ライフサイエンスコーパス: Ca2

1 Ca2+ binding to Miro1 halts mitochondrial transport by m

2 Ca2+ channel beta-subunit interactions with pore-forming

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+/calmodulin-dependent protein kinase II (CaMKII) acc

7 d in their oligosaccharide backbones or by a Ca2+-mediated process that involves the cargo-sorting pr

8 Hence, CMI1 is a Ca2+-dependent transducer of auxin-regulated gene expres

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

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

11 olecule 1 (STIM1) and Ca2+-release-activated Ca2+ channel 1 (Orai1) within ER-plasma membrane (PM) ju

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

13 e with atopic dermatitis but how they affect Ca2+ signalling and cell function is unknown.

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

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

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

17 d cellular mechanisms underlying the altered Ca2+ dynamics in the cells under obesity.

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

19 Although Ca2+ binds to the RNA aptamer with higher affinity than

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

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

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

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

24 ternans, and further caused AP alternans and Ca2+ transient alternans through Ca2+->AP coupling and A

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

26 sarcoplasmic reticulum (SR) Ca2+ content and Ca2+ transient amplitude.

27 auxin, a regulator of plant development, and Ca2+, a universal second messenger, have been proposed t

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

29 y, resulting in inhibition of Ca2+ entry and Ca2+-dependent gene expression.

30 y, resulting in inhibition of Ca2+ entry and Ca2+-dependent gene expression.

31 1R-mediated inositol monophosphate (IP1) and Ca2+ signaling in cell lines and on action potential fir

32 Circuit mapping and Ca2+ imaging using the trans-Tango system reveals second

33 nal SH3 domain tandem binds RIM, Munc13, and Ca2+ channels release machinery collectively.

34 se of RhoA activity are dependent on p63 and Ca2+/PKC, respectively, and further identified phosphory

35 Acidic pH and Ca2+ shifted the GP2 conformational equilibrium in favor

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

37 ) resulted in reduced Ca2+ store release and Ca2+ influx in response to all tested platelet agonists.

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

39 h stromal interaction molecule 1 (STIM1) and Ca2+-release-activated Ca2+ channel 1 (Orai1) within ER-

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

41 bi-directional coupling between voltage and Ca2+, forming a delayed feedback loop.

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

43 ing to intraflagellar pH (pHi), voltage and [Ca2+]i fluctuations.

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

45 annexins as mediators of membrane-associated Ca2+ release during membrane repair and annexin A6 as a

46 Annexins are a family of membrane-associated Ca2+-binding proteins implicated in repair, and annexin

47 Sevo disrupted astrocyte Ca2+ homeostasis both acutely and chronically, which led

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

49 re is the size of the overlap region between Ca2+ channel activation and inactivation, called the win

50 mutations were compared by Western blotting, Ca2(+) flux assays, differentiation of transduced HL-60

51 l protection of autophosphorylated CaMKII by Ca2+/CaM may be an important mechanism for regulation of

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

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

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

55 ough of mgtA by Mn2+ is much greater than by Ca2+.

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

57 osphate (IP3), inducing cytoplasmic calcium (Ca2+) influx.

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

59 the pancreas can elevate cytosolic calcium (Ca2+) levels, it is not known how transient pressure-act

60 (preBotC) interneurons that express calcium (Ca2+)-activated nonselective cationic current (ICAN) to

61 For example, a change in calcium (Ca2+) concentration in a cell in the present excitation

62 s tightly orchestrate intracellular calcium (Ca2+) dynamics to regulate cellular activities and maint

63 ng evidence that the store-operated calcium (Ca2+) channel Orai1 sustains Th17-driven inflammatory re

64 een calreticulin and store-operated calcium (Ca2+) entry (SOCE) machinery in megakaryocytes (Mks) fro

65 Intracellular calcium ([Ca2+]i) is a basic and ubiquitous cellular signal contro

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

67 Calreticulin (CRT) is a high-capacity Ca2+ protein whose expression is up-regulated during cel

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

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

70 steady-state as well as at elevated cellular Ca2+ levels to regulate auxin responses.

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

72 Furthermore, compartmentalized Ca2+ transients were also generated on discrete dendriti

73 eratinocytes trigger local compartmentalized Ca2+ transients within the melanocyte dendrites.

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

75 KCNMA1 encodes the large-conductance Ca2+- and voltage-activated K+ (BK) potassium channel al

76 atively regulate and thereby tightly control Ca2+ fluxes that are essential for mature T-cell activat

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

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

79 hosphatases (ABI2, PP2CA, HAB1) by cytosolic Ca2+ elevation, resolves the majority of the discrepanci

80 ment between repeated increases in cytosolic Ca2+ concentration and a self-sustaining feedback circui

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

82 ides new insights into the role of cytosolic Ca2+ oscillations in stomatal closure, revealing a mutua

83 will reach the state of saturated cytosolic Ca2+ concentration at a lower stimulus concentration, co

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

85 ted SOCE and generated spontaneous cytosolic Ca2+ flows.

86 This severely defective Ca2+ signaling translated into impaired thrombus formati

87 The localized dendritic Ca2+ transients could be triggered by two keratinocyte-s

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

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

90 determining inositol triphosphate-dependent Ca2+ release from the endoplasmic reticulum (ER).

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

92 andidate modules featuring voltage-dependent Ca2+-channels link these outputs to the downstream dynam

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

94 a2+ dynamics as they provide hubs for direct Ca2+ exchange between the organelles.

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

96 ocytes or spatially concordant or discordant Ca2+ and repolarization alternans in cardiac tissue.

97 such as subcellular concordant or discordant Ca2+alternans in cardiac myocytes or spatially concordan

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

99 scent indicators, action potential duration, Ca2+ alternans, and spontaneous calcium release (SCR) in

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

101 n type 1a receptor and a genetically encoded Ca2+ sensor.

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

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

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

105 Further, TRIC-A-dependent delay in ER Ca2+ store refilling contributes to shaping the pattern

106 Upon ER Ca2+ depletion, TRIC-A clusters with stromal interaction

107 ow significantly reduced electrically evoked Ca2+ release and force production.

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

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

110 Conversely, ATP-induced extracellular Ca2+ influx enhanced cell death, which confirmed the key

111 ocks caspase-4 or chelation of extracellular Ca2+, inhibited EPEC-induced cell death.

112 nal deletion of synaptotagmin-2, the fastest Ca2+ sensor for synaptic neurotransmitter release, from

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

114 dent protein kinase-1 (PDK1) is required for Ca2+-dependent platelet activation, but its role in MK d

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

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

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

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

119 is autaptic action affect cone voltage-gated Ca2+ channel (CaV channel) gating through changes in pH.

120 y the effects of MAM Ca2+ dynamics on global Ca2+ activities.

121 alternans through Ca2+->AP coupling and AP->Ca2+ coupling, respectively.

122 We have identified the single EF-hand Ca2+-binding protein Ca2+-dependent modulator of ICR1 (C

123 Specifically, we explore how Ca2+/CaM-binding may both stabilize CaMKII subunit activ

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

125 proterenol-induced arrhythmias, and improved Ca2+ homeostasis.

126 pression promoted external blebs enriched in Ca2+ and correlated with a reduction of intracellular Ca

127 umoniae, suggested previously to function in Ca2+ efflux.

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

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

130 G in Sa, Q193H in Sb, D168N in Ca1, P137S in Ca2, and F71L in Cb) were detected in variants from the

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

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

133 l duration by 24% (P<0.001, n=15), increased Ca2+ alternans by 300% (P<0.001, n=18), and promoted spo

134 n potential duration but only IL-6 increased Ca2+ alternans and promoted spontaneous calcium release

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

136 p size positively correlated with increasing Ca2+ concentrations.

137 ociates with the repression of auxin-induced Ca2+ increases in the lateral root cap and vasculature,

138 e lectin receptor (CLR) macrophage-inducible Ca2+-dependent lectin receptor (Mincle).

139 ects on beating parameters and intracellular Ca2+ flux in CMs and inhibition of tubulogenesis in ECs.

140 e role of MAMs is critical for intracellular Ca2+ dynamics as they provide hubs for direct Ca2+ excha

141 diomyocytes displayed improved intracellular Ca2+ signaling and a reduction of NADPH oxidase 2 (NOX2)

142 re was an enhanced response in intracellular Ca2+ and IL-17 expression, which was blocked by SOCE inh

143 b pathway inhibition increases intracellular Ca2+, induces apoptosis of activated T cells, and can co

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

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

146 correlated with a reduction of intracellular Ca2+ at the injury site.

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

148 ticulum (ER), a major store of intracellular Ca2+, and mitochondria, an important source of adenosine

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

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

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

152 rared (NIR) genetically encoded calcium ion (Ca2+) indicators (GECIs) can provide advantages over vis

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

154 The interaction between CMI1 and ICR1 is Ca2+-dependent and involves a conserved hydrophobic pock

155 This process is Ca2+-dependent and is required for invasive MDA-MB-231 c

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

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

158 However, these beta-less Ca2+ channels cannot be stimulated by beta-adrenergic pa

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

160 a hexa-coordinated metal cation, most likely Ca2+ or Mg2+.

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

162 ith genetics, we here identify the lysosomal Ca2+ channel Trpml as an essential player in the couplin

163 thematical model to study the effects of MAM Ca2+ dynamics on global Ca2+ activities.

164 of plasma membrane (PM) ion channels mediate Ca2+ entry signals triggered by the Ca2+ sensor Stromal

165 omplex, causing a decrease in Orai1-mediated Ca2+ current and SOCE.

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

167 tion of ryanodine receptor 2 (RyR2)-mediated Ca2+ oscillations and inositol 1,4,5-triphosphate recept

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

169 l amounts of certain divalent cations (Mg2+, Ca2+).

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

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

172 suppresses mitophagy, disturbs mitochondrial Ca2+ homeostasis, affects ATP production, and attenuates

173 n-regulation of CRT results in mitochondrial Ca2+ overload and induction of mitochondria permeability

174 RIC) channels have been proposed to modulate Ca2+ release from the endoplasmic reticulum (ER) and det

175 In the first module, [Ca2+]i-spike trains require the concerted action of a cl

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

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

178 ments over NIR-GECO1 for imaging of neuronal Ca2+ dynamics.

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

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

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

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

183 he Monte Carlo method to study the effect of Ca2+ signals on the dynamics of CaMKII phosphorylation i

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

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

186 IM stoichiometry, resulting in inhibition of Ca2+ entry and Ca2+-dependent gene expression.

187 IM stoichiometry, resulting in inhibition of Ca2+ entry and Ca2+-dependent gene expression.

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

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

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

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

192 illing contributes to shaping the pattern of Ca2+ oscillations.

193 unction that is compacted in the presence of Ca2+ or Mn2+ at a physiological Mg2+ concentration.

194 re closely associated with the regulation of Ca2+ dynamics.

195 In summary, the abnormal SOCE regulation of Ca2+ flows in Mks contributes to the pathophysiology of

196 , which confirmed the key regulatory role of Ca2+ in EPEC-induced pyroptosis.

197 ated Ca2+ entry (SOCE) is the major route of Ca2+ influx in platelets.

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

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

200 ially and temporally orchestrated series of [Ca2+]i spikes.

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

202 unrecognized feedback mechanism dependent on Ca2+c.

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

204 Store-operated Ca2+ entry (SOCE) is the major route of Ca2+ influx in p

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

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

207 gnals is based on attenuating store-operated Ca2+ entry (SOCE).

208 one formation, independent of weight loss or Ca2+/vitamin D deficiency.

209 Loss-of function mutations in Orai1 Ca2+ channels lead to a form of severe combined immunode

210 mic reticulum (ER) and determine oscillatory Ca2+ signals.

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

212 phosphatase, CaMKII monomers integrate over Ca2+ signals of certain frequencies through autophosphor

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

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

215 r (smFRET)-imaging, we found that acidic pH, Ca2+, and NPC1 binding synergistically induce conformati

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

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

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

219 In contrast, nonfailing hMSCs prevented Ca2+ alternans in human cardiac myocytes derived from in

220 RPML1], also known as MCOLN1), the principle Ca2+ release channel in the lysosome, as another direct

221 These produced Ca2+ transient alternans and AP alternans, and further c

222 fied the single EF-hand Ca2+-binding protein Ca2+-dependent modulator of ICR1 (CMI1) as an interactor

223 Rapid Ca2+ release correlated with colocalization of highly ph

224 chanistically, Tir clustering triggers rapid Ca2+ influx, which induces lipopolysaccharide (LPS) inte

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

226 (Bin2fl/fl,Pf4-Cre mice) resulted in reduced Ca2+ store release and Ca2+ influx in response to all te

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

228 e yybP-ykoY riboswitch functions to regulate Ca2+ efflux under these conditions.

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

230 its secondary structure at cellular resting Ca2+ concentrations ranging between 10-9 and 10-8 M.

231 Sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) activity was reduced and western blo

232 phospholamban, a sarco/endoplasmic reticulum Ca2+-ATPase inhibitor, consistent with a role for decrea

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

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

235 port ATPase increases sarcoplasmic reticulum Ca2+ concentration, thereby enhancing susceptibility to

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

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

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

239 due to the increased sarcoplasmic reticulum Ca2+-ATPase (SERCA) Ca2+ reuptake, modulated by increase

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

241 d sarcoplasmic reticulum Ca2+-ATPase (SERCA) Ca2+ reuptake, modulated by increased phospholamban (PLB

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

243 in Arabidopsis roots, auxin elicits specific Ca2+ signaling patterns that spatially coincide with the

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

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

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

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

248 ism has been suggested that the increased SR Ca2+ content and prolonged AP did not fully recover to t

249 e end of diastole, resulting in a smaller SR Ca2+ release and AP in the next beat.

250 by an increased sarcoplasmic reticulum (SR) Ca2+ content and Ca2+ transient amplitude.

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

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

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

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

255 Noting that Ca2+/CaM and protein phosphatases bind CaMKII at nearby

256 this hypothesis, we experimentally show that Ca2+ application to cellular lysates at physiological co

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

258 The Ca2+ sensor stromal interaction molecule 1 (STIM1) trigg

259 ell in the present excitation may affect the Ca2+ dynamics in the next excitation via bi-directional

260 mediate Ca2+ entry signals triggered by the Ca2+ sensor Stromal Interaction Molecule (STIM) proteins

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

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

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

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

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

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

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

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

269 -dependent phosphorylation by members of the Ca2+/calmodulin-dependent protein kinase (CaMK) group.

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

271 Since the Ca2+ dynamics inside the excitable cells are spatiotempo

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

273 SOCE by forming punctate structures with the Ca2+ channel Orai1 and the inositol trisphosphate recept

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

275 c envelope and temporal organisation of the [Ca2+]i-spike trains.

276 We show that the [Ca2+]i dynamics observed experimentally after sustained

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

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

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

280 ternans and Ca2+ transient alternans through Ca2+->AP coupling and AP->Ca2+ coupling, respectively.

281 Although key to Ca2+ signal generation, molecular understanding of this

282 protein of the SOCE machinery that leads to Ca2+ mobilization.

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

284 SVs to dock in defined nanoscale relation to Ca2+ channels.

285 RyR2 clusters with distinct sensitivities to Ca2+.

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

287 his pathway supported the increase in L-type Ca2+ channel activity and myogenic tone in two animal mo

288 or AC5 in PKA-dependent modulation of L-type Ca2+ channel activity and vascular reactivity during acu

289 between subpopulations of AC5 and the L-type Ca2+ channel pore-forming subunit CaV1.2.

290 iation is critical for stimulation of L-type Ca2+ channels in arterial myocytes and increased myogeni

291 inase A (PKA)-mediated stimulation of L-type Ca2+ channels in arterial myocytes resulting in increase

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

295 so-called "CaM trapping" phenomenon, wherein Ca2+/CaM may structurally exclude phosphatase binding an

296 g sites, we compare model scenarios in which Ca2+/CaM and protein phosphatase do or do not structural

297 STIM1-mediated SOC channel activation, while Ca2+ store content and agonist-induced IP3 production we

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

299 find that while abrogating RSS nicking with Ca2+ leads to substantially shorter PC lifetimes, analys

300 curtailed beta-adrenergic stimulation of WT Ca2+ channels, identifying an approach to specifically m