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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                  Evaluation of the effect of Ca2+ buffering and coupling coefficient in a network of
44 recruitment of mitochondria to enhance local Ca2+ buffering and energy supply.
45 g is surprisingly resistant to intracellular Ca2+ buffering and has steeply voltage-dependent gain, i
46 erdependence of SR Ca2+ content, cytoplasmic Ca2+ buffering and sarcolemmal Ca2+ fluxes.
47    Mitochondria participate in intracellular Ca2+ buffering and signalling.
48 ctors extrinsic to the RyR2 channel, such as Ca2+ buffers and diffusion, alter fluo-3 fluorescent res
49  employed in order to preserve intracellular Ca2+ buffers and other cellular constituents.
50  from significant pH interference, and their Ca2+-buffering and cross-reactivity with endogenous CaM
51  determined by the dynamics of Ca2+ sources, Ca2+ buffers, and Ca2+ extrusion mechanisms.
52 the number of channels, the fixed and mobile Ca2+ buffers, and the Ca2+ extrusion mechanism.
53 hese results indicate that the cell-permeant Ca2+ buffer, APTRA-AM, attenuates hippocampal excitabili
54 but not with high concentrations of the fast Ca2+ buffer BAPTA (10 mm).
55                   Pre-loading cells with the Ca2+ buffer BAPTA abolished the ATP-dependent responses
56  concentration in the patch electrode of the Ca2+ buffer BAPTA was lowered.
57                                    5 mM fast Ca2+ buffer (BAPTA (1,2-bis(2-aminophenoxy)ethane-N,N,N'
58         Precise knowledge of the cytoplasmic Ca2+ buffering behaviour in intact human red cells is es
59                              The cytoplasmic Ca2+ buffering behaviour in these cells was similar to t
60  assessed from the difference in cytoplasmic Ca2+ buffering between chelator-free and chelator-loaded
61                        A rapid intracellular Ca2+ buffer, bis(O-aminophenoxy)ethane-N,N,N',N'-tetra-a
62                           With intracellular Ca2+ buffered by EGTA in the recording pipette, vitronec
63      Noncoplanar PCBs, like PCB 95, alter SR Ca2+ buffering by an FKBP12-mediated mechanism.
64               Direct measurement of intra-SR Ca2+ buffering (by simultaneous [Ca2+]SR and [Ca]SRT mea
65 nt with the hypothesis that the BAPTA series Ca2+ buffers can activate those Ca2+-activated K+ channe
66 ghly conserved protein with Ca2+-sensing and Ca2+-buffering capabilities, is abundant in brain and se
67 rom RBCs was enhanced when the intraterminal Ca2+ buffer capacity was reduced.
68 and BAPTA into the red cells increased their Ca2+ buffering capacity by 300-600 mumol (340 g Hb)-1.
69  and are consistent with the hypothesis that Ca2+ buffering capacity contributes to the control of in
70                  A decrease in mitochondrial Ca2+ buffering capacity in cells affected by these lysos
71 n comparison, diminishment of the endogenous Ca2+ buffering capacity of nerve endings by treatment wi
72 nism that may play a key role in setting the Ca2+ buffering capacity of Purkinje cells.
73 kely to be associated with the intracellular Ca2+ buffering capacity that could regulate the sensitiv
74 ty (approximately 15 microM), high cytosolic Ca2+ buffering capacity, and the spatial separation of C
75                                The cytosolic Ca2+ buffering capacity, determined as the ratio of the
76 [Ca2+]SR, not to alterations in SR volume or Ca2+ buffering capacity.
77 ve attenuation was a function of cytoplasmic Ca2+ buffering capacity; i.e., loading increasing concen
78 trate that increasing neuronal mitochondrial Ca2+-buffering capacity is not beneficial in the R6/2 mo
79 Ca2+ release sites per micrometer3 in highly Ca2+-buffered cells, where diffusion of Ca2+ is limited
80 ading the SR with the low affinity exogenous Ca2+ buffer citrate exerted effects quantitatively simil
81 ored by loading the SR with the low-affinity Ca2+ buffer, citrate.
82                (iii) There was an additional Ca2+ buffering complex with a low capacity (approximatel
83    We suggest that an increase in the mobile Ca2+ buffer concentration in high-frequency hair cells (
84 were unable to activate Icrac under this low Ca2+ buffering condition.
85 tially sensitive to changes in intraterminal Ca2+ buffering conditions.
86  failed to generate macroscopic ICRAC in low Ca2+ buffering conditions.
87 + store with pump and channel; and cytosolic Ca2+ buffer) could not account for the observed [Ca2+]i
88 can be differentiated by the temperature and Ca2+ buffer dependence of wave speed.
89           At the whole-cell level, intra-SR [Ca2+] buffering dramatically increased the magnitude of
90 al fragmentation and decreased mitochondrial Ca2+ buffering efficiency.
91                     In cells loaded with the Ca2+ buffer EGTA (5 mmol/L) and the fluorescent Ca2+-ind
92 levels because it was greatly reduced by the Ca2+ buffers EGTA and BAPTA.
93               In the presence of 0.5 mM slow Ca2+ buffer (EGTA (ethylene glycolbis(2-aminoethylether)
94 otentiation effect of nifedipine, but a slow Ca2+ buffer, EGTA-AM, did not.
95                                With moderate Ca2+ buffer, however, sub-maximal ICRAC could be obtaine
96 nce of physiological levels of intracellular Ca2+ buffers, ICRAC was barely detectable when cells wer
97       (ii) Mitochondria may act as a spatial Ca2+ buffer in many cells, regulating the local Ca2+ con
98              By varying the concentration of Ca2+ buffer in the pipette, the mobile endogenous buffer
99  RyR1, lowers resting [Ca2+]SR and alters SR Ca2+ buffering in a way that copies the functional insta
100 ly developed method of measuring cytoplasmic Ca2+ buffering in intact red cells was applied to re-eva
101                                Intracellular Ca2+ buffering in pacemaker neurons results in dose-depe
102 nsport via the Na+-Ca2+ exchanger (NCX), and Ca2+ buffering in the altered Ca2+ transients of failing
103                                     Enhanced Ca2+ buffering in the SR was confirmed by an increase in
104 , supporting the importance of mitochondrial Ca2+ buffering in this subset of neurons.
105 where ATP and glutamate represented the only Ca2+ buffers in the pipette solution.
106                                The exogenous Ca2+ buffers in the SR also reduced the frequency of rep
107 creased during intracellular perfusion with [Ca2+] buffered in the range 1.0-20 microM.
108 hole-cell recordings without added exogenous Ca2+ buffers, indicating that the Ca2+-dependent charact
109  release mechanism by reducing the effective Ca2+ buffering inside the SR and/or by altering the resp
110        In the presence of high intracellular Ca2+ buffer, InsP3-F activated ICRAC to its maximal exte
111                      We also determined that Ca2+ buffering interacts synergistically with genetic ma
112 ht, suggesting that calnexin's function as a Ca2+ buffer is important for photoreceptor cell survival
113 dria, but neurotransmitter release and acute Ca2+ buffering is only impaired during prolonged stimula
114 te analysis of high-throughput intracellular Ca2+ buffer loading to demonstrate that Ca2+ signals coo
115 he data obtained suggest that alterations in Ca2+ buffering may provide a potent mechanism by which t
116 DP ratio decreases, causing energy-dependent Ca2+ buffering mechanisms to fail.
117 ing CICR, we assessed the impact of intra-SR Ca2+ buffering on global and local Ca2+ release properti
118                 The effects of intracellular Ca2+ buffering on hair cell mechanotransduction were stu
119 boring clusters, and 3) the influence of the Ca2+ buffers on the kinetics and localization of the mic
120                                        Since Ca2+ buffers only weakly affect CDI and CDF, we conclude
121 Ca2+ liberation rather than reduce cytosolic Ca2+ buffering or clearance.
122       Thus, the Cam3c1 mutation might affect Ca2+ buffering or interfere with the activation or inhib
123 e abolished when myocytes were dialyzed with Ca2+ buffers or after the Na+-Ca2+ exchanger was blocked
124  combination of IP3 and thapsigargin in high Ca2+ buffer, or passively with 10 mM EGTA or BAPTA.
125 ntra-SR free [Ca2+] ([Ca2+]SR), (2) intra-SR Ca2+ buffering, or (3) SR volume (as percentage of cell
126 from a physiological perspective is the weak Ca2+ buffer paradox: whereas macroscopic (whole cell) IC
127 bridges and probably utilizing intracellular Ca2+ buffers (parvalbumin) to spread out the time over w
128 e (ratio of flux and [Ca2+] gradient) and SR Ca2+ buffering power (B).
129 ined using measurements of the intracellular Ca2+ buffering power.
130 nhibitor, had no significant effect on total Ca2+ buffering power.
131 by targeted expression of varying doses of a Ca2+ buffer protein in transgenic Drosophila melanogaste
132  determine whether induced expression of the Ca2+ buffering protein parvalbumin (PV) in slow-twitch f
133 nd (4) unaltered levels of the intracellular Ca2+-buffering proteins calbindin-D28k or parvalbumin, e
134  model accounts for the presence of a mobile Ca2+ buffer, provided either that the buffer is unsatura
135  is likely to be the unavoidable increase in Ca2+ buffering rather than specific perturbation of CaM-
136                       (i) The known red cell Ca2+ buffer represented by alpha, with a large capacity
137 ysiological conditions of weak intracellular Ca2+ buffering, respiring mitochondria play a central ro
138 -free solutions nor increasing intracellular Ca2+ buffering speed and capacity altered Idelay.
139 a2+ release per [Ca2+]i transient, increased Ca2+ buffering strength, shortened action potentials, an
140 upport the conclusion that rapidly diffusing Ca2+ buffers (such as ATP) are important in shaping the
141 flux or by clamping [Ca2+]i with a cytosolic Ca2+ buffer suggesting that the process did not depend o
142  Icrac under conditions of low intracellular Ca2+ buffering suggests an additional site of action, pe
143 se-induced ICa inactivation to fast and slow Ca2+ buffers suggests that the process is mediated throu
144 passive Ca2+ influx and regulated by a large Ca2+ buffering system, Ca2+ extrusion via a PMCA and Ca2
145 lated with the concentration and the type of Ca2+ buffer that was dialysed into the cell: When Ca2+ b
146         The loss of a putative intraneuronal Ca2+ buffer, the Ca2+-binding protein calbindin (CB), fr
147 nely in the presence of strong intracellular Ca2+ buffer, the current is generally not detectable und
148 BL-1) cells dialysed with high intracellular Ca2+ buffer, the relationship is supra-linear with a Hil
149              In the absence of intracellular Ca2+ buffering, the application of soluble vitronectin (
150 tion and the lack of effect of intracellular Ca2+ buffers, the Ca2+-binding sites are probably locate
151        In recordings without added exogenous Ca2+ buffers, the time course of ICa inactivation was co
152                                Mitochondrial Ca2+ buffering therefore increases the dynamic range of
153 mplete tachyphylaxis even with intracellular Ca2+ buffered to low levels, whereas changes in nucleoti
154  by the removal of external Ca2+ or internal Ca2+ buffering to < or = 1 nM with EGTA.
155  means that it is possible for mitochondrial Ca2+ buffering to affect DCV exocytosis.
156 culated Ca2+ binding to the major myoplasmic Ca2+ buffers (troponin, ATP and parvalbumin); buffer con
157                 Increasing concentrations of Ca2+ buffer (up to 200 microM EGTA or BAPTA) were associ
158 thapsigargin, but at 0 mV the current in low Ca2+ buffer was as large as that seen in high Ca2+ buffe
159 ponse to InsP3-F in the presence of moderate Ca2+ buffer was due to partial depletion of the stores,
160                                         When Ca2+ buffer was omitted from the patch pipette solution,
161                                  Cytoplasmic Ca2+ buffering was analysed from plots of total cell cal
162 buffer that was dialysed into the cell: When Ca2+ buffering was minimized by dialysing cells with 0.5
163 with appropriate corrections for cytoplasmic Ca2+ buffering, we found that modulation extended the dy
164 channels is suppressed by strong cytoplasmic Ca2+ buffering, we investigated how factors that regulat
165 ng [Ca2+] to 200-300 nM, in solutions weakly Ca2+ buffered with 0.05 mM EGTA.
166            (iv) The cell content of putative Ca2+ buffers with submicromolar Ca2+ dissociation consta
167 sitised red cells is taken up by cytoplasmic Ca2+ buffers within the parasite.

 
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