia via apoptosis mediated by calcium release from the endoplasmic reticulum (ER), but
189 yR2-R4496C mutant HEK-293 cell line in which calcium release from the endoplasmic reticulum through t
191 ed CD36 function in FA uptake and FA-induced calcium release from the endoplasmic reticulum, supporti
193 as indicated by reduced RyR agonist-induced calcium release from the ER and RyR-mediated synaptic re
194 n induces endoplasmic reticulum (ER) stress, calcium release from the ER and subsequent uptake of cal
195 m overload in SOD1G93A astrocytes and excess calcium release from the ER during ATP stimulation.
196 d that purinergic stimulation induces excess calcium release from the ER stores in SOD1G93A astrocyte
197 FasL stimulation and found that LFG inhibits calcium release from the ER, a process that correlates w
202 oponin complex, CK-2017357 slows the rate of calcium release from troponin C and sensitizes muscle to
203 ner mechanistically dependent upon apoptotic calcium release from voltage-gated calcium channels.
205 either TMTC1 or TMTC2 caused a reduction of calcium released from the ER following stimulation, wher
207 tudy we examined the causal role of abnormal calcium releases from the sarcoplasmic reticulum in prod
208 > 10(-4) mol/g of dust, the amount of P (and calcium) released has a direct proportionality to the am
209 proaches, we demonstrated that IP(3)-induced calcium release (IICR) initiated the hypertrophy-associa
211 cium homeostasis, (ii) endoplasmic reticulum-calcium release, (iii) activation of the oxidative stres
212 ring inhibition of UTP-induced intracellular calcium release in 1321N1 astrocytoma cells stably trans
213 al slices, we show that increased RyR-evoked calcium release in 3xTg-AD mice "normalizes" an altered
214 s this question, sarcoplasmic reticulum (SR) calcium release in a mouse strain with a naturally occur
215 s for C/EPB homologous protein (CHOP) and ER calcium release in apoptosis, we hypothesized that apopt
216 imaging of zebrafish embryos shows defective calcium release in bin1 morphants, linking the presence
217 lt in exaggerated endoplasmic reticulum (ER) calcium release in cellular and animal models of Alzheim
220 ty of SDF1-ELP, as measured by intracellular calcium release in HL60 cells was dose dependent, and al
224 t amplitude variation in G-protein-activated calcium release in RAW264.7 macrophages is generally ext
225 tract, and fail to undergo calcium-dependent calcium release in response to electrical stimulation or
226 y capacity, protein kinase C expression, and calcium release in response to PMA and CF pathogens.
228 Calcium transient duration and diastolic calcium release in the mutant myocytes were tetrodotoxin
230 s study, we examined whether dysregulated ER calcium release in young 3xTg-AD neurons alters synaptic
231 inity binding of PSC-RANTES, analog-mediated calcium release (in desensitization assays), and analog-
232 We further show that endoplasmic reticulum calcium release-induced store-operated calcium entry con
236 vated chloride conductances by intracellular calcium release is the key factor underlying spontaneous
237 emonstrated that ATP dependent intracellular calcium release leads to an increase of nearly 100% in o
239 potent calcium messenger, is able to trigger calcium release, likely through two-pore channels (TPCs)
242 supported by a ROS-assisted calcium-induced calcium-release mechanism intimately involving ROS produ
243 a Ca(2+) diffusion-dominated calcium-induced calcium-release mechanism is insufficient to explain the
244 uated their ability to inhibit intracellular calcium release mediated by angiotensin II receptor type
245 the augmented synaptically evoked dendritic calcium release mediated by enhanced RyR calcium release
247 dramatically affect calcium homeostasis and calcium release mediated through the ryanodine receptor
248 ternal organelles, specialized intracellular calcium release membranes, come into close apposition wi
250 BAPTA chelation, and recruits intracellular calcium release on its way to activation of phosphatase
252 he results were corroborated by analyses for calcium release or uptake, tartrate-resistant acid phosp
254 content and sarcoplasmic reticulum-mediated calcium release, preserving cardiomyocyte contraction af
256 the effect of changing CSQ expression on the calcium release profile and the rate of spontaneous calc
257 at CAPN3 knockout muscles exhibit attenuated calcium release, reduced calmodulin kinase (CaMKII) sign
258 o indicate that enhanced mGluR signaling and calcium release regulated by InsP(3)R as underlying caus
260 ma 2 (AIM2), which led to higher cytoplasmic calcium release responsible for calpain activation under
263 cause triggered activity because spontaneous calcium release (SCR) activates sufficient Ca-sensitive
264 the atria from mice predisposed to abnormal calcium releases secondary to the absence of calsequestr
265 feedforward cycle between the increased RyR calcium release seen in presymptomatic AD mice and aberr
266 of luminal ATP translocation and ATP-evoked calcium release share common pharmacology, suggesting th
267 uous signaling system, translating a digital calcium release signal into calcium influx that can sign
269 Cmpt mice exhibited a faster decline in calcium release, suggesting a compromised ability to ref
272 e directly suppresses sarcoplasmic reticulum calcium release-the cellular mechanism responsible for t
273 e small molecule triptolide induces cellular calcium release through a polycystin-2-dependent pathway
274 ium activity during axophilic migration, and calcium release through IP3 receptors was found to stimu
277 acutely couples changes in pO(2) to altered calcium release through the ryanodine receptor-Ca(2+)-re
279 Consistent with these observations we found calcium release to be significantly reduced in fibers fr
281 s and were proposed to mediate endolysosomal calcium release triggered by the second messenger, nicot
282 fects of IVIg on several parameters, such as calcium release, tyrosine phosphorylation, BCR aggregati
284 um dynamics has revealed that the elementary calcium release units of the SR can become refractory in
285 bility to link microscopic properties of the calcium release units to whole cell behavior makes this
287 owth behaviors is due to Coronin-1-dependent calcium release via PLC-gamma1 signaling, which releases
288 ured from females, significantly potentiated calcium release via ryanodine receptors induced by caffe
289 s Akt phosphorylation, inhibited HSV-induced calcium release, viral entry, and plaque formation follo
291 neurons expressing actin-GFP or Lifeact-RFP, calcium release was found to stimulate leading process a
293 sis that ATP acts as a diffusible trigger of calcium release waves, local ejection of ATP triggered P
294 duration stimulus or a diastolic spontaneous calcium release, we observed that the stimulus needed wa
295 imilar kinetics and stronger intensity of ER calcium release were induced by the sarcoendoplasmic ret
296 litude and fractional sarcoplasmic reticulum calcium release were larger and action potential and QTc
298 sted selectively inhibited histamine-induced calcium release with the best being chlorprothixene (IC(
300 increase in ryanodine receptor (RyR)-evoked calcium release within synapse-dense regions of CA1 pyra
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