ライフサイエンスコーパス: Ca2 concentration

1 e PN, and a subsequent fast rise and fall of Ca2+ concentration.

2 g2+ and was independent of the extracellular Ca2+ concentration.

3 in response to changes in the intracellular Ca2+ concentration.

4 have shorter outer segments and a lower free-Ca2+ concentration.

5 able channel that is modulated by changes in Ca2+ concentration.

6 hesis stimulated by increasing intracellular Ca2+ concentration.

7 tor receptor is an increase in intracellular Ca2+ concentration.

8 s, must effectively respond to variations in Ca2+ concentration.

9 the exchanged fiber bundles as a function of Ca2+ concentration.

10 e channel activities by CaM depending on the Ca2+ concentration.

11 d with a transient rise in the nucleoplasmic Ca2+ concentration.

12 o neuron-wide changes in internal background Ca2+ concentration.

13 reticulum lumen to maintain a low cytosolic Ca2+ concentration.

14 gnaling and a biphasic rise in the cytosolic Ca2+ concentration.

15 tle or no change in bulk average cytoplasmic Ca2+ concentration.

16 cued" by transiently elevating extracellular Ca2+ concentration.

17 ode temporal and spatial changes in cellular Ca2+ concentration.

18 erences in stimuli into large differences in Ca2+ concentration.

19 f LTD depends on both stimulus frequency and Ca2+ concentration.

20 to reach the normal light-induced minimum in Ca2+ concentration.

21 ic acid-evoked increase in the intracellular Ca2+ concentration.

22 hysiological membrane potential and external Ca2+ concentration.

23 P triggered a strong increase in cytoplasmic Ca2+ concentrations.

24 moted over a relatively narrow range of free Ca2+ concentrations.

25 e calcium channels, leading to a decrease in Ca2+ concentrations.

26 monitor a simultaneous increase of cAMP and Ca2+ concentrations.

27 lectivity despite relatively low cytoplasmic Ca2+ concentrations.

28 e mutant inhibited GC only partially at high Ca2+ concentrations.

29 sphorylation due to a reduction in cytosolic Ca2+ concentrations.

30 entrations and a cytoplasmic pattern at high Ca2+ concentrations.

31 at cells, inhibited Ca2+ uptake at very high Ca2+ concentrations.

32 rge enhancement of GCAP activation under low Ca2+ concentrations.

33 with several agents that alter intracellular Ca2+ concentrations.

34 contact with eukaryotic cells, serum or low Ca2+ concentrations.

35 hannels and increasing resting intraterminal Ca2+ concentrations.

36 stinctly promoted at 1 to 15 micromolar free Ca2+ concentrations.

37 are thought to be key mediators of cytosolic Ca2+ concentrations.

38 ion of guanylyl cyclase at both high and low Ca2+ concentrations.

39 roM, but decreased ca 5- to 10-fold at lower Ca2+ concentrations.

40 are independent of changes in intracellular Ca2+ concentrations.

41 with Zn2+ were unaffected by up to equimolar Ca2+ concentrations.

42 fact open IP3Rs experience elevated "domain" Ca2+ concentrations.

43 essed in response to increased intracellular Ca2+ concentrations.

44 d convert the observed FRET ratio changes to Ca2+ concentrations.

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

46 ed, but rather CaM inhibited the RYR2 at all Ca2+ concentrations (100 nM to 1 mM).

47 ant membrane potential (-40 mV) and external Ca2+ concentration (2 mm).

48 urrents that were recorded routinely at high Ca2+ concentrations (20-110 mM) did not.

49 In contrast, at a reduced Ca2+ concentration a population of PMCA-CaM complexes ap

50 iates a biphasic elevation in cytosolic free Ca2+ concentration, a rapid initial peak observed within

51 within the cell can transiently elevate the Ca2+ concentration above the level expected from the ope

52 K+ exchanger, hence lowering the cytoplasmic Ca2+ concentration, activating guanylyl cyclase, raising

53 er constitutively or in response to elevated Ca2+ concentration allows the NCS proteins to discrimina

54 The resting level of intracellular Ca2+ concentrations also affects CaMKII/CaN operation: a

55 cant and sustained increase in intracellular Ca2+ concentration, although vitronectin-induced Ca2+ cu

56 es a biphasic increase in intracellular free Ca2+ concentration: an initial transient phase reflectin

57 ke a biphasic increase in intracellular free Ca2+ concentration: an initial transient release of Ca2+

58 prevents age-related decreases in myoplasmic Ca2+ concentration and consequently in specific force in

59 te decreased arteriole myocyte intracellular Ca2+ concentration and dilated brain slice arterioles an

60 ing proteome to identify regulators of basal Ca2+ concentration and found STIM2 as the strongest posi

61 cal activation of Yvc1p occurs regardless of Ca2+ concentration and is apparently independent of its

62 onse was still observed in low extracellular Ca2+ concentration and probably reflects mobilization of

63 ough spatiotemporal changes in the cytosolic Ca2+ concentration and subsequent interactions with Ca2+

64 The relationship between the free Ca2+ concentration and the apparent dissociation constan

65 nction of mGluR8 of modulating the cytosolic Ca2+ concentration and thereby potentially the release o

66 s within characteristic regimes of cytosolic Ca2+ concentration and time.

67 llular Ca2+ stores by lowering extracellular Ca2+ concentration and treatment with the Ca2+-ATPase in

68 sensitivity to alterations in intracellular Ca2+ concentration and underwent little rundown.

69 epsilonRI-induced elevation of intracellular Ca2+ concentrations and activation of protein kinase Cs

70 to account for increased intracellular free Ca2+ concentrations and changes in gene expression assoc

71 bly under conditions of normal extracellular Ca2+ concentrations and initiates tight junction assembl

72 he late phase through altering intracellular Ca2+ concentrations and K+ channel activity.

73 ction potentials that increase intracellular Ca2+ concentrations and of inhibitory signals through G(

74 f [Ca2+]o and [Ca2+]i are controlled by soil Ca2+ concentrations and transpiration rates.

75 ed Ca2+ dependent but was activated at lower Ca2+ concentrations and with a lower Ca2+ cooperativity

76 e, activated by a reduction in intracellular Ca2+ concentration, and inactivated by higher intracellu

77 by red light involves a rise in cytoplasmic Ca2+ concentration, and that a contribution to this end

78 d nuclear phospho-CREB levels, intracellular Ca2+ concentration, and transcription of c-fos.

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

80 second messenger pathways and intracellular Ca2+ concentrations, and is influenced by neuromodulator

81 nts correspond to bulk cytosolic and luminal Ca2+ concentrations, and the remaining 2N compartments r

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

83 ts that were recorded in quasi-physiological Ca2+ concentrations (approximately 2-5 mM) showed clear

84 round & Aims: Oscillations in cytosolic free Ca2+ concentration are a fundamental mechanism of intrac

85 In the AMP-PNP preincubation, low Ca2+ concentrations are not required, and retGC exists a

86 In turn, cytoplasmic Ca2+ concentrations are regulated by mitochondria.

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

88 that it is incompletely inactivated by high Ca2+ concentrations as should occur with dark adaptation

89 Thus, at low Ca2+ concentrations at pH 8.0, selective degradation of

90 immediately disassembled after lowering the Ca2+ concentration below 0.1 mM.

91 ng site eliminated CaM inhibition of RyR2 at Ca2+ concentrations below and above 1 microm.

92 eta and gamma heavy chains does not occur at Ca2+ concentrations below pCa 6 but is maximally activat

93 tion of membrane depolarization and elevated Ca2+ concentration, both consequences of oxidase activit

94 e [NaCl]L-dependent changes in intracellular Ca2+ concentration, but hydrochlorothiazide had no effec

95 Preventing the increase in intracellular Ca2+ concentration by the inhibitor of Galphaq or phosph

96 -700 polymorphism shifted the EC50 to higher Ca2+ concentrations (Ca Ser-700 EC50 of 950 microM and E

97 Raising intracellular Ca2+ concentration ([Ca]i) from 10 to 200 microM increas

98 Intracellular T-cell Ca2(+ )concentration, [Ca(2+)](i), was measured by the u

99 erms of neural activity and cytoplasmic-free Ca2+ concentration ([Ca2+]) is complicated by the nonlin

100 cyclic nucleotide levels, and intracellular Ca2+ concentration ([Ca2+]).

101 tes processes dependent on local cytoplasmic Ca2+ concentration ([Ca2+]c), particularly the flux of C

102 TP and ATP stimulated increases in cytosolic Ca2+ concentration ([Ca2+]c), with both nucleotides achi

103 es were used to monitor changes in cytosolic Ca2+ concentration ([Ca2+]c; fura-2FF) and mitochondrial

104 A transient increase in cytosolic Ca2+ concentration ([Ca2+]cyt) is thought to be a prereq

105 , a transient decrease in free extracellular Ca2+ concentration ([Ca2+]e), and a corresponding transi

106 wing simultaneous measurement of cytoplasmic Ca2+ concentration ([Ca2+]i) and [Ca2+]m, respectively.

107 onitor simultaneously changes in cytoplasmic Ca2+ concentration ([Ca2+]i) and mitochondrial potential

108 Intracellular Ca2+ concentration ([Ca2+]i) and NO production ([NO]i) o

109 d requires a transient rise in intracellular Ca2+ concentration ([Ca2+]i) but not concurrent activati

110 Modulation of cytoplasmic free Ca2+ concentration ([Ca2+]i) by receptor-mediated genera

111 duration of the signal conveyed by cytosolic Ca2+ concentration ([Ca2+]i) changes is regulated is not

112 The rate of intracellular Ca2+ concentration ([Ca2+]i) clearance was studied after

113 vealed a transient increase in intracellular Ca2+ concentration ([Ca2+]i) during brief (5-50 ms) depo

114 ying transient changes in intracellular free Ca2+ concentration ([Ca2+]i) evoked by pulsed infrared r

115 = 6.0 +/- 0.3 nM) increases in intracellular Ca2+ concentration ([Ca2+]i) in a proportion of dorsal r

116 late oscillations (spikes) in cytosolic free Ca2+ concentration ([Ca2+]i) in A7r5 rat vascular smooth

117 in modulating contraction and intracellular Ca2+ concentration ([Ca2+]i) in intact cardiac myocytes.

118 odulation and hence control of intracellular Ca2+ concentration ([Ca2+]i) in neuronal tissues.

119 hways leading to a rise in the intracellular Ca2+ concentration ([Ca2+]i) in pulmonary artery smooth

120 studied, the peak increase in intracellular Ca2+ concentration ([Ca2+]i) in response to depolarizati

121 ates robust oscillatory changes in cytosolic Ca2+ concentration ([Ca2+]i) in single cells by rapid, r

122 concentrations of NO increased intracellular Ca2+ concentration ([Ca2+]i) in somata, dendrites, and p

123 ut their contribution to the control of free Ca2+ concentration ([Ca2+]i) in the inner segments of ve

124 e CCK secretion and changes in intracellular Ca2+ concentration ([Ca2+]i) in two enteroendocrine cell

125 indicating that an increase in intracellular Ca2+ concentration ([Ca2+]i) is a potential pathway lead

126 tially restricted elevation of intracellular Ca2+ concentration ([Ca2+]i) on one side of the growth c

127 Changes in intracellular Ca2+ concentration ([Ca2+]i) play an important role in t

128 y test if acute hypoxia causes intracellular Ca2+ concentration ([Ca2+]i) rises through CCE in canine

129 membrane capacitance and intracellular free Ca2+ concentration ([Ca2+]i) showed that BDM action on O

130 roduce a sustained increase in intracellular Ca2+ concentration ([Ca2+]i) that was dependent on the c

131 We show that reduction of intracellular free Ca2+ concentration ([Ca2+]i) to <40 nM in Listeria monoc

132 inea-pig ventricular myocytes; intracellular Ca2+ concentration ([Ca2+]i) was measured with Indo-1.

133 nts in both ATP/ADP ratio and cytosolic free Ca2+ concentration ([Ca2+]i) were increased compared wit

134 Ca2+ release modulates the cytoplasmic free Ca2+ concentration ([Ca2+]i), providing a ubiquitous int

135 ymethyl ester to measure their intracellular Ca2+ concentration ([Ca2+]i), they were shown to possess

136 depended solely on the rise in intracellular Ca2+ concentration ([Ca2+]i), whereas the TRPC channel-m

137 onist-mediated oscillations in intracellular Ca2+ concentration ([Ca2+]i), which are driven by store-

138 nous oscillations in beta cell intracellular Ca2+ concentration ([Ca2+]i), which lead to pulsatile in

139 gulated, by an increase in the intracellular Ca2+ concentration ([Ca2+]i).

140 an appropriately elevated free intracellular Ca2+ concentration ([Ca2+]i).

141 cessitate tight regulation of free cytosolic Ca2+ concentration ([Ca2+]i).

142 R and a cAMP-dependent rise in intracellular Ca2+ concentration ([Ca2+]i).

143 activity of FDSs and on global intracellular Ca2+ concentration ([Ca2+]i).

144 cell shortening and changes in intracellular Ca2+ concentration ([Ca2+]i).

145 ponding transient rise in free intracellular Ca2+ concentration ([Ca2+]i).

146 tor rhod-2 was used to monitor mitochondrial Ca2+ concentration ([Ca2+]m) in gastric smooth muscle ce

147 was unaffected by lowering the extracellular Ca2+ concentration ([Ca2+]o) from 1.5 to 0.5 mM, but inc

148 cillations are synchronized to extracellular Ca2+ concentration ([Ca2+]o) oscillations largely throug

149 ability (P(r)) by changing the extracellular Ca2+ concentration ([Ca2+]o).

150 ptions: (i) that the resting myoplasmic free Ca2+ concentration ([Ca2+]R) and the total concentration

151 ISO application.Measurement of intra-SR-free Ca2+ concentration ([Ca2+]SR) showed an initial increase

152 In eukaryotes, changes in cytosolic Ca2+ concentrations ([Ca2+]cyt) are associated with a nu

153 hibition of either Na+ influx or the rise of Ca2+ concentrations ([Ca2+]i) at nerve terminals prevent

154 Mycoplasma flocculare on intracellular free Ca2+ concentrations ([Ca2+]i) in porcine ciliated trache

155 Intracellular Ca2+ concentrations ([Ca2+]i) in proliferating cortical

156 MCs) is poorly understood, but intracellular Ca2+ concentrations ([Ca2+]i) in the 2 cells are coordin

157 ent elevation of both cAMP and intracellular Ca2+ concentrations ([Ca2+]i).

158 Decreasing extracellular Ca2+ concentrations ([Ca2+]o) activated slow and sustain

159 ustained Rho-dependent increase in cytosolic Ca2+ concentration [Ca2+]i in endothelial cells overexpr

160 alpha) (PGF(2alpha)) increases intracellular Ca2+ concentration [Ca2+]i in vascular smooth muscle rem

161 n these findings, that at high intracellular Ca2+ concentrations, Ca2+-synaptotagmin I can displace G

162 n, repetitive increases in the intracellular Ca2+ concentration, [Ca2+]i, drive the completion of mei

163 Applying imaging of cytoplasmic free Ca2+ concentration, [Ca2+]i, we found that beta cell osc

164 skeletal muscle in which increasing internal Ca2+ concentration (Cai2+) in the range of 5 to 30 micro

165 ic flux, ATP-to-ADP ratio, and intracellular Ca2+ concentration) can dramatically enhance ROS product

166 g graded transmitter release, the background Ca2+ concentration changes evoked by low-threshold Ca2+

167 ardiomyocytes, given the extreme cytoplasmic Ca2+ concentration changes that underlie contraction, re

168 lts cannot be interpreted solely in terms of Ca2+ concentration changes, although the observations il

169 oponin, bound to the thin filaments, couples Ca2+-concentration changes to the movement of tropomyosi

170 We conclude that changes in Ca2+ concentration close to the intracellular opening of

171 to affect flash kinetics, the outer segment Ca2+ concentration closely follows the wave form of the

172 hTRPM3-expressing cells exhibited Ca2+ concentration-dependent Ca2+ entry.

173 Depression of Ca2+ extrusion produces Ca2+ concentration dynamics that depend on the history o

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

175 eneration or alter C5a-induced intracellular Ca2+ concentration elevations.

176 ta were gathered over a variety of lipid and Ca2+ concentrations, enabling the rigorous application o

177 it spontaneous oscillations in intracellular Ca2+ concentration, enhanced by tubular flow and luminal

178 inhibited the increase in free intracellular Ca2+ concentration evoked by depolarization; however, ef

179 ing exposure to steady background light, the Ca2+ concentration falls in proportion to the steady-sta

180 hatidylserine membranes occurs at micromolar Ca2+ concentrations for the cPLA2-alpha C2 domain, but r

181 2 domain, but requires 3- and 10-fold higher Ca2+ concentrations for the PKC-beta and Syt-IA C2 domai

182 binding with affinities corresponding to the Ca2+ concentrations found in the ER (Kd values range fro

183 r-induced current responses and intraciliary Ca2+ concentration from isolated salamander olfactory re

184 measurements cannot be made of intracellular Ca2+ concentration from the same cell using fluorescent

185 multiple determinations of photocurrent and Ca2+ concentration from the same cells.

186 ion of [3H]ryanodine binding above threshold Ca2+ concentrations (>or=0.3 microM), but MH mutations (

187 sicles is highly cooperative with respect to Ca2+ concentration (Hill constant approximately 7), ther

188 aMKII by itself showed a steep dependence on Ca2+ concentration [Hill coefficient (nH) approximately

189 induces a transient increase in cytoplasmic Ca2+ concentration in animal eggs that releases them fro

190 naling in T cells, we continuously monitored Ca2+ concentration in Bcl-2-positive and -negative clone

191 s in a manner consistent with increasing the Ca2+ concentration in both the +/+ and +/- mouse types.

192 + buffer in many cells, regulating the local Ca2+ concentration in cellular microdomains.

193 activity and elevated the rod outer segment Ca2+ concentration in darkness, measured by using fluo-5

194 tive at 250 nM free Ca2+, the normal resting Ca2+ concentration in darkness.

195 uR8 activity and modulation of the cytosolic Ca2+ concentration in mouse photoreceptors.

196 nsors can be modified further to measure the Ca2+ concentration in other cellular compartments, provi

197 that recent time-dependent data on the free Ca2+ concentration in pancreatic islets and beta-cell cl

198 e of Ca2+ oscillations and the intracellular Ca2+ concentration in perimacular cortical thick ascendi

199 sensing and transducing changes in cellular Ca2+ concentration in response to several biotic and abi

200 d increased the peak change in intracellular Ca2+ concentration in response to this lipid hydroperoxi

201 In longer studies, increasing the Ca2+ concentration in saline nutrient solutions resulted

202 ction-potential-induced transient changes in Ca2+ concentration in spines and dendrites of CA1 pyrami

203 om Ca2+ sensitivity in the fetal arteries to Ca2+ concentration in the adult vessels.

204 e of the [Ca2+]i transient depended upon the Ca2+ concentration in the bathing medium in the range 0-

205 In vivo, where the extracellular Ca2+ concentration in the endolymph surrounding the hair

206 In both cases, the Ca2+ concentration in the ER increased in response to ex

207 Basal Ca2+ concentrations in PS1 mutants were never lower than

208 capacitative calcium entry and intracellular Ca2+ concentrations in rat basophilic leukemia (RBL-2H3

209 ins that activate guanylyl cyclase when free Ca2+ concentrations in retinal rods and cones fall after

210 (protein SPCA1), responsible for controlling Ca2+ concentrations in the cytoplasm and Golgi in human

211 ns in the Ca2+ ATPase ATP2C1, which controls Ca2+ concentrations in the cytoplasm and Golgi of human

212 cient NADH shuttling, linked with changes in Ca2+ concentration, in sensitive cells of the central ne

213 Cytosolic Ca2+ concentrations, in turn, play a major role in the r

214 rn, regulated the differential intracellular Ca2+ concentration increase across the growth cone.

215 and produce prolonged increases in cytosolic Ca2+ concentrations increase calcineurin activity.

216 The mechanism by which intracellular Ca2+ concentrations increase remains unknown despite con

217 s for agonist-induced reductions in the free Ca2+ concentration inside the ER, we estimate that the c

218 Each of these agents reduced the Ca2+ concentration inside the nuclear envelope, and this

219 -induced contraction at experimentally fixed Ca2+ concentrations, involves (a) G protein activation,

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

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

222 en the cell is depolarized and the cytosolic Ca2+ concentration is elevated, and releases Ca2+ when t

223 However, the dark intraterminal Ca2+ concentration is lower in rods than in cones, as de

224 he onset of bright backgrounds, however, the Ca2+ concentration is markedly higher than expected from

225 fore demonstrate that the cone outer segment Ca2+ concentration is predominantly a function of the ra

226 lease triggered in wild-type synapses at low Ca2+ concentrations is physiologically asynchronous, and

227 at various stimulus frequencies and external Ca2+ concentrations is reproduced in both model simulati

228 2 activates retinal guanylyl cyclases at low Ca2+ concentration (<100 nM) and inhibits them at high C

229 activity-dependent changes in intracellular Ca2+ concentration may contribute to short-term synaptic

230 2+ sensors capable of real-time quantitative Ca2+ concentration measurements in specific subcellular

231 When treated with increasing Ca2+ concentrations, mitochondria from mutant huntingtin

232 caged Ca2+ chelator that changes in internal Ca2+ concentration modulate spike-mediated synaptic tran

233 aded with EGTA revealed significantly higher Ca2+ concentration near the interface, indicating Ca2+ i

234 pigment bleaching inevitably occurs, but the Ca2+ concentration nevertheless rises and falls in appro

235 be able to detect increases in extracellular Ca2+ concentrations observed in the pre-dentin matrix in

236 an increase in subsarcolemmal intracellular Ca2+ concentration occurred concomitantly with the last

237 Half-activation of the channel occurs at a Ca2+ concentration of 0.5 mM (at -80 mV).

238 The cytosolic Ca2+ concentration of acutely isolated rod photoreceptor

239 At intracellular Ca2+ concentrations of 250 nm, current activation was tr

240 te solutions containing 10 mm BAPTA and free Ca2+ concentrations of approximately 17 nm.

241 To assess the effects of cytosolic Ca2+ concentration on I(Ca), we used Ba2+ instead of Ca2

242 hibiting SOCE through lowering extracellular Ca2+ concentration or by application of 2-aminoethoxydip

243 During normal rhythmic activity, background Ca2+ concentration oscillates, and thus graded synaptic

244 of responding to increases in intracellular Ca2+ concentration over the narrow dynamic range of 200-

245 Consistent with this are recordings of free Ca2+ concentration, oxygen consumption, mitochondrial me

246 ed Ca2+ dependence in physiological range of Ca2+ concentrations (pCa 8-5); 2), in the same experimen

247 At normal Ca2+ concentration, platelets formed rolling as well as

248 Changes in cellular or subcellular Ca2+ concentrations play essential roles in plant develo

249 s by preventing an increase in intracellular Ca2+ concentration, potentiating ERK activation, and dec

250 By contrast, increases in intracellular Ca2+ concentration provoked by cell depolarization with

251 Golgi Ca2+ refill is slower, and the maximum Ca2+ concentration reached is significantly lower.

252 on occurs within a wide voltage range and at Ca2+ concentrations reached in the myocyte at rest and d

253 ranslocation is driven by the C2 domain when Ca2+ concentration reaches 1-3 microM.

254 5E) and S505A increased with the decrease in Ca2+ concentration, reaching >60-fold at 2.5 microm Ca2+

255 Guanine nucleotide binding and Ca2+ concentration reciprocally regulate TG's transamida

256 s is shown to report changes in luminal free Ca2+ concentration reliably.

257 Also flufenamic acid and zero external Ca2+ concentration, respectively, potentiated and reduce

258 ted in a rightward shift in both the PS- and Ca2+-concentration response curves for PKCalpha membrane

259 n the light and inhibits it in the dark when Ca2+ concentrations rise.

260 associate with the channel even before local Ca2+ concentration rises.

261 ontractile cells, increases in intracellular Ca2+ concentration serve as a second messenger to signal

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

263 hannels and have impaired intracellular free Ca2+ concentration-signaling responses to depolarization

264 ibres using synthetic localized increases in Ca2+ concentration, SLICs, generated by two-photon photo

265 Lowering the external Ca2+ concentration slowed both activation and adaptation

266 ingle, large wave of elevated free cytosolic Ca2+ concentration that emanates from the point of sperm

267 ge, transient increase in intracellular free Ca2+ concentration that is responsible for re-initiation

268 ning prevented the increase in intracellular Ca2+ concentration that normally follows H2O2 exposure.

269 ansmission follows the changes in background Ca2+ concentration that these baseline potential changes

270 ing to its kinase homology domain under high Ca2+ concentrations that allows large enhancement of GCA

271 y more responsive to caffeine than WTRyR1 at Ca2+ concentrations that approximate those in resting my

272 serves as a second messenger given the high Ca2+ concentrations that control contraction.

273 pecificity is achieved at physiological bulk Ca2+ concentrations that during a typical signaling even

274 ytoplasm is continually bathed with systolic Ca2+ concentrations that should maximally activate most

275 rapid and transient changes in intracellular Ca2+ concentrations that were blocked by the Ca2+ channe

276 At a high Ca2+ concentration, the distribution of modulation depth

277 In both Ca2+ concentrations, the conductance was positively corr

278 creases presynaptic, but not dendritic, free Ca2+ concentration; this Ca2+ rise is blocked by thapsig

279 C activation as shown here and to reduce the Ca2+ concentrations through cGMP phosphodiesterase activ

280 purinergic pathways that raise intracellular Ca2+ concentration to stimulate an alternate pathway to

281 n described by assigning continuously valued Ca2+ concentrations to one or more dyadic compartments.

282 ogical responses (increases in intracellular Ca2+ concentrations) to acid taste stimuli.

283 substantially to cytosolic free calcium ion (Ca2+) concentration transients and thereby modulate neur

284 rtension (IPAH), whereas a rise in cytosolic Ca2+ concentration triggers PASMC contraction and stimul

285 Perturbations in normal intracellular Ca2+ concentrations underlie many common pathological co

286 f ferricytochrome c, 2) monitoring fluxes in Ca2+ concentration using Fura 2-AM-loaded PMN, and 3) de

287 olgi Ca2+ stores, we measured intraorganelle Ca2+ concentrations using specifically targeted aequorin

288 The peak Ca2+ concentration values in response to prolonged stimu

289 ed HF by tachypacing in sheep; intracellular Ca2+ concentration was measured in voltage-clamped ventr

290 s and was greatly enhanced when the external Ca2+ concentration was reduced.

291 Js mediated the propagation of intracellular Ca2+ concentration waves in supporting cells by allowing

292 s of open and blocked times as a function of Ca2+ concentration were used to calculate rates of block

293 and activation attained at saturating PS and Ca2+ concentrations were in each case unaffected.

294 Intracellular Ca2+ concentrations were optically recorded in acutely i

295 in levels at both low and high extracellular Ca2+ concentrations when compared with normal control ke

296 y based on variations of their intracellular Ca2+ concentrations, which leads to glutamate release, t

297 iation constant for the complex and the free Ca2+ concentration, with a distance of 5-6 microM betwee

298 ne is the major determinant of outer segment Ca2+ concentration within the rod's normal operating lig

299 ack module that keeps basal cytosolic and ER Ca2+ concentrations within tight limits.

300 mans, physiological changes in extracellular Ca2+ concentrations would be an important determinant of