ライフサイエンスコーパス: Ca

1 Ca(2+) binding rigidifies elements along this pathway, t

2 Ca(2+) enters OSN cilia during the response through the

3 Ca(2+) is a ubiquitous intracellular messenger that cont

4 hesis translates classical AGP function as a Ca(2+) capacitor, pollen tube guide and wall plasticizer

5 y, our results support a role for CML36 as a Ca(2+) sensor that binds to and modulates ACA8, uncoveri

6 bly of CCPs, EGF stimulation also elicited a Ca(2+)- and PKC-dependent reduction in synaptojanin1 rec

7 ase in current density when switching from a Ca(2+)-containing solution to a divalent-free Na(+) one,

8 hrough calmodulin, which binds to TRPA1 in a Ca(2+)-dependent manner.

9 e-gated (CNG) channels and thereby induces a Ca(2+) influx, which leads to the increase in gap juncti

10 The mitochondrial calcium uniporter is a Ca(2+)-activated Ca(2+) channel complex mediating mitoch

11 Store-operated Ca(2+) entry (SOCE) is a Ca(2+)-entry process activated by the depletion of intra

12 Our work suggests a Ca(2+)-dependent process to regulate miRNA activity in n

13 ow that one isoform, AtMCU1, gives rise to a Ca(2+)-permeable channel activity that can be observed e

14 Accordingly, Ca(2+)-spark analysis in isolated TG cardiomyocytes reve

15 rial calcium uniporter is a Ca(2+)-activated Ca(2+) channel complex mediating mitochondrial Ca(2+) up

16 Here, we show that activated Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) s

17 ated cAMP Signaling (SOcAMPS) and activating Ca(2+) regulated adenylyl cyclases.

18 genetically encoded ER-targeted low-affinity Ca(2+) indicators optimized for examining axonal ER Ca(2

19 e metalation sites become more dynamic after Ca(2+) loss.

20 ory period for Ca(2+) spark initiation after Ca(2+) release in cardiac myocytes should inhibit furthe

21 ic arabinogalactan glycoprotein-calcium (AGP-Ca(2+) ) capacitor with tip-localized AGPs as the source

22 essary for efficient activity of eEF-2K, and Ca(2+) is shown to enhance the affinity of CaM toward eE

23 cantly enhanced [(3) H]ryanodine binding and Ca(2+) /calmodulin-dependent protein kinase II (CaMKII)

24 dentified as Candidatus Scalindua brodae and Ca.

25 ain chimera is permeable to Na(+), K(+), and Ca(2+) ions, and remarkably, is also robustly activated

26 eld the same information as mechanically and Ca(2+)-induced force kinetics (k+Pi(1) approximately k-P

27 iates salt tolerance by regulating Na(+) and Ca(2+) fluxes in the vacuole, cooperating with the vacuo

28 and glucose-stimulated insulin secretion and Ca(2+) uptake in the presence of glibenclamide, an inhib

29 ard, the phases were allowed to separate and Ca, K, Na, and Mg were determined in aqueous phase by me

30 ssessing both anion-vacancy order and Sr and Ca chemical order at the subnanometer scale, confirmed t

31 at is required for rapid synchronization and Ca(2+) cooperativity of vesicle release.

32 ith open probability being both voltage- and Ca(2+) -dependent.

33 is Ca(2+) -driven, electromechanically (APD-Ca(2+) ) concordant alternans becomes electromechanicall

34 g. membrane voltage or contractile apparatus Ca(2+) ion responses (force resolution 1microN, 0-10mN f

35 Synaptotagmins (Syts) act as Ca(2+) sensors in neurotransmitter release by virtue of

36 boring cells and exhibited asynchronous (AS) Ca transients.

37 However, whether resting astrocyte Ca(2+) can adjust to a new steady-state level, with an i

38 ily in the modulation of plant-autoinhibited Ca(2+) pumps.

39 th increased stimulation frequency; average [Ca(2+) ]i was a linear function of Ca entry per unit tim

40 Time-averaged [Ca(2+) ]i was increased by beta-adrenergic stimulation w

41 ude, whereas at low Pup by higher background Ca.

42 Using fluorescence-based Ca(2+) flux assays combined with pharmacology and gene k

43 exocytosis and endocytosis is assumed to be Ca(2+) dependent, but the exact role of Ca(2+) and its k

44 pectroscopy, suggesting substitution on both Ca and Zr sites.

45 SK channels were also activated by Ca(2+) influx through voltage-gated Ca(2+) channels and

46 indicating broad control of CCP assembly by Ca(2+) signals.

47 a metabolic model for autotrophic growth by Ca. P. anaerolimi whereby DPO drives CO2 reduction to fo

48 at distinct Ca(2+) domains are maintained by Ca(2+) uptake into mitochondria.

49 ecretion in pancreatic cells is regulated by Ca(2+) and ROS signaling through Ca(2+)-induced structur

50 , making release dependent on stimulation by Ca(2+)SIGNIFICANCE STATEMENT Syntaxin 1A (Syx) is a cent

51 on of the cardiac TF over the skeletal TF by Ca(2+) and lead to a mechanistic model for the regulatio

52 Calcium (Ca(2+)) and transverse-tubule imaging of ventricular myo

53 Calcium (Ca(2+)) is an essential second messenger required for di

54 ns exhibit spontaneous increases in calcium (Ca(2+)), but the mechanisms and functional significance

55 ed an accumulation of intracellular calcium (Ca(2+)) over time and cell death.

56 Ionic calcium (Ca(2+)) is an essential signal for axon guidance that me

57 y to conduct divalent cations, like calcium (Ca(2+)).

58 with all three fertilizers, but the calcium (Ca) and magnesium (Mg) was higher with ORG and 2xORG.

59 is promoted by increased cytosolic calcium ([Ca(2+)]cyto), aerobic glycolysis, and mitochondrial fiss

60 hat extinction recruited calcium/calmodulin (Ca(2+)/CaMK)-dependent protein kinase II (CaMKII) to the

61 tified as a direct inhibitor of CaMKIIdelta (Ca(2+)/calmodulin-dependent protein kinase IIdelta) acti

62 Overexcitation of the terminal causes Ca(2+) accumulation and swelling that can be prevented b

63 PMCA1 is required for maintaining cellular Ca(2+) homeostasis and electrical stability in murine at

64 CX) knockout (KO) mouse, a model of cellular Ca(2+) overload.

65 the low partial pressure of atmospheric CO2 (Ca ) experienced during the last glacial period is hypot

66 re; however the cells are able to compensate Ca(2+) homeostasis in an efficient way to minimize systo

67 otalea strains, extracted an almost complete Ca.

68 these mechanisms is that LCR exhibit complex Ca release propagation patterns (including merges and se

69 A mathematical model of a small conductance Ca(2)(+) -activated potassium (SK) channel was developed

70 ier current (IKs ) and the small conductance Ca(2+) -activated potassium (SK) current (ISK ).

71 enced the genomes of two additional cultured Ca.

72 educed the migration and the basal cytosolic Ca(2+) concentration of HCT116 colon cancer cell line an

73 highlight a potential link between cytosolic Ca(2+) signaling and the posttranslational control of re

74 AGPs as the source of tip-focussed cytosolic Ca(2+) oscillations: Hechtian adhesion between the plasm

75 ibe a mechanism by which increased cytosolic Ca(2+) negatively regulates adipokine secretion and have

76 activated by luminal Ca(2+) at low cytosolic Ca(2+) levels.

77 eau, as well as by the increase of cytosolic Ca(2+) associated with the Ca(2+) transient itself.

78 sensitization and lowering of the cytosolic Ca(2+) activation threshold.

79 cancer cell line and modified the cytosolic Ca(2+) oscillations induced by the sodium/calcium exchan

80 protein kinases (CDPKs) transduces cytosolic Ca(2+) flux into enzymatic activity, but how they functi

81 ed only a minor inhibition of P2X1-dependent Ca(2+) entry.

82 ed, while the capacity to maintain diastolic Ca(2+) is moderately increased.

83 ability of mitochondria to maintain distinct Ca(2+) domains.

84 We tested the hypothesis that distinct Ca(2+) domains are maintained by Ca(2+) uptake into mito

85 Ion-surface interactions between divalent Ca(2+) and Mg(2+) ions and the nanochannel walls reduced

86 e membrane potential, facilitates downstream Ca(2+) -dependent pathways and becomes concentrated in s

87 i metals (Li, K, Rb and Cs) and alkali-earth Ca.

88 (2+) pumps at the propagation front elevates Ca(2+) inside the SR locally, leading to luminal RyR sen

89 ating action potentials (bpAPs) could elicit Ca(2+) release from lysosomes in the dendrites.

90 ps particularly at C-domain of CaM, enabling Ca(2+) release.

91 coordination site, enabling Glu-88 to engage Ca(2+) and fucose.

92 termediate where loop 83-89 closes to engage Ca(2+) and mannose without triggering allostery that ope

93 indicators optimized for examining axonal ER Ca(2+).

94 TMEM16A provides a mechanism for enhanced ER Ca(2+) store release, possibly engaging Store Operated c

95 Here, we show that ER Ca(2+)-store depletion rapidly induces STIM1 phosphoryla

96 t that prolonged and aberrant hormone-evoked Ca(2+) increases may stimulate the production of mitocho

97 oteins (RabGAPs) inhibited histamine-evoked, Ca(2+)-dependent WPB exocytosis, presumably by inactivat

98 ution to a divalent-free Na(+) one, and fast Ca(2+)-dependent inactivation.

99 and morphologies to those that promote fast Ca(2+)-triggered release.

100 s by using a genetically encoded fluorescent Ca(2+) indicator.

101 phosphorylation functions to prime CPK28 for Ca(2+) activation and might also allow CPK28 to remain a

102 ondrial Ca(2+) uptake, a process crucial for Ca(2+) signaling, bioenergetics, and cell death.

103 This newly uncovered mechanism for Ca(2+) mobilization by beta2AR has broad implications fo

104 We also advance a new model for Ca(2+) transport by the enamel organ.

105 : The development of a refractory period for Ca(2+) spark initiation after Ca(2+) release in cardiac

106 amino acid identities revealed that the four Ca.

107 scular junctions (NMJs), where low-frequency Ca(2+) oscillations are required for synaptic refinement

108 tate)9(H2O) (MOF-1203), are constructed from Ca(2+) ions and l-lactate [CH3CH(OH)COO(-)], where Ca(2+

109 e in cardiac myocytes should inhibit further Ca(2+) release during the action potential plateau.

110 not conserved in CaV2 or CaV3 voltage-gated Ca(2+) channel subunits.

111 vated by Ca(2+) influx through voltage-gated Ca(2+) channels and synaptically activated NMDA receptor

112 It is generally accepted that voltage-gated Ca(2+) channels, CaV, regulate Ca(2+) homeostasis in exc

113 thesis, previous work has shown that glacial Ca limits vegetative growth in the wild progenitors of b

114 isplay characteristic hallmarks such as high Ca(2+) selectivity, an increase in current density when

115 ortant advance in understanding not only how Ca(2+) may improve coagulation outcomes, but also in pre

116 ich carry approximately 75% of the total IHC Ca(2+) current with slow inactivation and confer high se

117 to the interplay among: (i) ion fluxes, (ii) Ca(2+) release from the endoplasmic reticulum, (iii) int

118 lglycerol clearance from the PM and impaired Ca(2+)-triggered phosphatidylserine scrambling.

119 ptomatic characteristics, including impaired Ca(2+) transients, upregulation of Na(+)/Ca(2+) exchange

120 mutant, we explored the impacts of impaired Ca(2+) homeostasis on myofibril integrity.

121 in SK channel expression, but not changes in Ca(2+) -mediated activation of SK channels, contributes

122 CA)-mediated reuptake rather than changes in Ca(2+) influx capacity.

123 ase in SR Ca content but not the decrease in Ca(2+) transient amplitude.

124 hese results, E-Syt1 constructs defective in Ca(2+) binding in either C2A or C2C failed to rescue two

125 zation demonstrated only a 15% difference in Ca(2+) channel subunit densities.

126 with the glacial to postglacial increase in Ca , which matched the stimulation of photosynthesis, su

127 M to PSD-95 induced by a chronic increase in Ca(2+) influx is a critical molecular event in homeostat

128 findings indicate a major role for TRPV4 in Ca(2+) homeostasis and barrier function in human retinal

129 A induces an intracellular Ca(2+) increase ([Ca(2+)] i ) through PKA activation and subsequent cADPR

130 ed caffeine sensitivity as well as increased Ca(2+) in internal stores, which is consistent with incr

131 ls synchronize their openings via Ca-induced Ca release, generating high-amplitude local Ca signals k

132 ofibers exhibited increased caffeine-induced Ca(2+) release across a wide range of concentrations in

133 We show here that voltage-induced Ca(2+) transients elicited in dysferlin-null A/J myofibr

134 moral pituitaries, BIM-23A760 also inhibited Ca(2+) concentration, hormone secretion/expression and p

135 ion of 5RK promotes spontaneous and inhibits Ca(2+)-triggered release events.

136 ur findings provide mechanistic insight into Ca(2+)/calpain regulation of growth cone motility and ax

137 Intracellular Ca(2+) and Na(+) were simultaneously assessed using Fura

138 ure Mks because ABA induces an intracellular Ca(2+) increase ([Ca(2+)] i ) through PKA activation and

139 from wild type in both pH and intracellular Ca(2+) sensitivities.

140 nserved molecular link between intracellular Ca(2+) levels and energy homeostasis.

141 SK channels were activated by intracellular Ca(2+) sparks and mediated spontaneous transient outward

142 that they are not regulated by intracellular Ca(2+).

143 was significantly inhibited by intracellular Ca(2+)i chelation or CaM inhibition.

144 r cells through Orai1-mediated intracellular Ca(2+) oscillations and reveal a possible molecular basi

145 2 are involved in FXa-mediated intracellular Ca(2+) release in HUVEC and FXa reactive IgG from patien

146 zation, prolonged elevation of intracellular Ca(2+) and diminution of releasable synaptic vesicles.

147 unction, which also depends on intracellular Ca(2+) transport, could be affected by the loss of nBMP2

148 tions of EGTA, suggesting that intracellular Ca(2+) buffers play an important role in vesicle recruit

149 simultaneously monitoring the intracellular Ca(2+) responses of individual osteocytes by using a gen

150 very after photobleach during intracellular [Ca] recording.

151 Specifically, when alternans is Ca(2+) -driven, electromechanically (APD-Ca(2+) ) concor

152 cordingly, in the presence of isoproterenol, Ca(2+) transients and contraction amplitudes were smalle

153 n (the MID-domain), but is separate from its Ca(2+)-dependent priming function.

154 These findings uncover a critical K(+)-Ca(2+)-adrenergic signaling axis that acts to dampen the

155 S and CGA, some mineral elements, such as K, Ca and P, and essential amino acids, such as tryptophan,

156 a(2+) , through changes in expression of key Ca(2+) modelling protein densities, is drastically reduc

157 ents implied an approximately twofold larger Ca(2+) channel density in high release probability bouto

158 A group of "plant-like" Ca(2+)-dependent protein kinases (CDPKs) transduces cyto

159 irst-order sensory synapse and that limiting Ca(2+) accumulation in the terminal may protect against

160 how this is achieved, we have performed live Ca(2+) imaging in the nerve terminals of gonadotropin-re

161 Ca release, generating high-amplitude local Ca signals known as puffs in neurons and sparks in muscl

162 that controls growth cones is that of local Ca(2+) transients, which control the rate and direction

163 ivation of the RyRs by cytosolic and luminal Ca(2+) through a 'fire-diffuse-uptake-fire' (or FDUF) me

164 RyR1 was closed and not activated by luminal Ca(2+) at low cytosolic Ca(2+) levels.

165 hich is consistent with increased SR luminal Ca(2+) These findings define critical roles for Stac3 in

166 ecently have demonstrated that the lysosomal Ca(2+) release channel P2X4 regulates lysosome fusion th

167 ore-operated Ca(2+) entry (SOCE) is the main Ca(2+) influx pathway in lymphocytes and is essential fo

168 re-diffuse-uptake-fire' (or FDUF) mechanism: Ca(2+) uptake by SR Ca(2+) pumps at the propagation fron

169 -gated channel (CNGC) family members mediate Ca(2+) influx from cellular stores in plants.

170 wever, the properties of CaMKII that mediate Ca(2+) signals in spines remain elusive.

171 We propose that deficits in IP3-mediated Ca(2+) signaling represent a convergent hub function sha

172 Moreover, we ask whether TRPV4-mediated Ca(++)-influx evokes mast cell degranulation.

173 terminus of the Arabidopsis plasma membrane Ca(2+)-ATPase isoform 8 (ACA8) and that this interaction

174 Blocking mitochondrial Ca(2+) uniporter activity compromises the ability of mit

175 olecular mechanism that limits mitochondrial Ca(2+) overload to prevent cell death.

176 (2+) channel complex mediating mitochondrial Ca(2+) uptake, a process crucial for Ca(2+) signaling, b

177 c reticulum, a key mediator of mitochondrial Ca(2+) uptake.

178 n addition, treatment with the mitochondrial Ca(2+)-buffering protein parvalbumin significantly suppr

179 The role of mechanosensitive (MS) Ca(2+)-permeable ion channels in platelets is unclear, d

180 w honeys, with the exception of multifloral (Ca, Cr, Mo, Se), common heather (Mg, Na), bearberry (Ba,

181 The decay of Na(+) /Ca(2+) exchanger current that followed a stimulation pro

182 maker activity in the atrial-specific Na(+) /Ca(2+) exchange (NCX) knockout (KO) mouse, a model of ce

183 red Ca(2+) transients, upregulation of Na(+)/Ca(2+) exchanger function, reduction of Ca(2+) uptake to

184 ity, to quantify the interaction of neuronal Ca(2+)-Sensor proteins with their targets operating in p

185 t also led to elevated cytosolic and nuclear Ca(2+) levels.

186 experimental data, MD runs in the absence of Ca(2+) and Ax culminated in target binding site closure.

187 ofibrillar ATPase activity in the absence of Ca(2+) showed a significant increase in the presence of

188 brane potential leading to the activation of Ca(2+)-independent phospholipase A2gamma (iPLA2gamma) an

189 lecular underpinnings of lowered affinity of Ca(2+) for CaM in the presence of Ng13-49 by showing tha

190 e to give a three-dimensional arrangement of Ca(-COO, -OH) polyhedra supporting one-dimensional pores

191 e architecture dictates essential aspects of Ca signaling under both normal and diseased conditions.

192 Accordingly, increased binding of Ca(2+)/CaM to PSD-95 induced by a chronic increase in Ca

193 activity at physiological concentrations of Ca(2+) compared with the dephosphorylated protein, sugge

194 o measure total myocardial concentrations of Ca, Na, and other elements.

195 n increase in the amplitude and frequency of Ca(2+) influx through T-type and L-type Ca(2+) channels.

196 traction is proportional to the frequency of Ca(2+) oscillations within airway smooth muscle cells (A

197 average [Ca(2+) ]i was a linear function of Ca entry per unit time.

198 at rest, resulting in a continuous influx of Ca(2+) into the cell.

199 Here, we study the direct interaction of Ca(2+) with phosphatidylinositol 4,5-bisphosphate (PI(4,

200 ranslated into yield at subambient levels of Ca .

201 were not increased, and expression levels of Ca(2+)- or Na(+)-handling proteins were not altered.

202 ge and lower basal phosphorylation levels of Ca(2+)-cycling proteins including ryanodine receptor typ

203 tro as well as in cellulo in the presence of Ca(2+) and has been applied extensively for protein conj

204 their abundance in plants, the properties of Ca(2+) sensors and identification of novel target protei

205 a(+)/Ca(2+) exchanger function, reduction of Ca(2+) uptake to sarcoplasmic reticulum, reduced K(+) cu

206 ells, this is achieved by primary release of Ca(2+) from the endoplasmic reticulum via Ca(2+) release

207 o be Ca(2+) dependent, but the exact role of Ca(2+) and its key effector synaptotagmin-1 (syt1) in re

208 rticle, we will first review the key role of Ca(2+) in normal cardiac function-in particular, excitat

209 ors in neurotransmitter release by virtue of Ca(2+)-binding to their two C2 domains, but their mechan

210 ng chloride current by opening the olfactory Ca(2+)-activated chloride channel to amplify the respons

211 HIV-1-induced PS redistribution depends on Ca(2+) signaling triggered by Env-coreceptor interaction

212 effect on collagen-induced aggregation or on Ca(2+) influx via TRPC6 or Orai1 channels and caused onl

213 RPC1 resulted in a comparable suppression on Ca(2+) entry with double knockdown of both.

214 ighly compact conformation in which its open Ca(2+)-activated C-lobe and closed N-lobe cooperate to r

215 Store-operated Ca(2+) entry (SOCE) is a Ca(2+)-entry process activated

216 Store-operated Ca(2+) entry (SOCE) is the main Ca(2+) influx pathway in

217 er membrane pore formation by alamethicin or Ca(2+)-induced PTP opening.

218 ly and indirectly regulates the paracellular Ca(2+) transport pathway by modulating Cldn14 expression

219 tant stabilizes IP3R3 and induces persistent Ca(2+) mobilization and apoptosis.

220 ulations with analysis of in vivo two-photon Ca(2+) imaging data from somatosensory cortex of Fmr1 kn

221 Using chronic two-photon Ca(2+) imaging in hippocampal area CA1 of wild-type and

222 Here, we used two-photon Ca(2+) imaging to study visual processing in VGluT3-expr

223 The mechanism for reduced plateau [Ca(2+)]i upon stimulation was due to increased sarco/end

224 tunable, and often strategically positioned Ca(2+)-sensing elements.

225 ochondrial functions such as ATP production, Ca(2+) uptake and release, and substrate accumulation de

226 tions mediated by Synaptotagmin that promote Ca(2+) activation of the synaptic vesicle fusion machine

227 channels in diabetic cells exhibited reduced Ca(2+) sensitivity, single-channel open probability and

228 G cardiomyocytes revealed remarkably reduced Ca(2+) leakage and lower basal phosphorylation levels of

229 voltage-gated Ca(2+) channels, CaV, regulate Ca(2+) homeostasis in excitable cells following plasma m

230 due to increased sarco/endoplasmic reticulum Ca(2+) ATPase (SERCA)-mediated reuptake rather than chan

231 le 1 (STIM1), an endo/sarcoplasmic reticulum Ca(2+) sensor.

232 vealed both increased sarcoplasmic reticulum Ca(2+) spark frequency and disrupted JMC integrity.

233 s whereby beta2AR activation leads to robust Ca(2+) mobilization from intracellular stores via activa

234 ution 1microN, 0-10mN for the given sensor; [Ca(2+)] range 100nM-25microM).

235 In cardiac myocytes, there are several Ca(2+) -sensitive potassium (K(+) ) currents such as the

236 , which is different from the canonical SOCE/Ca(2+)-induced apoptosis in other tumors.

237 s to suppress GC growth through a novel SOCE/Ca(2+)/beta-catenin-mediated anti-proliferation of GC ce

238 re' (or FDUF) mechanism: Ca(2+) uptake by SR Ca(2+) pumps at the propagation front elevates Ca(2+) in

239 nsible for the age-associated increase in SR Ca content but not the decrease in Ca(2+) transient ampl

240 de that dysferlin prevents injury-induced SR Ca(2+) leak.

241 e, for the first time, we have shown that SR Ca content is increased in old atrial myocytes.

242 olecule-1 (STIM1), which functions as the SR Ca(2+) sensor, and Orai1, the Ca(2+)-permeable channel i

243 0 in mice led to impaired glucose-stimulated Ca(2+) dynamics and insulin secretion and recapitulated

244 CD8(+) T cells require sustained Ca(2+) signaling for inflammatory cytokine production an

245 The IHC ribbon synapse structure, synaptic Ca(2+) currents, and otoferlin distribution were unaffec

246 t the ability to dynamically change systolic Ca(2+) , through changes in expression of key Ca(2+) mod

247 Altogether, our data clearly establish that Ca(2+) entry exerts a feedback control on T-type channel

248 We found that Ca(2+) entry through mechanosensitive TRPV4 channels dur

249 We found that Ca(2+) influx through TRPV1 is necessary for capsaicin-i

250 Here, we show that Ca(2+) regulates TRPA1 through calmodulin, which binds t

251 Moreover, we could show that Ca(2+)-dependent adiponectin endocytosis contributes to

252 ak ICa-L offsets increased SR load such that Ca(2+) release from the SR was maintained during ageing.

253 e lectin domain closes loop 83-89 around the Ca(2+) coordination site, enabling Glu-88 to engage Ca(2

254 es open the beta-sheet structure between the Ca(2+) binding loops particularly at C-domain of CaM, en

255 This is well exemplified by the Ca(2+)-dependent inactivation of L-type Ca(2+) channels,

256 Upregulation of MCU clearly enhanced the Ca(2+) uptake into mitochondria, which significantly pro

257 Nixtamalization increased the Ca and Fe content, decreased the RS content to 4.19-4.43

258 tal to single-crystal cation metathesis, the Ca(2+) counterions of a preformed chiral MOF of formula

259 se findings demonstrate that the loss of the Ca(2+) channel alpha2delta-1 subunit function increases

260 ions as the SR Ca(2+) sensor, and Orai1, the Ca(2+)-permeable channel in the TT.

261 Munc13-4 promoted the Ca(2+)-stimulated fusion of VAMP8-containing liposomes w

262 nt channel (C1008-->A) in ECs suppressed the Ca(2+) entry response.

263 opsin expression gradient, we found that the Ca(2+) signals recorded from dendrites of dorsal horizon

264 We investigated whether the Ca(2+) -sensitive nature of SK channels could explain ar

265 ease of cytosolic Ca(2+) associated with the Ca(2+) transient itself.

266 ly to increase as the insects vectoring the "Ca.

267 ivation and, TRPM2-mediated increase in the [Ca(2+)]c to trigger the PYK2/MEK/ERK signalling pathway

268 This Ca(2+) release triggered the fusion of lysosomes with th

269 a result of the presence of a low threshold Ca(2+) channel, spike output functions are strongly modu

270 egulated by Ca(2+) and ROS signaling through Ca(2+)-induced structural changes promoting dimerization

271 Thus, [Ca(2+)]i controls myelin sheath development.

272 d to interconnect PI3K pathway activation to Ca(2+) signaling.

273 tion channel Piezo1, which may contribute to Ca(2+) entry and thrombus formation under arterial shear

274 the reducing-end mannose residue ligated to Ca(2+) in a primary binding site and the nonreducing ter

275 highly selective ion channel that transports Ca(2+) into the mitochondrial matrix to modulate metabol

276 and Cav2.2-NOS1 complexes voltage-triggered Ca(2+) influx through the Cav channels reliably initiate

277 For Syt1, the two Ca(2+)-saturated C2 domains have similar affinities for

278 l/L), whereas azithromycin suppressed L-type Ca(++) currents (rabbit ventricular myocytes, IC50=66.5+

279 meostatic changes were independent of l-type Ca(2+) channel activity but were contingent on the cruci

280 LCS are triggered by both L-type Ca(2+) channel activity during the action potential plat

281 hanced, increasing the probability of L-Type Ca(2+) channel opening events.

282 demonstrate that TRPC1 regulates the L-type Ca(2+) channel that contributes to the rhythmic activity

283 d decreases calcium influx across the L-type Ca(2+) channel.

284 coupling, activation of voltage-gated L-type Ca(2+) channels (LTCCs) in the plasma membrane can initi

285 that in turn pathologically recruits l-type Ca(2+) channels to facilitate coincidence detection duri

286 the Ca(2+)-dependent inactivation of L-type Ca(2+) channels, whose alteration contributes to the dra

287 y of Ca(2+) influx through T-type and L-type Ca(2+) channels.

288 itically links cellular properties of T-type Ca(2+) channels to their physiological roles.

289 For T-type Ca(2+) channels, a long-held view is that they are not r

290 trial myocytes increased significantly under Ca(2+) overload conditions and/or at higher frequency of

291 The channels synchronize their openings via Ca-induced Ca release, generating high-amplitude local C

292 of Ca(2+) from the endoplasmic reticulum via Ca(2+) release channels placed close to the physiologica

293 By coupling in vivo Ca(2+) imaging of dentate granule neurons with a novel,

294 hannels recorded in cultured astrocytes was [Ca(2+)]I dependent.

295 might also allow CPK28 to remain active when Ca(2+) levels are low.

296 ions and l-lactate [CH3CH(OH)COO(-)], where Ca(2+) ions are bridged by the carboxylate and hydroxyl

297 r findings reveal a novel mechanism by which Ca(2+) overload disrupts myofibril integrity by activati

298 lso in predicting the conditions under which Ca(2+) may prove beneficial.

299 -coil-alpha-helix transition associated with Ca(2+) uptake that involves just 7-8 out of a total of 1

300 atrial myocytes under basal conditions, with Ca(2+) overload leading to even greater prolongation.