ライフサイエンスコーパス: Ca2

1 Ca2+ -activated chloride channels (CaCCs) regulate numer

2 Ca2+ binding to Miro1 halts mitochondrial transport by m

3 Ca2+ entry through voltage-gated L-type Ca2+ channels tr

4 Ca2+ influx is negatively regulated by Ca2+ -activated K

5 Ca2+ influx mediates T cell function and immunity to inf

6 Ca2+ plays an important role not only in mineralizing de

7 Ca2+ transients in the dendrites of an individual Oregon

8 Ca2+-activated chloride currents (CaCCs) in vascular smo

9 The type 2 ryanodine receptor (RyR2) is a Ca2+ release channel on the endoplasmic reticulum (ER) o

10 We showed that the probability of a Ca2+ spark occurring when a single RyR2 in the cluster o

11 L. monocytogenes internalization requires a Ca2+ - and K+ -dependent internalization pathway that is

12 R membrane or by directly interacting with a Ca2+-release channel.

13 tion mutations in the Ca2+ release-activated Ca2+ (CRAC) channel genes ORAI1 and STIM1 abolish store-

14 iated by SOCE and the Ca2+ release-activated Ca2+ (CRAC) channel, the prototypical SOCE channel.

15 entry (SOCE) through Ca2+ release-activated Ca2+ (CRAC) channels.

16 When activated, [Ca2+]i-sensitive RyR2 open probability increases, and th

17 ethyl-D-aspartate (NMDA) receptors activates Ca2+/calmodulin signal transduction networks that either

18 evel of endogenous Miro1 but did not affect [Ca2+]c.

19 st verified the computational model against [Ca2+] and insulin secretion measurements in islets expre

20 des activation of PI3-kinase, IGF1R and Akt, Ca2(+)-sensitive transcription factors and also TGFbeta1

21 ural-CA1 pathway, phospho-alphaCaMKII (alpha Ca2(+)/calmodulin-dependent protein kinase II) level in

22 nans (ECG ALT) and Ca2+ transient alternans (Ca2+ALT) were induced by rapid pacing (300-120 ms) befor

23 Although Ca2+ is the principal regulator of contraction in striat

24 f cells exhibit synchronized, high amplitude Ca2+ release flux.

25 tly decreased ECG ALT (-77+/-9%, P<0.05) and Ca2+ ALT (-56+/-7%, P<0.05) and, importantly, reduced RO

26 In MI, ECG ALT (2.32+/-0.41%) and Ca2+ ALT (22.3+/-4.5%) were significantly greater compar

27 idant treatment had no effect on ECG ALT and Ca2+ ALT.

28 ECG T-wave alternans (ECG ALT) and Ca2+ transient alternans (Ca2+ALT) were induced by rapid

29 transposon-induced mutant alleles of Ca1 and Ca2 in maize (Zea mays).

30 thological consequences of elevated cGMP and Ca2+, which are induced by the Pde6 mutation.

31 electrides, such as 12 CaO7 Al2 O3 :e(-) and Ca2 N.

32 Accumulation of gluconate- and Ca2+ in the system over time correlated with lengthening

33 Deregulated protein and Ca2+ homeostasis underlie synaptic dysfunction and neuro

34 ultaneous electrophysiological recording and Ca2+ imaging in hippocampal neurons revealed that the sA

35 nct neutralizing Caton epitopes: Sa, Sb, and Ca2.

36 are closely interconnected with the SR, and Ca2+ is essential for optimal function of these organell

37 Electrical, structural, and Ca2+ -handling remodeling contribute to the perpetuation

38 we have identified a membrane structure and Ca2+-signaling complex that may enhance the speed of atr

39 for activity, but is inactive with Zn2+ and Ca2+.

40 sicles with low release probability, such as Ca2+-channel inactivation, and established unexpected bo

41 cell-to-cell heterogeneity of the astrocyte Ca2+ response was however large and increasing with stim

42 RNA sequencing identified a novel ATPase, Ca2+ transporting, plasma membrane 4(ATP2B4)-protein kin

43 Brain Ca2+ regulatory processes are altered during aging, disr

44 nced if paracellular barrier was impaired by Ca2+ depletion, proinflammatory cytokine tumor necrosis

45 or storing vesicles that is not modulated by Ca2+.

46 Ca2+ influx is negatively regulated by Ca2+ -activated K+ channels (SK-channels) which are in t

47 ations in transmission efficacy triggered by Ca2+ signals of different amplitudes at excitatory synap

48 to reactive oxygen species, cytosolic Ca2+ (Ca2+c), and heterotrimeric G-protein signaling.

49 Calcium (Ca2+) released from the sarcoplasmic reticulum (SR) is c

50 transport in response to cytosolic calcium (Ca2+) levels ([Ca2+]c) and mitochondrial damage.

51 temporal dynamics of intracellular calcium, [Ca2+]i, regulate the contractile function of cardiac mus

52 k provides novel perspectives on the cardiac Ca2+ release process and a general method for inferring

53 ng AP shape and duration, as well as to cell Ca2+ dynamics.

54 particular CISD2 mutation disturbs cellular Ca2+ homeostasis with enhanced Ca2+ flux from the ER to

55 Chronic [Ca2+]i dysregulation amplifies Cdk5-ATM signaling, possi

56 , and the myoplasmic calcium concentration ([Ca2+]i) during excitation-contraction coupling.

57 Resting cytoplasmic calcium concentration ([Ca2+]i) in cultured preCGG hippocampal neurons is chroni

58 Large conductance Ca2(+)-activated K(+) (BKCa) channels in buffering pheny

59 PPT also inhibited a small conductance Ca2+-activated K+ (SK) current; blockade of the SK curre

60 ntaneously giving rise to spatially-confined Ca2+ release events known as "sparks." RyR2s are organiz

61 ch act as the major mediators of contractile Ca2+ release, upon a physiologically-realistic cellular

62 ux from the ER to mitochondria and cytosolic Ca2+ abnormalities in patient-derived fibroblasts.

63 ntial cation channels to attenuate cytosolic Ca2+ influx, implicating a mechanism by which overexpres

64 ster fraction, thereby maintaining cytosolic Ca2+ signaling despite decreases in RyR2 cluster density

65 regard to reactive oxygen species, cytosolic Ca2+ (Ca2+c), and heterotrimeric G-protein signaling.

66 As a rise in the cytosolic Ca2+ concentration is a versatile signal that can modula

67 depolarizations and triggered beats, delayed Ca2+ transients and frequent spontaneous Ca2+ release ev

68 etory defect was distal to glucose-dependent Ca2+ influx and resulted from reduced proinsulin biosynt

69 ochondrial Calcium Uniporter (MCU)-dependent Ca2+ clearance.

70 lates MCU expression, mitochondria-dependent Ca2+ clearance, and thereby, presynaptic release propert

71 Action potential-dependent Ca2+ transients were recorded in neurons of all six laye

72 In cardiomyocytes, RyR2-dependent Ca2+ release is critical for excitation-contraction coup

73 ng beta cells, and opening voltage-dependent Ca2+ channels to elicit insulin exocytosis.

74 and subsequent opening of voltage-dependent Ca2+ channels to elicit insulin granule exocytosis.

75 In combination with spectrally different Ca2+ indicators, such as OGB-1, Cal-590 can be readily u

76 aM binding proteins are "tuned" to different Ca2+ flux signals by their unique binding and activation

77 However, direct Ca2+-binding of the mutant was nearly similar to the wil

78 ormones, cause oxidative stress, and disrupt Ca2+-mediated signal transduction.

79 ntry through NCX1, as well as less efficient Ca2+ clearance.

80 r pressure overload is due to more efficient Ca2+ clearance because this isoform of NKA preferentiall

81 Elevated [Ca2+]i, ROS, and DDR signals are normalized with dantrol

82 ng electrophysiology and genetically encoded Ca2+ sensors targeted to the mitochondrial matrix or to

83 urbs cellular Ca2+ homeostasis with enhanced Ca2+ flux from the ER to mitochondria and cytosolic Ca2+

84 The magnitudes of the ensuing Ca2+ transients within dendritic spines are thought to d

85 e SERCA2-inhibitor thapsigargin, depletes ER Ca2+ stores, leading to constitutive ER stress and incre

86 significantly attenuated electrically evoked Ca2+ transient amplitude and prolonged the 50% decay tim

87 T at 70 mmHg) and augmented glutamate-evoked Ca2+ (Fura-2) signals.

88 (Kd=561 nM), single-action potential-evoked Ca2+ transients were discernable in most neurons with a

89 perparathyroidism that accompanies excretory Ca2+ losses induced by aldosteronism in which elevated p

90 lls, we demonstrate that these cells express Ca2+ -handling molecules and mediate Ca2+ influx through

91 al-muscle channels (NaV1.4), we uncover fast Ca2+ regulation eerily similar to that of Ca2+ channels.

92 Here, we tested the red-shifted fluorescent Ca2+ indicator Cal-590 for deep tissue experiments in th

93 e the relatively low affinity of Cal-590 for Ca2+ (Kd=561 nM), single-action potential-evoked Ca2+ tr

94 A common mechanism for Ca2+ influx is store-operated Ca2+ entry (SOCE).

95 roteins (eg, claudin-4) as receptors to form Ca2+-permeable pores in the membrane, damaging epithelia

96 n data, which revealed the molecular formula Ca2[(HO3PC6H3COOH)2]2[(HO3PC6H3(COO)2H)(H2O)2].

97 mutant was less sensitive to changes in free Ca2+, resulting in a constitutively active form under ph

98 Voltage gated Ca2+ channels, K(+)ATP channels and the alpha-gustducin

99 d by NMDA-receptor (NMDAR) and voltage-gated Ca2+ -channel (VGCC) activation is thought to determine

100 However, global Ca2+ levels in cells rarely reach such levels and, there

101 g FKBP1b underlies aging-related hippocampal Ca2+ dysregulation.

102 However, Ca2+ accumulation can impair mitochondrial function, lea

103 Our aim was to determine if Ca2+ influx through transient receptor potential canonic

104 cated in delayed repolarization and impaired Ca2+ handling in heart failure (HF).

105 Most alterations in Ca2+ homeostasis were prevented by 100 nm tetrodotoxin.

106 ivating the kinase in response to changes in Ca2+ concentrations.

107 We observed strong Hofmeister effects in Ca2+/Na+ exchange on a permanently charged surface over

108 The increase in Ca2+ spark rate is thought to be due to an increase in r

109 ed stretching, the X-ROS-induced increase in Ca2+ spark rate is transient, so that long-sustained str

110 lopment, the molecular machinery involved in Ca2+ homeostasis in ameloblasts remains poorly understoo

111 rovide a map of all of the genes involved in Ca2+ signaling and link these genes to human genetic dis

112 efficiency of bipolar NEFO was preserved in Ca2+-free conditions and thus cannot be explained by the

113 l activation and the subsequent reduction in Ca2+ influx through NMDARs and L-type VGCCs results in a

114 the spatial resolution to which changes in [Ca2+]i can be detected.

115 these structure-induced heterogeneities in [Ca2+]i can appear in line scan data.

116 Significant recoveries in [Ca2+] and insulin secretion were predicted for many muta

117 wever, our model predicted the variation in [Ca2+]i to be between 0.3 and 12.7 muM (~3 to 100 fold fr

118 yme complex dephosphorylates and inactivates Ca2(+)/calmodulin-dependent protein kinase I (CaMKI), an

119 ss-induced endothelial responses, including [Ca2+]i transients, activation of the endothelial NO synt

120 a2+ release per [Ca2+]i transient, increased Ca2+ buffering strength, shortened action potentials, an

121 he range of moderate hypokalaemia, increases Ca2+ levels in ventricular myocytes by reducing the pump

122 This increases Ca2+ binding to ligand-gated channels known as ryanodine

123 In addition, we found that increasing Ca2+ concentrations elevated ASL viscosity, in part, ind

124 myocytes and are activated on Ca2+ -induced Ca2+ release.

125 LysASA induced Ca2+ fluxes and EDN release, but not CysLT secretion fro

126 l for lymphocyte function, and intracellular Ca2+ concentrations are regulated by store-operated Ca2+

127 our results present astrocyte intracellular Ca2+ activity as a nonlinear integrator of glutamate-dep

128 must be mechanisms that focus intracellular Ca2+ transients towards the ANO1 channels.

129 C3 expression; calcium influx; intracellular Ca2+ concentration; and calcineurin activity.

130 ic glutamate receptor-mediated intracellular Ca2+ waves, SK and TRPC channel activity.

131 At 4 weeks, optical mapping of intracellular Ca2+ and ROS was performed.

132 pharmacological inhibition of intracellular Ca2+ leak in CPVT-associated RyR2-expressing mice, in hu

133 hey may support the process of intracellular Ca2+ release, either indirectly by manipulating ionic fl

134 ed as regulators or targets of intracellular Ca2+ signals.

135 en co-localize with sources of intracellular Ca2+ signals.

136 n and required mobilization of intracellular Ca2+.

137 ls from these animals revealed intracellular Ca2+ leak via oxidized and nitrosylated RyR2 channels, a

138 le (TT) invaginations and slow intracellular Ca2+ propagation but exhibits rapid contractile activati

139 and temporal distribution of intracellular [Ca2+] and [H+], cells such as cardiac myocytes can exerc

140 in mutant SOD1-related ALS we investigated [Ca2+]c and Miro1 levels in ALS mutant SOD1 expressing ne

141 In hippocampal neurons, calcium ion (Ca2+) flux through N-methyl-D-aspartate (NMDA) receptors

142 Signal transduction via calcium ions (Ca2+) represents a fundamental signaling pathway in all

143 ne potential depolarization, increased islet Ca2+ influx, and enhanced second-phase GSIS.

144 g properties, its Ca2+/Mg2+-binding, and its Ca2+-induced conformational changes in comparison to the

145 parameters of its activating properties, its Ca2+/Mg2+-binding, and its Ca2+-induced conformational c

146 apid increases in the phosphorylation of key Ca2+ handling proteins, including ryanodine receptor and

147 We determined that less Ca2+ release per [Ca2+]i transient, increased Ca2+ buffe

148 esponse to cytosolic calcium (Ca2+) levels ([Ca2+]c) and mitochondrial damage.

149 es similar to that found in the literature ([Ca2+]i approximately 1 muM; F/F0 approximately 5.5).

150 l insulin 1 (INS1) cells for which localized Ca2+ influx triggers exocytosis with high probability an

151 Measuring [Ca2+]i flux is central to the study of mechanisms that u

152 express Ca2+ -handling molecules and mediate Ca2+ influx through SOCE.

153 tamate release driven NMDA receptor mediated Ca2+ transients often occur at the same synapse, these t

154 tivity and ryanodine receptor (RyR)-mediated Ca2+ release, but underlying molecular mechanisms are po

155 ll immunophilin that stabilizes RyR-mediated Ca2+ release in cardiomyocytes, declines in hippocampus

156 ted with a decrease in parallel RyR-mediated Ca2+ transients.

157 n mice and was associated with TRPC-mediated Ca2+ entry.

158 nity or translocation to cellular membranes (Ca2+/myristoyl switch).

159 Microscopy, Ca2+ monitoring, and electrophysiological data showed th

160 In the extracellular milieu, Ca2+ -EMP interactions occur at different levels.

161 but not IP3R2, channels cause mitochondrial Ca2+ overload and dysfunction in HF.

162 diastolic SR Ca2+ leak causes mitochondrial Ca2+ overload and dysfunction in a murine model of postm

163 establishment of MCU-dependent mitochondrial Ca2+ uptake at glutamatergic synapses rescues the altere

164 leaky RyR2 channels result in mitochondrial Ca2+ overload, dysmorphology, and malfunction.

165 eart failure (HF), but whether mitochondrial Ca2+ plays a mechanistic role in HF remains unresolved.

166 e, which permits some degree of reverse-mode Ca2+ entry through NCX1, as well as less efficient Ca2+

167 agonist modulator (DREAM), a multifunctional Ca2+-binding protein, is reduced in murine in vivo and i

168 orders uncovered 1470 diseases with mutated 'Ca2+ genes'.

169 ale ventricular myocytes and altered myocyte Ca2+ handling, particularly spontaneous Ca2+ release fro

170 The impact of BPS on myocyte Ca2+ handling was mediated by estrogen receptor beta sig

171 ady-state force while increasing myofilament Ca2+ sensitivity.

172 ampal FKBP1b in young rats augments neuronal Ca2+ responses.

173 n filament regulatory unit in the absence of Ca2+.

174 tic plasticity by differential activation of Ca2+ -sensitive enzymes such as calmodulin.

175 ntal observations of decreased activation of Ca2+/CaM-dependent protein kinase II in knockout models

176 KBP1b overexpression reversed key aspects of Ca2+ dysregulation and cognitive impairment in aging rat

177 zation, treating cells with a combination of Ca2+ and K+ ionophores but not with individual ionophore

178 t in the cytoplasmic compartmentalization of Ca2+ without requiring a partitioning membrane.

179 cribe the binding and activation dynamics of Ca2+/CaM signal transduction and can be used to guide fo

180 by the reversal of electrophoretic flows of Ca2+.

181 voltage-sensitive Ca2+ channels and flux of Ca2+ into the cells.

182 s a stability threshold for the formation of Ca2+ sparks in terms of the RyR2 gating transition rates

183 There are two forms of Ca2+ release channels on cardiac SR: type 2 ryanodine re

184 lusters strongly influences the frequency of Ca2+ sparks.

185 kinases (CDPKs) comprise the major group of Ca2+-regulated kinases in plants and protists.

186 of transmembrane potential and induction of Ca2+/Calcineurin-mediated retrograde signaling.

187 for Hebbian synaptic plasticity is influx of Ca2+ into postsynaptic dendritic spines.

188 haffer collateral synapses the magnitudes of Ca2+ transients during plasticity induction do not match

189 rin on human mast cells with measurements of Ca2+ flux and PGD2 release.

190 Using a 3-dimensional model of Ca2+ and calmodulin dynamics within an idealised, but bi

191 Using an explicit model of Ca2+, CaM, and seven highly-expressed hippocampal CaM bi

192 in many cell types and chose eight models of Ca2+ signalling networks which exhibit similar behaviour

193 Here we studied regulation of Ca2+ spark refractoriness in mouse ventricular myocytes

194 Their openings cause cell-wide release of Ca2+, which in turn causes muscle contraction and the ge

195 renergic stimulation influenced sequences of Ca2+ sparks originating from individual RyR clusters.

196 oordinated activation of distinct sources of Ca2+ and mGluR1-dependent facilitation of NMDAR function

197 crystals, which depend on a robust supply of Ca2+.

198 st Ca2+ regulation eerily similar to that of Ca2+ channels.

199 l model, we simulated reaction-diffusion of [Ca2+]i during the rising phase of the transient (first 3

200 The magnitude of [Ca2+] increase caused by NMDA-receptor (NMDAR) and volta

201 Here, we report the occurrence and role of [Ca2+]cyto signals during the entire double fertilization

202 good correspondence between suppression of [Ca2+] and clinical presentation of different NDM mutatio

203 se ventricular myocytes and are activated on Ca2+ -induced Ca2+ release.

204 tion of IRE1alpha was partially dependent on Ca2+ oscillation mediated by inositol 1,4,5-trisphosphat

205 unrecognized feedback mechanism dependent on Ca2+c.

206 We focussed on Ca2+ signalling in response to hormone stimulation, whic

207 ncentrations are regulated by store-operated Ca2+ entry (SOCE) through Ca2+ release-activated Ca2+ (C

208 genes ORAI1 and STIM1 abolish store-operated Ca2+ entry (SOCE), and patients with these CRAC channel

209 mechanism for Ca2+ influx is store-operated Ca2+ entry (SOCE).

210 assumed that CDPKs are activated, like other Ca2+-regulated kinases, by derepression of the kinase do

211 In contrast to other Ca2+-regulated kinases, the regulatory domain of TgCDPK1

212 maging experiments in combination with other Ca2+ indicators.

213 We determined that less Ca2+ release per [Ca2+]i transient, increased Ca2+ buffering strength, sho

214 as bursting electrical activity and periodic Ca2+ entry in beta-cells.

215 uch events have been attributed to perturbed Ca2+ handling in cardiac myocytes leading to spontaneous

216 al-590 is well suited for in vivo two-photon Ca2+ imaging experiments in all layers of mouse cortex.

217 nstitutively active form under physiological Ca2+-concentration, showed significantly higher activati

218 Presynaptic Ca2+ homeostasis plays a critical role in specifying neu

219 in a bouton-specific way through presynaptic Ca2+ clearance.

220 ent ROS production on RyR2 open probability, Ca2+ sparks, and the myoplasmic calcium concentration ([

221 table to a failure of subcellular propagated Ca2+ release due to an increased cytosolic buffering str

222 Rapid Ca2+ release correlated with colocalization of highly ph

223 This model reproduces realistic Ca2+ waves and DADs driven by stochastic Ca2+ release ch

224 results suggest that increasing pH, reducing Ca2+ concentration, and/or altering electrostatic intera

225 molecular mechanism underlying aging-related Ca2+ dysregulation and unhealthy brain aging and pointin

226 rteries, I-1 and sarco/endoplasmic reticulum Ca2+ -ATPase expression is specific to contractile vascu

227 I-1 and sarco/endoplasmic reticulum Ca2+ -ATPase synergistically induce the vascular smooth

228 horylated PLB on sarco/endoplasmic reticulum Ca2+-ATPase, Ad-PLB transduction significantly attenuate

229 protein levels of the sarcoplasmic reticulum Ca2+ ATPase (SERCA) regulatory protein sarcolipin, which

230 ing proteins, such as sarcoplasmic reticulum Ca2+ ATPase (SERCA2a), located in the sarcoplasmic retic

231 include cytosolic and sarcoplasmic reticulum Ca2+ concentrations, inwardly rectifying potassium curre

232 S signaling increases sarcoplasmic reticulum Ca2+ leak and contributes to global oxidative stress, th

233 Increased diastolic sarcoplasmic reticulum Ca2+ leak and related delayed after-depolarizations/trig

234 y because of enhanced sarcoplasmic reticulum Ca2+ leak.

235 ignificantly increase sarcoplasmic reticulum Ca2+ leak; and 4) when the chemical reducing capacity of

236 on that overexpressing FKBP1b should reverse Ca2+ -mediated manifestations of brain aging.

237 rs of intracellular ryanodine receptor (RyR) Ca2+ -release channels in mouse brain neurons, most prom

238 probability of sarcolemmal voltage-sensitive Ca2+ channels and flux of Ca2+ into the cells.

239 tion of NMDARs followed by voltage-sensitive Ca2+ channels within dendritic spines.

240 We conclude that the red-shifted Ca2+ indicator Cal-590 is well suited for in vivo two-ph

241 At 30 ms, the average peak of the simulated [Ca2+]i transient and of the simulated fluorescence inten

242 astroglia, which elicits spontaneous somatic Ca2+ transients, synaptogenic thrombospondin 1 (TSP-1) r

243 t the mechanisms regulating synapse-specific Ca2+ homeostasis in the mammalian brain are still poorly

244 Specifically Ca2+/calmodulin activated kinase II, protein kinase A an

245 yed Ca2+ transients and frequent spontaneous Ca2+ release events and at the whole heart level, increa

246 tic events from a limited set of spontaneous Ca2+ release profiles is presented.

247 cyte Ca2+ handling, particularly spontaneous Ca2+ release from the sarcoplasmic reticulum.

248 g in cardiac myocytes leading to spontaneous Ca2+ release and delayed afterdepolarizations (DADs).

249 st time, to our knowledge, that diastolic SR Ca2+ leak causes mitochondrial Ca2+ overload and dysfunc

250 R2 mutations that either cause or inhibit SR Ca2+ leak, we found that leaky RyR2 channels result in m

251 steepness of the sarcoplasmic reticulum (SR) Ca2+ release slope.

252 xM1 demonstrated enhanced glucose-stimulated Ca2+ influx, which resulted in improved glucose toleranc

253 ow progressively greater glucose-stimulated [Ca2+] and insulin secretion following expression of ATP-

254 tic Ca2+ waves and DADs driven by stochastic Ca2+ release channel (RyR) gating and is used to study m

255 ain of Troponin C with its natural substrate Ca2+.

256 ATP channel mutations found in NDM suppress [Ca2+], and the role of gap junction coupling in this sup

257 e the functional significance of supralinear Ca2+ signals, we examined activity-dependent fluctuation

258 cells is mediated by CRAC channels and that Ca2+ signals enhance the expression of EMPs.

259 Our findings demonstrate that Ca2+ influx via store-operated CRAC channels is essentia

260 These data indicate that Ca2+ influx in LS8 cells and enamel organ cells is media

261 We evaluated the possibility that Ca2+ influx in enamel cells might be mediated by SOCE an

262 Here, we show that Ca2+/calmodulin-dependent protein kinase gamma (CaMKIIga

263 amel cells might be mediated by SOCE and the Ca2+ release-activated Ca2+ (CRAC) channel, the prototyp

264 ive RyR2 open probability increases, and the Ca2+ spark rate changes in a manner consistent with expe

265 cular dynamics simulations for comparing the Ca2+-saturated inhibiting state of GCAP1 with the Mg2+-b

266 inherited mutations in the gene encoding the Ca2+ channel ORAI1 or its activator stromal interaction

267 Loss-of-function mutations in the Ca2+ release-activated Ca2+ (CRAC) channel genes ORAI1 a

268 giotensin II receptor type 1 (AGTR1), in the Ca2+/AT-IIR/alpha-AR signaling pathway.

269 active oxygen species (ROS) and increase the Ca2+ spark rate in a process called X-ROS signaling.

270 In hippocampal pyramidal neurons, the Ca2+ -dependent slow afterhyperpolarization (sAHP) exhib

271 nt a stochastic contact network model of the Ca2+ spark initiation process.

272 ing diastole, increases the magnitude of the Ca2+ transient; 3) during prolonged stretching, the X-RO

273 ced chloride secretion and activation of the Ca2+-activated chloride channel (CaCC) anoctamin 1 (ANO1

274 ing of Cl- channels; in TRPM5-GFP+ OSNs, the Ca2+ -activated Cl- ANO2 (anoctamin 2) channel is not ex

275 sence of competitors shifts and sharpens the Ca2+ frequency-dependence of CaM binding proteins.

276 's ability to represent perturbations to the Ca2+ regulatory mechanism by analyzing twitch records me

277 with scale-free properties appeared when the Ca2+ genes were mapped to their associated genetic disor

278 this study that: (i) heterogeneities in the [Ca2+]i transient are due not only to heterogeneous distr

279 tions, we demonstrate the robustness in the [Ca2+]i transient to differences in RyR cluster distribut

280 This Ca2+ dysregulation was associated with increased ER-mito

281 This Ca2+ release silencing was attributable to a failure of

282 Whether this Ca2+-independent activation (CIA) occurs under physiolog

283 significantly lower flexibility, when three Ca2+ or two Mg2+ were bound forming probably the structu

284 o activate human mast cells directly through Ca2+ flux and PGD2 release.

285 by store-operated Ca2+ entry (SOCE) through Ca2+ release-activated Ca2+ (CRAC) channels.

286 c nucleotide-gated (CNG) channel, leading to Ca2+ gating of Cl- channels; in TRPM5-GFP+ OSNs, the Ca2

287 cit activation of the CNG channel leading to Ca2+ gating of TRPM5.

288 arrhythmia substrate that has been linked to Ca2+ cycling proteins, such as sarcoplasmic reticulum Ca

289 RyR2 clusters with distinct sensitivities to Ca2+.

290 In mouse AM, AT structures triggered Ca2+ release from the SR approximately 2 times faster at

291 increased sAHP results from elevated L-type Ca2+ channel activity and ryanodine receptor (RyR)-media

292 quires Munc13-mediated recruitment of L-type Ca2+ channels in close proximity to insulin granules.

293 Ca2+ entry through voltage-gated L-type Ca2+ channels triggers exocytosis of insulin-containing

294 rtened action potentials, and reduced L-type Ca2+ current contribute to a stunning reduction of intra

295 to an increased driving force for the L-type Ca2+ current during the action potential, which explains

296 ling within cytoplasm, which produces uphill Ca2+ transport energized by spatial H+ ion gradients, an

297 In this work, we view Ca2+/CaM as a limiting resource in the signal transducti

298 In vivo Ca2+ imaging of neuronal populations in deep cortical la

299 bles, we determined that alternans onset was Ca2+-driven rather than voltage-driven and occurred as a

300 Activation with Ca2(+)/calmodulin engages additional interactive surface