ライフサイエンスコーパス: Ca

1 Ca(2+) binding restricts the dynamics in the Ca(2+)-bind

2 Ca(2+) dysregulation is thought to cause rod and cone ph

3 Ca(2+) has been assumed to be a key mediator of this cou

4 Ca(2+) induces tight binding of synaptotagmin-1 to PIP(2

5 Ca(2+) influx through NMDA receptors leads to channel in

6 Ca(2+) is a fundamental second messenger in all cell typ

7 Ca(2+) release-activated Ca(2+) (CRAC) channels elevate

8 Ca(2+) transient amplitude, 50% decay rate, and sarcopla

9 Ca(2+) transients in ICC-SS occurred by release from sto

10 Ca(2+)-dependent inactivation (CDI) is a regulatory feed

11 Ca(2+)-free synaptotagmin-1 binds to SNARE complexes anc

12 metals in the heterometallic nodes of MUV-10(Ca) enables controlled metal exchange in soft positions

13 ce of physiological concentrations of Mg(2+) Ca(2+) binding triggers an increase in protein multidoma

14 beta-cells through voltage-dependent Ca(2+) (Ca(V) ) channels.

15 an increase in the intracellular [Ca(2+)] ([Ca(2+)](i)) and high-molecular-weight glycoprotein secre

16 the mode of action and efficacy of REP 2139-Ca against HDV in 12 treatment-naive HBV/HDV co-infected

17 cation are effectively inhibited by REP 2139-Ca.

18 f development, which are driven by Ca(V) 1.3 Ca(2+) channels.

19 Solutions of variable NaNO(3), Ca(NO(3))(2), and humic acid (HA) concentrations were us

20 lecular ion and the internal states of a (40)Ca(+) atomic ion(2).

21 Further analysis of 770 Ca.

22 ciates with PM via a polybasic cluster and a Ca(2+)-binding loop.

23 (+) cells also express Ano1, which encodes a Ca(2+) -activated Cl(-) conductance that serves as a pri

24 expose negatively charged phospholipids in a Ca(2+)-dependent manner.

25 The mitochondrial calcium uniporter is a Ca(2+)-gated ion channel complex that controls mitochond

26 ers increased intracellular Ca(2+) through a Ca(2+)/calmodulin-dependent protein kinase II (CaMKII)-m

27 mGlu(2)/Gqo5-expressing HEK293 cells using a Ca(2+) imaging assay and a [(3)H]ketanserin binding assa

28 PDE4B deficiency leads to abnormal Ca(2+) handling and PDE4B is decreased in pressure overl

29 ontaining particles in the PMCs and acquired Ca-L(2,3) X-ray absorption near-edge spectra of these Ca

30 tical role for ER Ca(2+) depletion-activated Ca(2+) current in mediating Ca(2+)-induced insulin secre

31 Ca(2+) release-activated Ca(2+) (CRAC) channels elevate cytoplasmic Ca(2+) concen

32 tor stimulation are Ca(2+) release-activated Ca(2+) (CRAC) channels.

33 ACC activates Ca(2+)-containing ion currents via GLUTAMATE RECEPTOR-LI

34 proton countertransport occurring in active Ca(2+) transport.

35 We therefore expressed a low affinity Ca(2+) indicator (ER-GCaMP6-150) in the ER, and measured

36 s developed for further determination of Al, Ca, Cr, Cu, Fe, K, Mn, Mo and Ni in rice samples by ICP

37 Fluoride exposure did not alter Ca(2+) homeostasis or increase the expression of ER stre

38 fluorescently tagged actin, mutant analyses, Ca(2+) imaging and controlled Ca(2+) release to determin

39 ymphatic muscle cells expressed Ca(v)3.1 and Ca(v)3.2 and produced functional T-type VGCC currents wh

40 scade, which leads to increased H(2)O(2) and Ca(2+) levels and F-actin reorganization, but the mechan

41 as a function of the constituent Mn(2+) and Ca(2+) ions in genetically engineered membranes of the c

42 eous optical monitoring of CaCC activity and Ca(2+) dynamics revealed that the TRPV1 ligand capsaicin

43 C stimulates transient Ca(2+) elevation, and Ca(2+) influx in octuple mutant ovules rescues LURE1.2 s

44 n originates from increased excitability and Ca(2+) transients in the presynaptic terminals, where Kv

45 Crystal structures of Ca(2+)-free and Ca(2+)-bound EhActn2 reveal a calmodulin-like domain (Ca

46 his mutation on cardiac function, I(K1), and Ca(2+) handling, to determine the underlying cellular ar

47 ther with the potential release of Na(+) and Ca(2+) cations, revealing suitable for RT albumin remova

48 which CaCO(3) is decarbonated at low pH and Ca(OH)(2) is precipitated at high pH, concurrently produ

49 2Y(11)/ P2Y(11)-like receptors, AC5, PKA and Ca(V)1.2 into nanocomplexes at the plasma membrane of hu

50 by voltage and Ca(2+), and that voltage and Ca(2+) activations interact, less is known about the mec

51 hat BK channels are activated by voltage and Ca(2+), and that voltage and Ca(2+) activations interact

52 o moderate dietary sources of Se, Ni, Zn and Ca.

53 he ionic conditions-specifically [H(+)] and [Ca(2+)] -modulated the sol-gel transition pH, isoelectri

54 s following antigen receptor stimulation are Ca(2+) release-activated Ca(2+) (CRAC) channels.

55 quent signaling and cellular events, such as Ca(2+) mobilization, gamete formation, and gametes egres

56 periodic table, in particular metals such as Ca, Al, Na, Zn, and Fe and halogens like Cl and F, occur

57 and EDX) and diffraction indicated that U-As-Ca- and U-Ca-bearing solids resemble uranospinite [Ca(UO

58 hannel with a peripheral membrane-associated Ca(2+)-binding protein, likely ANXA1.

59 role for CaMKII in neuronal TRPV4-associated Ca(2+) responses, the importance of tightly regulated Ca

60 Here we simultaneously monitored astrocytic Ca(2+) and cAMP and demonstrate that astrocytic second m

61 ess in this pathway underscores asynchronous Ca(2+) release and arrhythmia.

62 at diastolic cytoplasmic [Ca(2+)] but not at Ca(2+) levels in the dyadic cleft during systole.

63 , suggesting a counteracting effect to avoid Ca(2+) overload.

64 2))(2)(AsO(4))(2).10H(2)O] and becquerelite [Ca(UO(2))(6)O(4)(OH)(6).8(H(2)O)].

65 Our data suggest a causal link between Ca(2+) dysregulation and primary, nonapoptotic degenerat

66 SNAREpins associated with Synaptotagmin-1 by Ca(2+) is sufficient to trigger rapid (<100 msec) and sy

67 e stages of development, which are driven by Ca(V) 1.3 Ca(2+) channels.

68 major F-actin bundlers that are inhibited by Ca(2+) in nonmuscle cells.

69 mportantly, these processes are regulated by Ca(2+) signals that occur at rest.

70 lts demonstrate that inactivation of RyR2 by Ca(2+)-CaM is a major determinant of Ca(2+) alternans, m

71 Calcium (Ca(2+) ) transients were measured in isolated cardiomyoc

72 in secretion (GSIS) is regulated by calcium (Ca(2+) ) entry into pancreatic beta-cells through voltag

73 elicited X-ROS primes intracellular calcium (Ca(2+) ) channels for synchronized activation in the hea

74 nules is dependent on intracellular calcium (Ca(2+)) signals.

75 t control mobilization of cytosolic calcium [Ca(2+)](i) are key for regulation of numerous eukaryotic

76 CaMKII (Ca(2+)/calmodulin-dependent protein kinase-II) protein-e

77 Changing activity of cardiac Ca(V)1.2 channels under basal conditions, during sympath

78 In beta cells, Ca(2+), cyclic adenosine monophosphate (cAMP), and Prote

79 with a protection from TAC-induced cellular Ca(2+) signaling alterations (increased SOCE, decreased

80 s, NCKX, are important mediators of cellular Ca(2+) efflux, particularly in neurons associated with s

81 ants that estimate stationary single-channel Ca(2+) nanodomains with great accuracy in broad regions

82 creased intracellular Ca(2+) concentration ([Ca(2+)](i)).

83 Concerning Ca(V)3.1, the compound did not alter the shape of the in

84 of ACh-mediated effects to small-conductance Ca(2+)-activated potassium (SKs) channels.

85 We used confocal Ca(2+) imaging in myocytes and HEK-RyR2 (ryanodine recep

86 tant analyses, Ca(2+) imaging and controlled Ca(2+) release to determine the mechanisms regulating a

87 s, a highly selective and tightly controlled Ca(2+) channel of the inner mitochondrial membrane that

88 Optogenetic approaches for controlling Ca(2+) channels provide powerful means for modulating di

89 e into microcircuits that exhibit correlated Ca(2+) signals.

90 d Ca(2+) (CRAC) channels elevate cytoplasmic Ca(2+) concentration, which is essential for T cell acti

91 caused inhibition at diastolic cytoplasmic [Ca(2+)] but not at Ca(2+) levels in the dyadic cleft dur

92 which, in turn, reduces diastolic cytosolic Ca(2+), leading to alternations in diastolic cytosolic C

93 ading to alternations in diastolic cytosolic Ca(2+), RyR2 inactivation, and sarcoplasmic reticulum Ca

94 GLR3.3 in the amino acid-elicited cytosolic Ca(2+) increase in Arabidopsis seedling roots.

95 e used a functional assay based on cytosolic Ca(2+) imaging.

96 e, duration, and duty cycle of the cytosolic Ca(2+) contraction signal and spatial localization have

97 H(i) (6.75-6.25) together with the cytosolic Ca(2+) rise accelerated G(i/o) -mediated TRPC4 activatio

98 nhibitory effects of even resting cytosolic [Ca(2+)] on I(Na).

99 ling alterations (increased SOCE, decreased [Ca(2+)](i) transients amplitude and decay rate, lower SR

100 ytes, which exhibit norepinephrine-dependent Ca(2+) elevations during vigilance, are not well underst

101 creatic beta-cells through voltage-dependent Ca(2+) (Ca(V) ) channels.

102 ecreased myocyte contractility and disrupted Ca(2+) cycling.

103 The disturbed Ca(2+) regulation in mut(PG1)JPH2 overexpressing myocyte

104 rovide powerful means for modulating diverse Ca(2+)-specific biological events in space and time.

105 kidney 293 cells) cells, biochemistry, dual Ca(2+)/voltage optical mapping in intact hearts from alc

106 amma can bind to PLCbeta but does not elicit Ca(2+) signals.

107 We employed Ca(2+) imaging of colonic ICC-IM in situ, using mice exp

108 eered flies expressing a genetically encoded Ca(2+) indicator in the photoreceptor ER.

109 ration of K328Q actin significantly enhanced Ca(2+) sensitivity of RTF activation relative to control

110 , dependent on mGluR5 and linked to enhanced Ca(2+) influx.

111 meostasis and apoptosis, and iii) altered ER Ca(2+) homeostasis in kidney disease, including podocyto

112 these results support a critical role for ER Ca(2+) depletion-activated Ca(2+) current in mediating C

113 on: i) Ca(2+) homeostasis in the ER, ii) ER Ca(2+) dyshomeostasis and apoptosis, and iii) altered ER

114 cent studies have highlighted the role of ER Ca(2+) imbalance caused by dysfunction of sarco/ER Ca(2+

115 Emei disruption reduces ER Ca(2+) level and subsequently leads to JNK activation an

116 imbalance caused by dysfunction of sarco/ER Ca(2+) ATPase, ryanodine receptor, and inositol 1,4,5-tr

117 lls to suppress action potential (AP)-evoked Ca(2+) signals.

118 was found that mechanical stimulation-evoked Ca(2+) responses in astrocytes of the rat brainstem were

119 Of note, OR2W3-evoked [Ca(2+)](i) mobilization and ASM relaxation required Ca(2

120 well-crystallized minerals and exchangeable Ca(2+) regardless of the presence or absence of CaCO(3),

121 to sex-specific regulation of excitability, [Ca(2+)](i), and myogenic tone in arterial myocytes.

122 lar cells subjected to hypokalemia exhibited Ca(2+) overload and increased generation of both spontan

123 that mouse lymphatic muscle cells expressed Ca(v)3.1 and Ca(v)3.2 and produced functional T-type VGC

124 positive feedback mechanism in which fluxed Ca(2+) activates nearby RyRs.

125 onally high affinity of the EhActn2 CaMD for Ca(2+), binding of which can only be regulated in the pr

126 nd an auxiliary subunit, EMRE, essential for Ca(2+) transport(3-8).

127 d the presence of an alternative pathway for Ca(2+) uptake into photoreceptor mitochondria.

128 their electrical activity and cytosolic free Ca(2+) oscillations.

129 els had suggested that several voltage-gated Ca(2+) channels (VGCCs) regulated critical signaling eve

130 ls (64% of total) generated rhythmic, global Ca(2+) transients at the SW frequency that were synchron

131 In the presence of RyRp at high Ca(2+), the closed conformation shifts to a more compact

132 titutively-bound calmodulin, whereas higher [Ca(2+) ] exerts inhibitory effect during depolarization.

133 OVX showed the lowest and ZOL the highest Ca and Pi contents in femur and maxilla (P < 0.05).

134 channel possesses similar features as human Ca(V)2.1 and other Ca(V)2 channels, including high volta

135 oxidant reduced AF burden, restored I(Na), I(Ca,L), I(Kur), action potential duration, and reversed a

136 This mini-review is focused on: i) Ca(2+) homeostasis in the ER, ii) ER Ca(2+) dyshomeostas

137 d sarcoplasmic reticulum Ca(2+) release (ie, Ca(2+) alternans).

138 esence of L-NNA and MRS 2500 enhanced ICC-IM Ca(2+) transients.

139 ency (basal) hair cells was also affected in Ca(V) 1.3(-/-) mice, but to a much lesser extent than ap

140 ion afforded 10, which was a full agonist in Ca(2+)-release assays; its potency and binding affinity

141 iomyocyte model demonstrated that changes in Ca(2+) and Na(+) homeostasis are responsible for the sur

142 evidence indicates that localized changes in Ca(2+) in oligodendrocytes can regulate the formation an

143 n kinase II (CaMKII) plays a central role in Ca(2+) signaling throughout the body.

144 s that are larger in external Ba(2+) than in Ca(2+); voltage-dependent kinetics of activation, inacti

145 whereas neostigmine and carbachol increased Ca(2+) transients.

146 ted to the compacted cells and the increased Ca(2+)-cross linked cell-cell adhesion.

147 ur study is that IP(3)R activation increases Ca(2+) transient duration for a broad range of IP(3)R pr

148 r astrocytes of mice brain is able to induce Ca(2+)-dependent gene expression without any mechanical

149 nsitivity of ost1 mutants, the cold-induced [Ca(2+) ](cyt) elevation in the ost1-3 mutant was reduced

150 on in the expression of mitochondrial influx Ca(2+) transporter genes, but upregulation in the genes

151 Nitrergic agonists inhibited Ca(2+) transients in ICC-SS, and stimulation of intrinsi

152 cyclopiazonic acid and reduced by inhibiting Ca(2+) influx via Orai channels.

153 responses to EFS were ablated by inhibiting Ca(2+) stores with cyclopiazonic acid and reduced by inh

154 Rhythmic action potentials and intercellular Ca(2+) waves are generated in smooth muscle cells of col

155 bstrate hydrolysed by PLC, and intracellular Ca(2+) .

156 ivated by membrane voltage and intracellular Ca(2+).

157 A sustained increase in intracellular Ca(2+) concentration (referred to hereafter as excitotox

158 bition prevents both increased intracellular Ca(2+) and neurotoxicity in Drosophila and cultured prim

159 in but it can follow increased intracellular Ca(2+) concentration ([Ca(2+)](i)).

160 RPV4(R269C) triggers increased intracellular Ca(2+) through a Ca(2+)/calmodulin-dependent protein kin

161 y monitoring ionomycin-induced intracellular Ca(2+) elevations with fluorometry.

162 vitro assay, and the levels of intracellular Ca(2+) uptake and Na, K-ATPase mRNA were determined in t

163 impact of such discoveries on intracellular Ca(2+) dynamics and biophysical properties.

164 sured were an increase in the intracellular [Ca(2+)] ([Ca(2+)](i)) and high-molecular-weight glycopro

165 Whole cell CRAC current is Ca(2+) -selective.

166 ptic release sites, and synapse structure is Ca(V)2 independent.

167 of B21 produce widespread increases in its [Ca(2+)](i) via activation of a nifedipine-sensitive curr

168 the results from cancerous cervical cells, K(Ca)3.1-dependent H33258 uptake was rarely observed in ep

169 es the analysis of 20 elements (Mg, P, S, K, Ca, V, Cr, Mn, Fe, Co, Cu, Zn, Se, Br, Rb, Sr, Mo, I, Cs

170 Therapeutic control of late Ca(2+) spark activity may provide an additional approach

171 vanilloid 4 (TRPV4) ion channels are a major Ca(2+) influx pathway in endothelial cells, and regulato

172 protein cofilin but does not depend on major Ca(2+)-dependent cascades in astrocytes.

173 ajor determinant of Ca(2+) alternans, making Ca(2+)-CaM dependent regulation of RyR2 an important the

174 classes of LCCBs activate STIM/ORAI-mediated Ca(2+) entry in VSMCs.

175 not its analogues, suppressed RyR2-mediated Ca release at clinically relevant concentrations.

176 in CH but decreases (tau for SERCA-mediated Ca(2+) removal changed from 6.3 to 3.0 s(-1) ) in HF.

177 crease in spark frequency and spark-mediated Ca(2+) leak.

178 (3)R channel activity and InsP(3)R-mediated [Ca(2+)](i) signaling in cells by controlling an interact

179 letion-activated Ca(2+) current in mediating Ca(2+)-induced insulin secretion in response to ER stres

180 Concentrations of 16 elements (K, Na, Mg, Ca, Fe, Zn, Hg, Se, As, Cu, Cd, Mn, Ni, Cr, Pb and Co) w

181 Low Mg/Ca, and high U/Ca, Mo/Ca, and V/Ca potentially suggest a

182 s from bioenergetic crisis and mitochondrial Ca(2+) overload during periods of nutrient stress.

183 channel complex that controls mitochondrial Ca(2+) entry and regulates cell metabolism.

184 was associated with decreased mitochondrial Ca(2+) uptake, collectively suggesting that induction of

185 BAT activates a PKA-dependent mitochondrial Ca(2+) extrusion via the mitochondrial Na(+)/Ca(2+) exch

186 on activity-driven presynaptic mitochondrial Ca(2+) uptake to accelerate ATP production.

187 ac inducible gene that reduces mitochondrial Ca(2+) influx and permeability transition pore opening a

188 nvestigate the hypothesis that mitochondrial Ca(2+) uptake via MCU influences phototransduction and e

189 lation in the genes related to mitochondrial Ca(2+) efflux pathways, suggesting a counteracting effec

190 effects of a physiologically relevant (2 mM) Ca(2+) concentration on zwitterionic phosphatidylcholine

191 Low Mg/Ca, and high U/Ca, Mo/Ca, and V/Ca potentially suggest a decreased abundance o

192 We followed changes in cardiac myocyte Ca(2+) and Na(+) regulation from the formation of compen

193 w that loss of gammaC0C7 reduced myofilament Ca(2+) sensitivity and increased cross-bridge cycling (k

194 t rapid store depletion is mediated by Na(+)/Ca(2+) exchange across the ER membrane induced by Na(+)

195 The family of K(+)-dependent Na(+)/Ca(2+)-exchangers, NCKX, are important mediators of cell

196 Ca(2+) extrusion via the mitochondrial Na(+)/Ca(2+) exchanger, NCLX.

197 rentially host the mitochondrial NCLX (Na(+)/Ca(2+) exchanger).

198 ention of Na(i) overload or inhibition of Na/Ca(mito) may be a new approach to ameliorate metabolic d

199 Plume pharmacology and plume-like neural Ca(2+) events were consistent with action-potential-inde

200 is requires Galpha(i2) and Gbeta(2), but not Ca(2+) signaling, and membrane protrusive activity is pr

201 onal dynamics in the presence and absence of Ca(2+) Only AtSCS-A has the features of a calcium sensor

202 ystis sp. PCC6803 to elucidate the action of Ca(2+) and peripheral proteins.

203 is caused by beta-adrenergic augmentation of Ca(V)1.2 voltage-gated calcium channels(1-4).

204 These increases are prevented by blockade of Ca(2+) channels and depend on downstream recruitment of

205 ate-limiting steps of the catalytic cycle of Ca(2+) transport.

206 RyR2 by Ca(2+)-CaM is a major determinant of Ca(2+) alternans, making Ca(2+)-CaM dependent regulation

207 itical to transduce the inhibitory effect of Ca(2+) and the stimulatory effect of thrombomodulin on t

208 MDIMP is a promising member of the family of Ca(2+) channel blockers, with possible application to th

209 for the discovery of the cadherin family of Ca(2+)-dependent cell-cell adhesion proteins, which play

210 Although these proxy measurements of Ca(2+) provided insight into the synchronization mechani

211 o specify the spatiotemporal mobilization of Ca(2+) to drive cell migration.

212 cellular responses through the modulation of Ca(2+) signaling, actin organization, vesicle traffickin

213 eta(3) activation and enhanced the number of Ca(2+) transients.

214 of Syt1 both in the absence and presence of Ca(2+).

215 nels and depend on downstream recruitment of Ca(2+)-activated potassium channels to the plasma membra

216 To examine how the source of Ca(2+) affects CDI, we recorded one-channel Na(+) curren

217 The main sources of Ca(2+) influx in mammalian lymphocytes following antigen

218 Crystal structures of Ca(2+)-free and Ca(2+)-bound EhActn2 reveal a calmodulin

219 Here, we identified a type of Ca(2+) "mini-sensor" in YfkE, a bacterial CAX homolog fr

220 ties, but the effect of IP(3)R activation on Ca(2+) transient amplitude is dependent on IP(3) concent

221 sure in enamel cells to assess its impact on Ca(2+) signaling.

222 P(i) accumulation and a potential impact on Ca(2+) signaling.

223 ects of mutations in the polybasic region on Ca(2+)-dependent synaptotagmin-1-PIP(2)-membrane interac

224 STIM/ORAI proteins mediate store-operated Ca(2+) entry (SOCE) and drive fibro-proliferative gene p

225 ncludes the potential role of store-operated Ca(2+) entry in these processes.

226 similar features as human Ca(V)2.1 and other Ca(V)2 channels, including high voltage-activated curren

227 ) muscles from SOD1(G37R) mice and performed Ca(2+)-imaging to monitor PSC activity and used immunohi

228 Here, we have combined two-photon Ca(2+) imaging and single-cell electrophysiology in awak

229 voked mechanisms akin to Hebbian plasticity: Ca(2+)-permeable AMPA receptor upregulation, L-type Ca(2

230 hich was prevented by chelating postsynaptic Ca(2+) or blocking nicotinic receptors.

231 RAs(3) where R = Ca, Sr, thus, offers a unique opportunity to realize an

232 Reduced Ca(V) 1.3 activity might open new ways to understand sym

233 GS967 suppressed PVT incidences by reducing Ca(2+)-mediated EADs and focal activity during isoproter

234 sponses, the importance of tightly regulated Ca(2+) dynamics for mitochondrial axonal transport, and

235 f type-2 ryanodine receptors (RyR2s) release Ca(2+) from the sarcoplasmic reticulum (SR) via a positi

236 [Ins(1,4,5)P(3)R] and the ability to release Ca(2+) from intracellular stores via type 1 Ins(1,4,5)P(

237 (i) mobilization and ASM relaxation required Ca(2+) flux through the store-operated calcium entry (SO

238 cy and neuronal signalling, neuronal resting Ca(2+) signals warrant further mechanistic analysis that

239 that dysregulation of sarcoplasmic reticulum Ca(2+) ATPase (SERCA) pump is one of the key determinant

240 , 50% decay rate, and sarcoplasmic reticulum Ca(2+) content were not different between WT (n=18) and

241 yR2 inactivation, and sarcoplasmic reticulum Ca(2+) release (ie, Ca(2+) alternans).

242 activation diminishes sarcoplasmic reticulum Ca(2+) release, which, in turn, reduces diastolic cytoso

243 Second, active zone proteins may scaffold Ca(V)2s to presynaptic release sites, and synapse struct

244 uman keratinocyte stem cells to show similar Ca(++)-induced differentiation, resulting in increased 5

245 inhibition of SERCA, and binding of a single Ca(2+) ion is sufficient to shift the protein population

246 pe Ca(2+) channel activation, enhanced spine Ca(2+) transients, nuclear translocation of a CaM shuttl

247 Spontaneous Ca(2+) transients activate Ano1 channels in ICC-SS.

248 and increased generation of both spontaneous Ca(2+) waves and delayed afterdepolarizations.

249 to IHCs, immature OHCs elicited spontaneous Ca(2+) action potentials (APs), but only during the firs

250 found that OHCs, like IHCs, fire spontaneous Ca(2+) -induced action potentials (APs) during immature

251 ates sensitize cardiomyocytes to spontaneous Ca(2+)-releases and arrhythmogenic afterdepolarizations,

252 ransients amplitude and decay rate, lower SR Ca(2+) load and depressed cellular contractility) and SE

253 determinant of beta-cell glucose-stimulated Ca(2+) entry and thus the set-point of GSIS.

254 oxygen consumption rate, glucose-stimulated Ca(2+) flux, and reduced insulin content associated with

255 ermining the set-point of glucose-stimulated Ca(2+) influx and insulin secretion.

256 cross-bridge cycling (k(tr)) at submaximal [Ca(2+)].

257 Submicromolar [Ca(2+) ] activates the channel via constitutively-bound

258 NOX4 silencing suppressed Ca(2+) oscillations, and the patch-clamped K(ATP) channe

259 mplex through the primary interface and that Ca(2+) releases this interaction, inducing PIP(2)/membra

260 elective receptor antagonists, we found that Ca(2+) mobilization downstream of P2Y(1) was essential f

261 e EF domain to the active site suggests that Ca(2+) binding is relevant to the catalytic activity.

262 The Ca(2+) ATPase NCA-2 was found to be involved in the init

263 The Ca(2+)-facilitated hydrogen-bonding network forms the st

264 Ca(2+) binding restricts the dynamics in the Ca(2+)-binding region.

265 transient and examine the sensitivity of the Ca(2+) transient shape to properties of IP(3)R activatio

266 lack of Ube3a-mediated ubiquitination of the Ca(2+)-activated small conductance potassium channel, SK

267 imicking activation of the C2A domain of the Ca(2+)-sensor Synaptotagmin-1 (Syt1), by adding a positi

268 yanodine receptor and IP(3)R channels on the Ca(2+) transient and examine the sensitivity of the Ca(2

269 methionyl-leucylphenylalanine (fMLP), or the Ca(2+) ionophore, A23187.

270 Thus, the Ca(2+)-independent, Arg-containing NrfA from G. lovleyi

271 ibrinogen binding events correlated with the Ca(2+) transient amplitude and frequency, respectively.

272 ators: i) the stimulus function and ii) the [Ca(2+)](i) changes.

273 ponent of the machinery that maintains these Ca(2+)-sensitive fraction of spontaneous release events.

274 X-ray absorption near-edge spectra of these Ca-rich particles.

275 Thus, [Ca(2+)](ER) is a major regulator of InsP(3)R channel act

276 TMEM16 Ca(2+)-activated phospholipid scramblases (CaPLSases) me

277 ncreased the sensitivity of CREB activity to Ca(2+) elevations and prolonged the duration of CREB act

278 tion channelrhodopsins, it is impermeable to Ca(2+) ions.

279 cal data reveal that OSCA1.3 is permeable to Ca(2+), and that BIK1-mediated phosphorylation on its N

280 In ovules, ACC stimulates transient Ca(2+) elevation, and Ca(2+) influx in octuple mutant ov

281 tal structure revealed an EF domain with two Ca(2+)-binding motifs inserted within the catalytic doma

282 vidence that ketamine is an effective L-type Ca(2+) channel (Cav1.2) antagonist that directly inhibit

283 permeable AMPA receptor upregulation, L-type Ca(2+) channel activation, enhanced spine Ca(2+) transie

284 A role for L-type Ca(2+) channels (Cav(L)) and anoctamin 1 (ANO1) was test

285 Only the L-type Ca(2+) current exhibits a day versus night difference in

286 that TSPAN-7 modulation of beta-cell L-type Ca(V) channels is a key determinant of beta-cell glucose

287 , CCL-2 secretion was decreased after L-type Ca(V) inhibition.

288 nd diffraction indicated that U-As-Ca- and U-Ca-bearing solids resemble uranospinite [Ca(UO(2))(2)(As

289 Low Mg/Ca, and high U/Ca, Mo/Ca, and V/Ca potentially suggest a decreased abun

290 The FRET efficiency is modulated upon Ca(2+) ion binding.

291 d U-Ca-bearing solids resemble uranospinite [Ca(UO(2))(2)(AsO(4))(2).10H(2)O] and becquerelite [Ca(UO

292 s to memory consolidation during sleep using Ca(2+) imaging in freely moving mice.

293 voltage-gated ion channels, including Na(V), Ca(V), and K(V) channels.

294 Low Mg/Ca, and high U/Ca, Mo/Ca, and V/Ca potentially suggest a decreased abundance of "centers

295 rengthening of GABA(A) receptor synapses via Ca(2+)/calmodulin-dependent protein kinase II.

296 CaM is enriched in subcellular domains where Ca(V) channels reside, such as the cardiac dyad.

297 n excitatory and inhibitory synapses whereby Ca(2+)-entering through postsynaptic NMDARs promotes the

298 In particular, the molecular basis by which Ca(2+) binding affects structure and enhances the functi

299 -nlacZ) and TRPV1-Cre:tdTomato combined with Ca(2+) imaging revealed specific localization of TRPV1 t

300 However, infection with Ca.