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1 es, and interaction with the plasma-membrane Ca2+ pump.
2 the Golgi, a hitherto unusual location for a Ca2+ pump.
3 are considered, including reversal of the SR Ca2+ pump.
4 the Ca2+ spark was also influenced by the SR Ca2+ pump.
5 as largely dependent on leaks through the SR Ca2+ pump.
6 d active Ca2+ efflux via the plasma membrane Ca2+ pump.
7 rs to involve further Ca2+ efflux via the SR Ca2+ pump.
8 ectiveness of oxidized CaM in activating the Ca2+ pump.
9 in the ATP2A2 gene, which encodes the SERCA2 Ca2+ pump.
10 lation and the consequent reversal of the SR Ca2+ pump.
11 microM, consistent with inhibition of the SR Ca2+ pump.
12 nsitive protein kinase and the intracellular Ca2+ pump.
13 ted K+-channel and possibly also not for the Ca2+-pump.
14 iculum (53%) than with plasma membrane (32%) Ca2+ pumps.
15 TP-dependent and sensitive to blockers of ER Ca2+ pumps.
16 tly thapsigargin (Tg), an inhibitor of SR/ER Ca2+ pumps.
17 plicing within the family of plasma membrane Ca2+ pumps.
18 ional work involved in insulin secretion and Ca2+ pumping.
19 ast, the corresponding C-terminal peptide of Ca2+ pump 2b interacted weakly with PDZ1 + 2 and not at
20                                              Ca2+ pump 4b bound strongly to PDZ1 + 2 + 3 of hDlg on f
21 id assays demonstrated strong interaction of Ca2+ pump 4b with the PDZ1 + 2 domains of several mammal
22 ers, including plasma membrane H+ pump AHA3, Ca2+ pump ACA9, and K+ channel SPIK, further support the
23  In this issue, Ryken et al. show that three Ca2+ pumps (ACAs) play an important role in the maintena
24                       We examined whether SR-Ca2+ pumps account for a larger proportion of the energy
25 rates the inadequacy of a two-state model of Ca2+ pump activation and suggests a regulatory role for
26 report here the first direct measurements of Ca2+ pump activity in human red cells infected with Plas
27                                              Ca2+ pump activity was measured by the Co2+-exposure met
28 tion in calmodulin-dependent plasma membrane Ca2+ pump activity.
29  highly thapsigargin-resistant intracellular Ca2+ pumping activity capable of accumulating Ca2+ withi
30  study investigated the role of this unusual Ca2+ pumping activity in maintaining cytosolic Ca2+, gen
31 preparation indicated a 3-4-fold increase in Ca2+ pumping activity in the transfected cells, and the
32 e mutant showed high H+/Ca2+-antiport but no Ca2+-pump activity.
33 ge portion of neuronal endoplasmic reticulum Ca2+ pumps against thapsigargin inhibition.
34        It is a potent inhibitor of the SERCA Ca2+ pumps (all isoforms), inhibiting Ca2+-dependent ATP
35 table cells (consisting of a plasma membrane Ca2+ pump and channel; Ca2+ store with pump and channel;
36 1cnb1) lacks a Golgi and a vacuolar membrane Ca2+ pump and grows very poorly on Ca2+-depleted medium.
37 action on the cardiac sarcoplasmic reticulum Ca2+ pump and myocardial relaxation, may prove valuable
38 ived the most attention because it expresses Ca2+ pumps and Ca2+ channels, thus endowing it with the
39 ulating Ca2+(i) stores via interactions with Ca2+ pumps and channels that regulate those stores.
40 ma membrane (PMCA) and intracellular (SERCA) Ca2+ pumps and characterizing their role in initiation a
41          The ATP utilization rates of the SR-Ca2+ pumps and crossbridges were measured using a couple
42                         The number of bundle Ca2+ pumps and magnitude of resting Ca2+ efflux suggeste
43 concentration of sarcoplasmic reticulum (SR)-Ca2+ pumps and parvalbumin, (b) fast off-rate of Ca2+ fr
44 xpected, the relative proportions used by SR-Ca2+ pumps and the crossbridges were similar to other mu
45 total energy has been found to be used by SR-Ca2+ pumps and the remainder by crossbridges.
46  SERCA2a, the cardiac sarcoplasmic reticulum Ca2+ pump, and SERCA2b, which is expressed in all tissue
47 co/endoplasmic reticulum Ca2+-ATPase (SERCA) Ca2+ pumps, and additionally increases ion leakage acros
48 nd re-uptake of the released Ca2+ via the SR Ca2+ pump are well-coordinated processes.
49 dephosphorylation cycles regulating IP3R and Ca2+ pumps are a controlling factor for sustained Ca2+ o
50 ed as intermediates of the reaction cycle of Ca2+-pumping ATPases.
51 ises a synthetic, light-driven transmembrane Ca2+ pump based on a redox-sensitive, lipophilic Ca2+-bi
52         Store-operated Ca2+ entry induced by Ca2+ pump blockade or in response to muscarinic or B cel
53 pletion of Ca2+ pools using the irreversible Ca2+ pump blocker, thapsigargin, induces DDT1MF-2 smooth
54                            The intracellular Ca2+ pump blocker, thapsigargin, induces emptying of Ca2
55 ndoplasmic reticulum calcium ATPase (SERCA) (Ca2+ pump) blocker.
56 he concept of vectorial Ca2+ efflux in which Ca2+ pumping by SERCA reduces [Ca2+]c after stimulation.
57 iated with inhibition of the plasma membrane Ca2+ pump (by 29 +/- 3 %, P < 0.01) and increased Ca2+ s
58 rvalbumin) to spread out the time over which Ca2+ pumping can occur.
59 g agonist stimulation, but much less so in a Ca2+ pumping-deficient PMCA4b mutant.
60 lts revealed that the thapsigargin-resistant Ca2+ pump does maintain physiological Ca2+ levels, is ab
61  these complexes include: (a) binding of the Ca2+-pump domain to only the C-terminal part of CaM (b)
62          This may involve reversal of the SR Ca2+ pump, due to local ADP accumulation.
63 s all the conserved domains common to P-type Ca2+ pumps (EC 3.6.1.38).
64 is counterbalanced by unidirectional forward Ca2+ pump flux.
65 es in the EC50 of the sarcoplasmic reticulum Ca2+ pump for CA2+ and increases in the contractile para
66 finity of the cardiac sarcoplasmic reticulum Ca2+ pump for Ca2+, represses both the rates of relaxati
67 )plasmic reticulum Ca2+-ATPase 1 (SERCA1), a Ca2+ pump found in the muscle sarcoplasmic reticulum (SR
68 tudy the structure/function relationships of Ca2+ pumps from eukaryotes.
69                                        Thus, Ca2+ pump function is largely conserved in parasitised c
70 C of isoform 4a of the human plasma membrane Ca2+ pump (hPMCA4a) was studied using the COS cell expre
71 t ECA1 encodes an endoplasmic reticulum-type Ca2+ pump in Arabidopsis.
72    Vanadate (1 mM) inhibited the Vmax of the Ca2+ pump in inosine-fed cells by 99.7%.
73 ts suggest that PLB is a regulator of the SR Ca2+ pump in mouse aorta and plays a regulatory role in
74  There appear to be three different types of Ca2+ pumps in mammalian tissues: the sarco(endo)plasmic
75 tructure, role, and regulation of individual Ca2+ pumps in plants, we have used yeast as a heterologo
76 with sarco/endoplasmic reticulum Ca2+ ATPase Ca2+ pumps in the internal stores can give rise to eithe
77                                 In contrast, Ca2+ pumps in the plasma membrane (PMCA) and sarco-endop
78 psigargin (and cyclopiazonic acid)-sensitive Ca2+-pump in cooperation with a H+-dependent Ca2+ transp
79 of animal sarcoplasmic/endoplasmic reticulum Ca2+ pumps, inhibited the formation of the phosphoprotei
80 ating that the pentamer is not essential for Ca2+ pump inhibition and that the monomer is the more ac
81 lso occurred following application of the SR Ca2+ pump inhibitor cyclopiazonic acid (CPA).
82 tively abolished by pretreatment with the SR Ca2+ pump inhibitor cyclopiazonic acid (CPA).
83 ow depletion of the ER by exposure to the ER Ca2+ pump inhibitor cyclopiazonic acid resulted in a del
84                             The sarcoplasmic Ca2+ pump inhibitor thapsigargin reduced the outward cur
85        The potent and specific intracellular Ca2+ pump inhibitor, thapsigargin, blocks Ca2+ accumulat
86 e was also absent in cells treated with a SR Ca2+-pump inhibitor, cyclopiazonic acid.
87 n and thapsigargin, an endoplasmic reticulum Ca2+-pump inhibitor, were effective inducers of apoptosi
88 al [Ca2+]i, while endoplasmic reticulum (ER) Ca2+ pump inhibitors and release channel activators (tha
89 esting that the dissociation of PLB from the Ca2+ pump is complete, not partial, when the pump binds
90         The inhibition of 2-APB on the SERCA Ca2+ pumps is isoform-dependent, with SERCA 2B being mor
91 odine receptor and Ca2+ re-uptake via the SR Ca2+ pump) is controlled, is the change in the Ca2+ conc
92 boxyl-terminal region of the plasma membrane Ca2+ pump isoform 4b contains two autoinhibitory regions
93 ata demonstrate a direct physical binding of Ca2+ pump isoform 4b to MAGUKs via their PDZ domains and
94  C termini of alternatively spliced "b"-type Ca2+ pump isoforms resemble those of K+ channels and N-m
95 an up-regulation of specific plasma membrane Ca2+ pump isoforms.
96                                       The SR Ca2+ pump may contribute to Ca2+ removal over a low [Ca2
97                          We suggest that the Ca2+ pump modulates ISOC by regulating [Ca2+]i in the re
98  whether, and to what extent, alterations in Ca2+ pump numbers can affect contraction and relaxation
99 und that extrusion through the ATP-dependent Ca2+ pump of the plasma membrane is the dominant form of
100 earance by either Na(+)-Ca2+ exchange or the Ca2+ pumps of the plasma and reticular membranes.
101 uate the effects of overexpression of the SR Ca2+ pump on cardiac contractility, we used the isolated
102 ential and external Na+/K+ concentrations on Ca2+ pump performance.
103            Inhibition of the plasma membrane Ca2+ pump (PMCA) by extracellular allkalinisation (pH 9)
104 t CA1 pyramidal neurons that plasma membrane Ca2+ pumps (PMCAs) and Na+/Ca2+ exchangers are the major
105           Yeast mutants defective in a Golgi Ca2+ pump (pmr1) or both Golgi and vacuolar Ca2+ pumps (
106  Ca2+ pump (pmr1) or both Golgi and vacuolar Ca2+ pumps (pmr1 pmc1 cnb1) were sensitive to growth on
107  a yeast mutant defective in both endogenous Ca2+ pumps, PMR1 and PMC1.
108  disruption of the Golgi apparatus-localized Ca2+ pump Pmr1p.
109                   The thapsigargin-resistant Ca2+ pumping pool was capable of generating rapid cytoso
110  or partially emptied thapsigargin-sensitive Ca2+ pumping pool.
111 stantial Ca2+ accumulation within a specific Ca2+-pumping pool.
112       The release of Ca2+ from intracellular Ca2+ pumping pools and the entry of extracellular Ca2+ a
113 id-induced recovery of bradykinin-releasable Ca2+-pumping pools, whereas cyclooxygenase and lipoxygen
114 igh (20%) serum treatment, which induces new Ca2+ pump protein, return of Ca2+ pools, and reentry of
115 th the plasma membrane Ca2+-ATPase (PMCA), a Ca2+ pump regulated by binding of CaM.
116 ression in a yeast strain lacking endogenous Ca2+ pumps reveals further functional differences from h
117 n by varying the level of activity of the ER Ca2+ pump (SERCA), CICR and release-activated Ca2+ trans
118  of Ca2+ by the sarco-/endoplasmic reticulum Ca2+ pump (SERCA).
119                            Overexpression of Ca2+ pump SERCA1, Ca2+/H+ antiporter Vcx1, or a Mn2+ tra
120       For the skeletal muscle isoform of the Ca2+ pump (SERCA1), the inhibition of curcumin is noncom
121 overning the interaction between the cardiac Ca2+ pump (SERCA2a) and phospholamban (PLB).
122 mains of phospholamban (PLB) and the cardiac Ca2+ pump (SERCA2a) have been investigated by chemical c
123 Ca2+ ATPase isoform 3 (SERCA3) is one of two Ca2+ pumps serving intracellular Ca2+ signaling pools in
124 y both thapsigargin-sensitive and -resistant Ca2+ pumps; since these pumps accumulate Ca2+ in distinc
125 drugs that inhibit the endoplasmic reticulum Ca2+ pump (thapsigargin, cyclopiazonic acid, and tert-bu
126 umen and it is this negative feedback on the Ca2+ pump that controls the Ca2+ store content.
127 TPase isoform 2 (SERCA2) is an intracellular Ca2+ pump that replenishes ER Ca2+, and it seems likely
128 get domains derived from the plasma membrane Ca2+-pump, the Ca2+-activated K+-channel, the Ca2+/CaM-d
129 cific inhibitor of the endoplasmic reticulum Ca2+ pump, to analyse the effects of Ca2+ released from
130 2+-saturated Ca2+ extrusion rate through the Ca2+ pump (Vmax) of parasitised red cells was marginally
131 tribution of the sarcoplasmic reticulum (SR) Ca2+ pump (vs. diffusion) to the kinetics of [Ca24]i dec
132 ' of the Ca2+ sparks was longest when the SR Ca2+ pump was blocked, intermediate in control and short
133 out in human red cells whose plasma membrane Ca2+ pump was inhibited either by depleting the cells of
134 full Ca2+ equilibration, the plasma membrane Ca2+ pump was inhibited either by depleting the cells of
135                              The recombinant Ca2+ pump was produced in high yield, contributing 20% o
136 tapsigargin), indicating that the ATP-driven Ca2+ pump was somehow activated by CaMK II.
137         Specific and polarized expression of Ca2+ pumps was observed in all epithelial cells examined
138      To identify and characterize individual Ca2+ pumps, we have expressed an Arabidopsis ECA1 gene e
139 e-operated Ca2+ channels and plasma membrane Ca2+ pump were present and functional in hCPCs, they had
140 r NCX: L-type Ca2+ currents and plasmalemmal Ca2+ pumps were not affected.
141                         Inhibition of the SR Ca2+ pump with cyclopiazonic acid (CPA) markedly reduced
142 Finally, we inhibited sarcoplasmic reticulum Ca2+ pumping with cyclopiazonic acid (CPA), an inhibitor
143 tion, as occurs after inhibition of internal Ca2+ pumps with thapsigargin.
144 bsequent block of the sarcoplasmic reticulum Ca2+ pump (with cyclopiazonic acid) abolished Ca2+ oscil
145 lows the hair cell to remove H+ generated by Ca2+ pumping without ATP hydrolysis in the cell.

 
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