ライフサイエンスコーパス: Ca2 buffer

1 ndoplasmic reticulum (ER) as a high-capacity Ca2+ buffer.

2 eters identified with the cell's cytoplasmic Ca2+ buffer.

3 model included mobile molecules as the only Ca2+ buffer.

4 he activation of ICRAC in weak intracellular Ca2+ buffer.

5 rev)) upon switching to a sodium-free, 10 mM Ca2+ buffer.

6 rate and to a similar extent in low or high Ca2+ buffer.

7 a2+ buffer was as large as that seen in high Ca2+ buffer.

8 as very similar in low or high intracellular Ca2+ buffer.

9 y changes in either concentration or type of Ca2+ buffer.

10 half-maximal DSI in the absence of exogenous Ca2+ buffers.

11 ls as reservoirs of exchangeable Ca2+ and as Ca2+ buffers.

12 eatly prolonged in the presence of exogenous Ca2+ buffers.

13 the presence of rapid stationary and mobile Ca2+ buffers.

14 apacitance measurement and the photolysis of Ca2+ buffers.

15 the entry site, and binds to fixed or mobile Ca2+ buffers.

16 hat were unexpected from behavior as passive Ca2+ buffers.

17 ent and differentially modulated by distinct Ca2+ buffers.

18 properties are modulated by mobile cytosolic Ca2+ buffers.

19 cording conditions that preserved endogenous Ca2+ buffers.

20 -20 mm extracellular Ca2+ with intracellular Ca2+ buffered.

21 The difference was accounted for by Ca2+ buffering.

22 d reduction, or alterations in intracellular Ca2+ buffering.

23 oncentration and the degree of intracellular Ca2+ buffering.

24 unction of [Ca2+]i, ICa density, or cellular Ca2+ buffering.

25 r Ca2+ signal, is regulated by mitochondrial Ca2+ buffering.

26 be seen under conditions of low cytoplasmic Ca2+ buffering.

27 ) cells under conditions of weak cytoplasmic Ca2+ buffering.

28 Under conditions of low intracellular Ca2+ buffering (0.1 mM BAPTA), adenophostin A-induced Ca

29 M N-terminal lobe and present only with mild Ca2+ buffering (0.5 mM EGTA) characteristic of many neur

30 Addition of the "fast" Ca2+ buffer 1,2-bis(2-aminophenoxy)ethanetetraacetic aci

31 e and KCl internal saline with low levels of Ca2+ buffering, 10 microM ADP evoked [Ca2+]i oscillation

32 High concentration of Ca2+ buffers (2-5 mM EGTA plus 1 mM fluo-3) completely a

33 effects of the neuroprotective cell-permeant Ca2+ buffer, 2-aminophenol-N,N,O-triacetic acid acetoxym

34 e of desensitization was reduced by stronger Ca2+ buffering (20 mM BAPTA, without added Ca2+), or by

35 Exogenous, low-affinity Ca2+ buffers (5 to 20 mmol/L ADA, citrate or maleate) we

36 When cells were field stimulated in 2.0 mM Ca2+ buffer, a transverse confocal line scan (500 Hz) sh

37 the Ca2+/Mg2+ occupancy and consequently the Ca2+ buffering ability of the RLC.

38 level by a high concentration of a selective Ca2+ buffer, acetylcholine evoked the usual depletion of

39 ethane-N,N,N',N'-tetraacetic acid (MAPTA), a Ca2+ buffering agent, and the effect of CPT-cAMP on TC u

40 CRAC even in the presence of low cytoplasmic Ca2+ buffering, albeit at a slow rate.

41 than by subsarcomeric inhomogeneities of the Ca2+ buffer and transport system.

42 nd oligomycin together because mitochondrial Ca2+ buffering and ATP production were both inhibited.

43 recruitment of mitochondria to enhance local Ca2+ buffering and energy supply.

44 g is surprisingly resistant to intracellular Ca2+ buffering and has steeply voltage-dependent gain, i

45 erdependence of SR Ca2+ content, cytoplasmic Ca2+ buffering and sarcolemmal Ca2+ fluxes.

46 Mitochondria participate in intracellular Ca2+ buffering and signalling.

47 ctors extrinsic to the RyR2 channel, such as Ca2+ buffers and diffusion, alter fluo-3 fluorescent res

48 employed in order to preserve intracellular Ca2+ buffers and other cellular constituents.

49 from significant pH interference, and their Ca2+-buffering and cross-reactivity with endogenous CaM

50 determined by the dynamics of Ca2+ sources, Ca2+ buffers, and Ca2+ extrusion mechanisms.

51 the number of channels, the fixed and mobile Ca2+ buffers, and the Ca2+ extrusion mechanism.

52 hese results indicate that the cell-permeant Ca2+ buffer, APTRA-AM, attenuates hippocampal excitabili

53 but not with high concentrations of the fast Ca2+ buffer BAPTA (10 mm).

54 Pre-loading cells with the Ca2+ buffer BAPTA abolished the ATP-dependent responses

55 concentration in the patch electrode of the Ca2+ buffer BAPTA was lowered.

56 5 mM fast Ca2+ buffer (BAPTA (1,2-bis(2-aminophenoxy)ethane-N,N,N'

57 Precise knowledge of the cytoplasmic Ca2+ buffering behaviour in intact human red cells is es

58 The cytoplasmic Ca2+ buffering behaviour in these cells was similar to t

59 assessed from the difference in cytoplasmic Ca2+ buffering between chelator-free and chelator-loaded

60 A rapid intracellular Ca2+ buffer, bis(O-aminophenoxy)ethane-N,N,N',N'-tetra-a

61 With intracellular Ca2+ buffered by EGTA in the recording pipette, vitronec

62 Noncoplanar PCBs, like PCB 95, alter SR Ca2+ buffering by an FKBP12-mediated mechanism.

63 Direct measurement of intra-SR Ca2+ buffering (by simultaneous [Ca2+]SR and [Ca]SRT mea

64 nt with the hypothesis that the BAPTA series Ca2+ buffers can activate those Ca2+-activated K+ channe

65 ghly conserved protein with Ca2+-sensing and Ca2+-buffering capabilities, is abundant in brain and se

66 rom RBCs was enhanced when the intraterminal Ca2+ buffer capacity was reduced.

67 and BAPTA into the red cells increased their Ca2+ buffering capacity by 300-600 mumol (340 g Hb)-1.

68 and are consistent with the hypothesis that Ca2+ buffering capacity contributes to the control of in

69 A decrease in mitochondrial Ca2+ buffering capacity in cells affected by these lysos

70 n comparison, diminishment of the endogenous Ca2+ buffering capacity of nerve endings by treatment wi

71 nism that may play a key role in setting the Ca2+ buffering capacity of Purkinje cells.

72 kely to be associated with the intracellular Ca2+ buffering capacity that could regulate the sensitiv

73 ty (approximately 15 microM), high cytosolic Ca2+ buffering capacity, and the spatial separation of C

74 The cytosolic Ca2+ buffering capacity, determined as the ratio of the

75 [Ca2+]SR, not to alterations in SR volume or Ca2+ buffering capacity.

76 ve attenuation was a function of cytoplasmic Ca2+ buffering capacity; i.e., loading increasing concen

77 trate that increasing neuronal mitochondrial Ca2+-buffering capacity is not beneficial in the R6/2 mo

78 Ca2+ release sites per micrometer3 in highly Ca2+-buffered cells, where diffusion of Ca2+ is limited

79 ading the SR with the low affinity exogenous Ca2+ buffer citrate exerted effects quantitatively simil

80 ored by loading the SR with the low-affinity Ca2+ buffer, citrate.

81 (iii) There was an additional Ca2+ buffering complex with a low capacity (approximatel

82 We suggest that an increase in the mobile Ca2+ buffer concentration in high-frequency hair cells (

83 were unable to activate Icrac under this low Ca2+ buffering condition.

84 tially sensitive to changes in intraterminal Ca2+ buffering conditions.

85 failed to generate macroscopic ICRAC in low Ca2+ buffering conditions.

86 + store with pump and channel; and cytosolic Ca2+ buffer) could not account for the observed [Ca2+]i

87 can be differentiated by the temperature and Ca2+ buffer dependence of wave speed.

88 At the whole-cell level, intra-SR [Ca2+] buffering dramatically increased the magnitude of

89 al fragmentation and decreased mitochondrial Ca2+ buffering efficiency.

90 In cells loaded with the Ca2+ buffer EGTA (5 mmol/L) and the fluorescent Ca2+-ind

91 levels because it was greatly reduced by the Ca2+ buffers EGTA and BAPTA.

92 In the presence of 0.5 mM slow Ca2+ buffer (EGTA (ethylene glycolbis(2-aminoethylether)

93 otentiation effect of nifedipine, but a slow Ca2+ buffer, EGTA-AM, did not.

94 With moderate Ca2+ buffer, however, sub-maximal ICRAC could be obtaine

95 nce of physiological levels of intracellular Ca2+ buffers, ICRAC was barely detectable when cells wer

96 (ii) Mitochondria may act as a spatial Ca2+ buffer in many cells, regulating the local Ca2+ con

97 By varying the concentration of Ca2+ buffer in the pipette, the mobile endogenous buffer

98 RyR1, lowers resting [Ca2+]SR and alters SR Ca2+ buffering in a way that copies the functional insta

99 ly developed method of measuring cytoplasmic Ca2+ buffering in intact red cells was applied to re-eva

100 Intracellular Ca2+ buffering in pacemaker neurons results in dose-depe

101 nsport via the Na+-Ca2+ exchanger (NCX), and Ca2+ buffering in the altered Ca2+ transients of failing

102 Enhanced Ca2+ buffering in the SR was confirmed by an increase in

103 , supporting the importance of mitochondrial Ca2+ buffering in this subset of neurons.

104 where ATP and glutamate represented the only Ca2+ buffers in the pipette solution.

105 The exogenous Ca2+ buffers in the SR also reduced the frequency of rep

106 creased during intracellular perfusion with [Ca2+] buffered in the range 1.0-20 microM.

107 hole-cell recordings without added exogenous Ca2+ buffers, indicating that the Ca2+-dependent charact

108 release mechanism by reducing the effective Ca2+ buffering inside the SR and/or by altering the resp

109 In the presence of high intracellular Ca2+ buffer, InsP3-F activated ICRAC to its maximal exte

110 We also determined that Ca2+ buffering interacts synergistically with genetic ma

111 ht, suggesting that calnexin's function as a Ca2+ buffer is important for photoreceptor cell survival

112 dria, but neurotransmitter release and acute Ca2+ buffering is only impaired during prolonged stimula

113 te analysis of high-throughput intracellular Ca2+ buffer loading to demonstrate that Ca2+ signals coo

114 he data obtained suggest that alterations in Ca2+ buffering may provide a potent mechanism by which t

115 DP ratio decreases, causing energy-dependent Ca2+ buffering mechanisms to fail.

116 ing CICR, we assessed the impact of intra-SR Ca2+ buffering on global and local Ca2+ release properti

117 The effects of intracellular Ca2+ buffering on hair cell mechanotransduction were stu

118 boring clusters, and 3) the influence of the Ca2+ buffers on the kinetics and localization of the mic

119 Since Ca2+ buffers only weakly affect CDI and CDF, we conclude

120 Ca2+ liberation rather than reduce cytosolic Ca2+ buffering or clearance.

121 Thus, the Cam3c1 mutation might affect Ca2+ buffering or interfere with the activation or inhib

122 e abolished when myocytes were dialyzed with Ca2+ buffers or after the Na+-Ca2+ exchanger was blocked

123 combination of IP3 and thapsigargin in high Ca2+ buffer, or passively with 10 mM EGTA or BAPTA.

124 ntra-SR free [Ca2+] ([Ca2+]SR), (2) intra-SR Ca2+ buffering, or (3) SR volume (as percentage of cell

125 from a physiological perspective is the weak Ca2+ buffer paradox: whereas macroscopic (whole cell) IC

126 bridges and probably utilizing intracellular Ca2+ buffers (parvalbumin) to spread out the time over w

127 e (ratio of flux and [Ca2+] gradient) and SR Ca2+ buffering power (B).

128 ined using measurements of the intracellular Ca2+ buffering power.

129 nhibitor, had no significant effect on total Ca2+ buffering power.

130 by targeted expression of varying doses of a Ca2+ buffer protein in transgenic Drosophila melanogaste

131 determine whether induced expression of the Ca2+ buffering protein parvalbumin (PV) in slow-twitch f

132 nd (4) unaltered levels of the intracellular Ca2+-buffering proteins calbindin-D28k or parvalbumin, e

133 model accounts for the presence of a mobile Ca2+ buffer, provided either that the buffer is unsatura

134 is likely to be the unavoidable increase in Ca2+ buffering rather than specific perturbation of CaM-

135 (i) The known red cell Ca2+ buffer represented by alpha, with a large capacity

136 ysiological conditions of weak intracellular Ca2+ buffering, respiring mitochondria play a central ro

137 -free solutions nor increasing intracellular Ca2+ buffering speed and capacity altered Idelay.

138 a2+ release per [Ca2+]i transient, increased Ca2+ buffering strength, shortened action potentials, an

139 upport the conclusion that rapidly diffusing Ca2+ buffers (such as ATP) are important in shaping the

140 flux or by clamping [Ca2+]i with a cytosolic Ca2+ buffer suggesting that the process did not depend o

141 Icrac under conditions of low intracellular Ca2+ buffering suggests an additional site of action, pe

142 se-induced ICa inactivation to fast and slow Ca2+ buffers suggests that the process is mediated throu

143 passive Ca2+ influx and regulated by a large Ca2+ buffering system, Ca2+ extrusion via a PMCA and Ca2

144 lated with the concentration and the type of Ca2+ buffer that was dialysed into the cell: When Ca2+ b

145 The loss of a putative intraneuronal Ca2+ buffer, the Ca2+-binding protein calbindin (CB), fr

146 nely in the presence of strong intracellular Ca2+ buffer, the current is generally not detectable und

147 BL-1) cells dialysed with high intracellular Ca2+ buffer, the relationship is supra-linear with a Hil

148 In the absence of intracellular Ca2+ buffering, the application of soluble vitronectin (

149 tion and the lack of effect of intracellular Ca2+ buffers, the Ca2+-binding sites are probably locate

150 In recordings without added exogenous Ca2+ buffers, the time course of ICa inactivation was co

151 Mitochondrial Ca2+ buffering therefore increases the dynamic range of

152 mplete tachyphylaxis even with intracellular Ca2+ buffered to low levels, whereas changes in nucleoti

153 by the removal of external Ca2+ or internal Ca2+ buffering to < or = 1 nM with EGTA.

154 means that it is possible for mitochondrial Ca2+ buffering to affect DCV exocytosis.

155 culated Ca2+ binding to the major myoplasmic Ca2+ buffers (troponin, ATP and parvalbumin); buffer con

156 Increasing concentrations of Ca2+ buffer (up to 200 microM EGTA or BAPTA) were associ

157 thapsigargin, but at 0 mV the current in low Ca2+ buffer was as large as that seen in high Ca2+ buffe

158 ponse to InsP3-F in the presence of moderate Ca2+ buffer was due to partial depletion of the stores,

159 When Ca2+ buffer was omitted from the patch pipette solution,

160 Cytoplasmic Ca2+ buffering was analysed from plots of total cell cal

161 buffer that was dialysed into the cell: When Ca2+ buffering was minimized by dialysing cells with 0.5

162 with appropriate corrections for cytoplasmic Ca2+ buffering, we found that modulation extended the dy

163 channels is suppressed by strong cytoplasmic Ca2+ buffering, we investigated how factors that regulat

164 ng [Ca2+] to 200-300 nM, in solutions weakly Ca2+ buffered with 0.05 mM EGTA.

165 (iv) The cell content of putative Ca2+ buffers with submicromolar Ca2+ dissociation consta

166 sitised red cells is taken up by cytoplasmic Ca2+ buffers within the parasite.