ライフサイエンスコーパス: Ca2 uptake

1 s release of mitochondrial Ca2+ and prevents Ca2+ uptake.

2 ired for optimal activation of mitochondrial Ca2+ uptake.

3 O. produced by SR-associated NOS inhibits SR Ca2+ uptake.

4 s not directly involved in A beta P-mediated Ca2+ uptake.

5 cts are mediated by changes in mitochondrial Ca2+ uptake.

6 urther increasing cytosolic Ca2+ by reducing Ca2+ uptake.

7 ng depolarization, may involve mitochondrial Ca2+ uptake.

8 ng site is responsible for the inhibition of Ca2+ uptake.

9 not directly involved in the AbetaP-mediated Ca2+ uptake.

10 e-induced Ca2+ release, without affecting SR Ca2+ uptake.

11 exon, cAMP failed to regulate Na+-dependent Ca2+ uptake.

12 -ATPase activity paralleled their effects on Ca2+ uptake.

13 I may have stimulatory effects on ICa and SR Ca2+ uptake.

14 en prolonged Ca2+ transients, and augment SR Ca2+ uptake.

15 ly implicated in mating pheromone-stimulated Ca2+ uptake.

16 ecrease in [Ca2+] within the bath, due to SR Ca2+ uptake.

17 a2+ efflux pathway rather then inhibition of Ca2+ uptake.

18 tochondrial membrane potential and decreased Ca2+ uptake.

19 how that pigmentation requires mitochondrial Ca2+ uptake.

20 pling between Ca2+ release and mitochondrial Ca2+ uptake.

21 nel sensitive to inhibitors of mitochondrial Ca2+ uptake.

22 secondary to Ca2+-dependent activation of SR Ca2+ uptake.

23 and demonstrates a role for TRPC3 in apical Ca2+ uptake.

24 e uniporter responsible for energy-dependent Ca2+ uptake.

25 ndently published data sets on mitochondrial Ca2+ uptake.

26 ation within the SR, resulting in maintained Ca2+ uptake.

27 2+ without further increase in mitochondrial Ca2+ uptake.

28 induced a significant (P < 0.05) increase in Ca2+ uptake accompanied by membrane depolarization (9 mV

29 investigated how inhibition of mitochondrial Ca2+ uptake affects transmitter release from mouse motor

30 store [Ca2+] signals as greatly accelerated Ca2+ uptake after Ca2+ release from internal stores.

31 The kinetics of microsomal Ca2+ uptake after phospholamban phosphorylation or tryps

32 Mitochondrial Ca2+ uptake also increases the dynamic range over which

33 (iii) Impaired mitochondrial Ca2+ uptake alters the spatiotemporal characteristics of

34 Impaired sarcoplasmic reticular (SR) Ca2+ uptake and a greater dependence on Na+/Ca2+ exchang

35 have a higher capacity for energy-dependent Ca2+ uptake and a greater resistance to Ca(2+)-induced r

36 Ts) temperature-sensitive growth which block Ca2+ uptake and accumulation, suggesting that cytosolic

37 acellular Na+ ([Na+]i) affects mitochondrial Ca2+ uptake and bioenergetics.

38 + overload by reducing the driving force for Ca2+ uptake and by activating cyclosporin-sensitive Ca2+

39 cid (EC50 approximately 3 microM) stimulated Ca2+ uptake and calcium-activated ATP hydrolysis at subm

40 Quercetin had a biphasic effect on Ca2+ uptake and calcium-stimulated ATP hydrolysis in iso

41 opsis thaliana rhd2 mutants are defective in Ca2+ uptake and consequently cell expansion is compromis

42 rotein exhibit a defect in pheromone-induced Ca2+ uptake and consequently lose viability upon mating

43 mic reticulum, because endoplasmic reticulum Ca2+ uptake and content were reduced in betaIRS1-A cells

44 ances, however, are active in modifying both Ca2+ uptake and efflux through oat and pea leaf protopla

45 lism, and the possibility that mitochondrial Ca2+ uptake and extrusion modulate free cytosolic [Ca2+]

46 Measuring both 12-min Ca2+ uptake and initial Ca2+ uptake rates, the apparent

47 In contrast, Ca2+ uptake and InsP3-independent Ca2+ release were very

48 ons, suggesting that the activity of both SR Ca2+ uptake and Na(+)-Ca2+ exchange is affected by lacta

49 Under these conditions, mitochondrial Ca2+ uptake and Na+/Ca2+ exchange do not significantly i

50 effect of NO depended on the initial rate of Ca2+ uptake and on the concentration of ATP and was abol

51 oss the inner mitochondrial membrane blocked Ca2+ uptake and pacemaker currents in cultured ICC and b

52 s as a critical determinant of mitochondrial Ca2+ uptake and pigmentation.

53 gly, keratin5 in turn augments mitochondrial Ca2+ uptake and potentiates melanogenesis by regulating

54 a2+ load mechanistically due to increased SR Ca2+ uptake and reduced SR Ca2+ leak.

55 , these knockdown myotubes exhibited reduced Ca2+ uptake and reduced stored Ca2+ release by UTP (400

56 nctions, several inhibitors of mitochondrial Ca2+ uptake and release (tetraphenylphosphonium or TPP+,

57 Thapsigargin (5 microM) prevented Ca2+ uptake and release by the sarcoplasmic reticulum.

58 ) the plasma membrane electrophysiology; (b) Ca2+ uptake and release from the sarcoplasmic reticulum

59 was prevented by inhibitors of mitochondrial Ca2+ uptake and release mechanisms.

60 tary time courses of mitochondrial versus ER Ca2+ uptake and release suggest that these organelles pa

61 Inhibitors of Ca2+ influx, SR Ca2+ uptake and release, mitochondrial Ca2+ uptake, mito

62 tive and dynamic recording of endo-lysosomal Ca2+ uptake and release.

63 In contrast, 20 mM oxalate increased Ca2+ uptake and the [Ca2+] within the bath continued to

64 not due to a change in the driving force for Ca2+ uptake and therefore must be due to an enhanced Ca2

65 d Ca2+ release without affecting the rate of Ca2+ uptake and/or extrusion.

66 nsiently cease without affecting the rate of Ca2+ uptake and/or extrusion.

67 hat evoke[Ca2+]i oscillations, mitochondrial Ca2+ uptake, and a nuclear [Ca2+] delay, CCh also evoked

68 ed cardiac myocyte SERCA2 levels, augment SR Ca2+ uptake, and shorten prolonged excitation-contractio

69 he Ca2+ current; (ii) sarcoplasmic reticulum Ca2+ uptake; and (iii) mRNA expression of important comp

70 .1 mM), completely inhibited the PCP-induced Ca2+ uptake as well as the membrane depolarization eithe

71 Ca2+ uptake assays in a membrane preparation indicated a

72 Ca2+ uptake assays showed 44+/-8% reduction of Vmax in c

73 Sarcoplasmic reticulum Ca2+ uptake assays showed that the Vmax was decreased by

74 Maintained Ca2+ uptake associated with Ca-Pi precipitation was not

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

76 L6, but not Jurkat cells, inhibited Ca2+ uptake at very high Ca2+ concentrations.

77 Mn2+ until the point at which mitochondrial Ca2+ uptake became apparent.

78 FK-506 did not affect SR Ca2+ uptake but modestly decreased Ca2+ extrusion via Na

79 line of [Ca2+]SR was not due to decreased SR Ca2+ uptake, but instead was the result of increased SRC

80 Pi inhibits net SR Ca2+ uptake, but this appears to result from activation

81 Ca2+ release occurred after abolition of SR Ca2+ uptake by ATP withdrawal.

82 ugmented store-operated channel activity and Ca2+ uptake by intracellular organelles.

83 Inhibition of Ca2+ uptake by mitochondria did not change the effects o

84 was inhibited by ruthenium red, a blocker of Ca2+ uptake by mitochondria.

85 exin V liposomes, are blocked by Zn2+, as is Ca2+ uptake by MV incubated in synthetic cartilage lymph

86 the mechanism of inhibition of mitochondrial Ca2+ uptake by Ru360 and its specificity in vitro in iso

87 nneling expands the SOCE microdomain through Ca2+ uptake by SERCA into the ER lumen where it diffuses

88 Despite their polarized expression, Ca2+ uptake by SERCA pumps and Ca2+ efflux by PMCA resul

89 ld be dysregulated at the level of cytosolic Ca2+ uptake by SERCA2a, its inhibitory subunit (phosphol

90 Inhibition of SR Ca2+ uptake by thapsigargin in cells already preloaded w

91 ased cytosolic Ca2+ was due to inhibition of Ca2+ uptake by the endoplasmic reticulum, because endopl

92 associated with mislocalization and reduced Ca2+ uptake by the mitochondria of stimulated Mist1-/- c

93 These data demonstrate that Ca2+ uptake by the mitochondria suppresses the local pos

94 Ca2+ uptake by the mitochondrial store is sensitive (thr

95 In contrast, inhibition of Ca2+ uptake by the sarcoplasmic reticulum ATPase does no

96 This does not depend on Ca2+ uptake by the sarcoplasmic reticulum but may reflec

97 Inhibition of Ca2+ uptake by the sarcoplasmic reticulum with cyclopiaz

98 d Ca2+ transient is dependent on the rate of Ca2+ uptake by the SR and (ii) prolongation associated w

99 A reduction in the rate of net Ca2+ uptake by the SR slows the decay of the Ca2+ transi

100 l membranes and that excessive mitochondrial Ca2+ uptake can impair electron transport and oxidative

101 rebellar granule cells demonstrated a higher Ca2+ uptake capacity (686 +/- 71 nmol/mg protein) than t

102 expressing cells had a reduced mitochondrial Ca2+ uptake capacity in comparison with wild type cells.

103 mPTP opening, were necessary to increase the Ca2+ uptake capacity of synaptic versus nonsynaptic mito

104 -induced Ca2+ load was less than the maximal Ca2+ uptake capacity of the mitochondria determined in v

105 pression of bcl-2 enhanced the mitochondrial Ca2+ uptake capacity using either digitonin-permeabilize

106 in the presence of ADP and the decreases in Ca2+ uptake capacity were abolished in the presence of P

107 Ca2+ was a smaller percentage of the maximal Ca2+ uptake capacity.

108 Mitochondrial Ca2+ uptake controls the rate of energy production, shap

109 LCT1-dependent increase in Ca2+ uptake correlated with the observed phenotype.

110 phore uncoupler that decreases mitochondrial Ca2+ uptake, decreased K+on but not K+off.

111 was most probably mediated by an enhanced SR Ca2+ uptake due to an augmentation of mitochondria-depen

112 f divalent cations, also are likely sites of Ca2+ uptake during contraction and the first step in con

113 Mitochondrial Ca2+ uptake during depolarizing stimulation caused depol

114 ermore, NOS blockade increased mitochondrial Ca2+ uptake during NMDA.

115 erated map analysis revealed that because SR Ca2+ uptake efficiency was much higher in control atrial

116 Pore opening does not occur following Ca2+ uptake, even though ruthenium red-inhibited rat liv

117 e the consequences of impaired mitochondrial Ca2+ uptake for cell function?' and finally (iv) 'What a

118 apeutic potential of targeting mitochondrial Ca2+ uptake for clinical management of pigmentary disord

119 mately 10.8-fold, indicating active, dynamic Ca2+ uptake from cytosol into the granules.

120 increased pump levels result in increased SR Ca2+ uptake function.

121 beta-Adrenergic stimulation of SR Ca2+ uptake in cells from failing hearts sufficed only t

122 Mitochondrial Ca2+ uptake in combination with NO production triggers t

123 hatase) corrected [Ca2+]er and mitochondrial Ca2+ uptake in DKO cells, restoring apoptotic death in r

124 acemaker currents and rhythmic mitochondrial Ca2+ uptake in ICC were also blocked by inhibitors of IP

125 s studied on the membrane potential (Vm) and Ca2+ uptake in isolated single skeletal muscle cells of

126 These data suggest that mitochondrial Ca2+ uptake in response to an increase of cytosolic Ca2+

127 ore expression caused enhanced mitochondrial Ca2+ uptake in response to ER Ca2+ release induced by th

128 nts of a yeast Ca2+ channel that may mediate Ca2+ uptake in response to mating pheromone, salt stress

129 l distribution and the role of mitochondrial Ca2+ uptake in shaping the spatial and temporal properti

130 t on the 10-min time course of ATP-dependent Ca2+ uptake in the absence of the luminal Ca2+ chelator

131 t cations such as Li+, suggesting a role for Ca2+ uptake in the calcineurin-dependent ion stress resp

132 Bcl-2 overexpression maintains Ca2+ uptake in the ER of TG-treated cells and prevents a

133 It also inhibits ATP-dependent Ca2+-uptake in a variety of microsomal membranes, althou

134 by manipulations that blocked mitochondrial Ca2+ uptake, including replacement of extracellular Ca2+

135 mycin on Ca2+ release evoked by agonists and Ca2+ uptake induced by antagonists.

136 Mitochondrial Ca2+ uptake inhibition prevented the NO increase, wherea

137 educed in cells treated with a mitochondrial Ca2+ uptake inhibitor, carbonyl cyanide m-chlorophenylhy

138 s (pool 1) and perpetuated through cycles of Ca2+ uptake into and release from Ca2+-induced Ca2+ rele

139 ctifying, making it especially effective for Ca2+ uptake into energized mitochondria.

140 ellular Ca2+ pools by blocking LTP-dependent Ca2+ uptake into intracellular compartments, blocked the

141 racellular acidosis is due to enhancement of Ca2+ uptake into intracellular stores as a result of a r

142 asmic reticulum Ca2+-ATPase (SERCA)-mediated Ca2+ uptake into intracellular stores is also accelerate

143 zonic acid (CPA, 20-40 microM), a blocker of Ca2+ uptake into intracellular stores.

144 ns of Ca(2+)-releasing agonists by promoting Ca2+ uptake into intracellular stores.

145 We conclude that Ru360 specifically blocks Ca2+ uptake into mitochondria and can be used in intact

146 responses were recorded from cells in which Ca2+ uptake into mitochondria had been inhibited by micr

147 ltage-clamped ventricular myocytes prevented Ca2+ uptake into mitochondria in situ where the cells we

148 However, the specificity of Ru360 on Ca2+ uptake into mitochondria in vitro or in intact cell

149 Ruthenium red is a well known inhibitor of Ca2+ uptake into mitochondria in vitro.

150 However, its utility as an inhibitor of Ca2+ uptake into mitochondria in vivo or in situ in inta

151 The IC50 of 103Ru360 for the inhibition of Ca2+ uptake into mitochondria was also 0.2 nM, indicatin

152 ruthenium red (IC50 = 6.85 nM) in inhibiting Ca2+ uptake into mitochondria.

153 chloride channels appears to be regulated by Ca2+ uptake into mitochondria.

154 s in ciliated cells are caused by stimulated Ca2+ uptake into mitochondria.

155 Ca2+ uptake into some mitochondria is activated by Ca2+

156 pH did not affect the rate of ATP-dependent Ca2+ uptake into stores, but did modify the rate of Ca2+

157 doplasmic reticulum) of isolated microsomes, Ca2+ uptake into streptolysin O-permeabilized cells, and

158 ns in a manner consistent with inhibition of Ca2+ uptake into the endoplasmic reticulum.

159 ment with thapsigargin (TG), an inhibitor of Ca2+ uptake into the endoplasmic reticulum.

160 inacidil decreased the rate and magnitude of Ca2+ uptake into the mitochondrial matrix with an IC50 o

161 influx via L-type Ca2+ current and stimulate Ca2+ uptake into the sarcoplasmic reticulum (SR), thereb

162 that SERCA2 protein and maximal velocity of Ca2+ uptake into the sarcoplasmic reticulum were reduced

163 2+ influx in intact platelets and to monitor Ca2+ uptake into the stores in permeabilized platelets,

164 + content of internal stores, measurement of Ca2+ uptake into the thapsigargin- and oxalate-sensitive

165 We show that Ca2+ uptake is ATP-dependent and sensitive to blockers o

166 This suggests that SR Ca2+ uptake is balanced by an efflux under these conditi

167 Mitochondrial Ca2+ uptake is critical for wave propagation, and mitoch

168 Thus, mitochondrial Ca2+ uptake is essential for sustaining phasic release,

169 ate that maximal activation of mitochondrial Ca2+ uptake is evoked by IP3-induced perimitochondrial [

170 This suggests that SR Ca2+ uptake is faster in these myocytes.

171 Thus, SR Ca2+ uptake is markedly downregulated in failing hearts,

172 ar and platelet microsomes, a stimulation in Ca2+ uptake is observed at low curcumin concentrations (

173 The rate of mitochondrial Ca2+ uptake is sensitive to extracellular [Ca2+], indica

174 ggesting that the net sarcoplasmic reticulum Ca2+ uptake is smaller in the presence of lactate.

175 This Ca2+ uptake is undertaken by the mitochondrial Ca2+ unip

176 ss induced by t-BuOOH enhances mitochondrial Ca2+ uptake, leading to increased matrix Ca2+, increased

177 We find that mitochondrial Ca2+ uptake limits the rise and underlies the rapid deca

178 This proficient mitochondrial Ca2+ uptake may avert a large rise in cytosolic Ca2+ con

179 ns high for long enough, while mitochondrial Ca2+ uptake may be important when [Ca2+]i is high.

180 t perinuclear mitochondria and mitochondrial Ca2+ uptake may differentially shape nuclear [Ca2+] sign

181 ciation with oxidative stress, mitochondrial Ca2+ uptake may trigger pathological states that lead to

182 mitochondrial Ca2+ uniporter is the primary Ca2+ uptake mechanism in respiring mitochondria.

183 sympathetic ganglion neurons exhibit a novel Ca2+ uptake mechanism, release-activated calcium transpo

184 d the maximal rate of thapsigargin-sensitive Ca2+ uptake mediated by SERCA in sarcoplasmic vesicles a

185 x, SR Ca2+ uptake and release, mitochondrial Ca2+ uptake, mitochondrial permeation transition pore, c

186 SR in the pathogenesis of HF, with abnormal Ca2+ uptake, more than Ca2+ release, contributing to the

187 ?' (ii) 'What is the impact of mitochondrial Ca2+ uptake on Ca2+ signalling?' (iii) 'What are the con

188 ns: (i) 'What is the impact of mitochondrial Ca2+ uptake on mitochondrial function?' (ii) 'What is th

189 epresent a first plant cDNA encoding a plant Ca2+ uptake or an organellar Ca2+ transport pathway in p

190 mpared with other interventions that inhibit Ca2+ uptake or reduce the sensitivity of the SR Ca2+ rel

191 produced no effect on sarcoplasmic reticulum Ca2+ uptake or release, sarcolemmal Na+/Ca2+ exchange, a

192 lum Ca2+-ATPase, disruption of mitochondrial Ca2+ uptake, or inhibition of the Na+-Ca2+ exchanger did

193 A number of specific cellular Ca2+ uptake pathways have been described in many differe

194 ial membrane potential (DeltaPsim)-dependent Ca2+ uptake plays a central role in neurodegeneration af

195 In conclusion, mitochondrial Ca2+ uptake plays a major role in Ca2+ clearance by rapi

196 Consequently, mitochondrial Ca2+ uptake plays a substantial role in shaping [Ca2+]c

197 ge-clamp technique to ascertain whether this Ca2+ uptake process influences the time course of the su

198 in, and triadin) were downregulated, whereas Ca2+-uptake proteins (Ca2+-ATPase and phospholamban) wer

199 pensate for depressed sarcoplasmic reticular Ca2+ uptake, provide inotropic support through reverse-m

200 iazonic acid (CPA), a sarcoplasmic reticulum Ca2+ uptake pump inhibitor.

201 iazonic acid (CPA), a sarcoplasmic reticulum Ca2+-uptake pump inhibitor.

202 mM oxalate resolved a thapsigargin-sensitive Ca2+ uptake rate (IC50 approximately 1 nM thapsigargin)

203 At very low [ATP], a reduction in the SR Ca2+ uptake rate may also contribute to the decrease in

204 d the Ca2+ transient, SR Ca2+ content and SR Ca2+ uptake rate to the same levels as control cells in

205 rawal may also reflect a decrease in the net Ca2+ uptake rate.

206 Ca2+ uptake rates by the SR and the amount of Ca2+ store

207 easuring both 12-min Ca2+ uptake and initial Ca2+ uptake rates, the apparent thapsigargin sensitivity

208 CA pump for Ca2+ and the maximum velocity of Ca2+ uptake rates.

209 d by mitochondrial depolarization, swelling, Ca2+ uptake, reactive oxygen species production, and res

210 ee hypotheses were tested: (1) Mitochondrial Ca2+ uptake regulates [Ca2+]i and production of force in

211 , cytosolic Ca2+ increase, and mitochondrial Ca2+ uptake remain obscure.

212 Mitochondrial Ca2+ uptake responds dynamically and sensitively to chan

213 fluctuations were triggered by mitochondrial Ca2+ uptake since they were inhibited by both ruthenium

214 We conclude that each mitochondrial Ca2+ uptake site faces multiple IP3R, a concurrent activ

215 anced Ca2+ permeability of the mitochondrial Ca2+ uptake sites (uniporter).

216 of high [Ca2+], saturation of mitochondrial Ca2+ uptake sites by released Ca2+, connection of multip

217 may utilize activation of the mitochondrial Ca2+ uptake sites by the large local [Ca2+]c rise occurr

218 n SR/ER Ca2+ release sites and mitochondrial Ca2+ uptake sites, including transient microdomains of h

219 However, after mitochondrial Ca2+ uptake starts, mitochondria continually take up Mn2

220 e roles of the L-type Ca2+ current (ICa), SR Ca2+ uptake, storage and release, Ca2+ transport via the

221 inal free [Ca2+] after inhibition of further Ca2+ uptake, submaximal concentrations of InsP3 caused r

222 fter inhibition of the endoplasmic reticulum Ca2+ uptake system (SERCA).

223 ger and inhibition of a pheromone-stimulated Ca2+ uptake system, suggesting that Tcn1p functions down

224 types, as expected after removal of a major Ca2+ uptake system.

225 ity in pancreatic islets, which mediates the Ca2+ uptake that triggers insulin secretion.

226 re the procedures to specifically measure SR Ca2+ uptake, the formation and decomposition of SERCA ph

227 released Ca2+ is modulated by mitochondrial Ca2+ uptake, the interactions between ER and mitochondri

228 At all stages of Ca2+ uptake, the potassium channel openers depolarized t

229 d the mitochondrial energization that drives Ca2+ uptake through it.

230 ll and coupling Ca2+ entry and mitochondrial Ca2+ uptake to Ca2+ release.

231 m promoting quiescence via BK channels or SR Ca2+ uptake, to promoting Ca2+ entry and contractility a

232 ANT plays an important role in mitochondrial Ca2+ uptake under ischemic conditions by reversing its a

233 potential and unidirectional measurements of Ca2+ uptake using 45Ca2+.

234 e that core directly increases mitochondrial Ca2+ uptake via a primary effect on the uniporter.

235 The maximum velocity of Ca2+ uptake (Vmax) was increased by 37%, demonstrating t

236 The threshold [Ca2+]c for mitochondrial Ca2+ uptake was 300-500 nM, similar to that without Mn2+

237 Mitochondrial Ca2+ uptake was also dependent on the nature and duratio

238 34.5% augmentation of oxalate-facilitated SR Ca2+ uptake was also documented in SERCA2 adenovirus-inf

239 F, respectively, revealed that mitochondrial Ca2+ uptake was also inhibited by ruthenium red and Ru36

240 d [Ca2+]m by 0.2 microM, total mitochondrial Ca2+ uptake was approximately 13 mumol (1 mitochondria)-

241 bmaximal IP3 was enhanced when mitochondrial Ca2+ uptake was blocked with ruthenium red or uncoupler.

242 Mitochondrial Ca2+ uptake was calculated from the difference between [

243 Mitochondrial Ca2+ uptake was dependent on glutamate concentration, wh

244 reased 2.5-fold, and the maximal velocity of Ca2+ uptake was increased 1.7-fold in TG hearts, demonst

245 tage-clamped cells show that the PCP-induced Ca2+ uptake was independent of the PCP-induced depolariz

246 ation that MT-AEQ was in a compartment whose Ca2+ uptake was inhibited 82% with carbonyl cyanide p-tr

247 When mitochondrial Ca2+ uptake was inhibited by depolarizing mitochondria w

248 Net Ca2+ uptake was markedly reduced in the presence of 30 m

249 red treatment, suggesting that mitochondrial Ca2+ uptake was required for the mechanism of action.

250 The initial rate of Ca2+ uptake was similar in microsomes from transfected a

251 +/- 1.4% (mean +/- s.e.m., n = 16), while SR Ca2+ uptake was unaffected.

252 razone (CCCP), an inhibitor of mitochondrial Ca2+ uptake, was investigated on the properties of Ca(2+

253 DeltaPsim dissipation reduces mitochondrial Ca2+ uptake, we hypothesized that NO mediates the NMDA-i

254 store-operated Ca2+ entry, and mitochondrial Ca2+ uptake, we used two IP3-binding proteins (IP3BP): 1

255 sphosphate (IP3) receptors and mitochondrial Ca2+ uptake were tested on the generation of slow waves

256 Inhibition of mitochondrial Ca2+ uptake with cyanide, carbonyl cyanide p-trifluorome

257 Inhibition of SR Ca2+ uptake with cyclopiazonic acid (CPA, 30 microM) slo

258 Inhibition of endoplasmic reticular Ca2+ uptake with cyclopiazonic acid also had little effe

259 was abolished by inhibition of mitochondrial Ca2+ uptake with ruthenium red and Ru360.

260 Inhibition of sarcoplasmic reticulum Ca2+ uptake with thapsigargin (100 nM) reduced the under

261 nd (2) elevated [Na+]i impairs mitochondrial Ca2+ uptake, with consequent effects on energy supply an