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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 tly thapsigargin (Tg), an inhibitor of SR/ER Ca2+ pumps.
16 plicing within the family of plasma membrane Ca2+ pumps.
17 ional work involved in insulin secretion and Ca2+ pumping.
18 ast, the corresponding C-terminal peptide of Ca2+ pump 2b interacted weakly with PDZ1 + 2 and not at
20 id assays demonstrated strong interaction of Ca2+ pump 4b with the PDZ1 + 2 domains of several mammal
21 ers, including plasma membrane H+ pump AHA3, Ca2+ pump ACA9, and K+ channel SPIK, further support the
23 rates the inadequacy of a two-state model of Ca2+ pump activation and suggests a regulatory role for
24 report here the first direct measurements of Ca2+ pump activity in human red cells infected with Plas
27 highly thapsigargin-resistant intracellular Ca2+ pumping activity capable of accumulating Ca2+ withi
28 study investigated the role of this unusual Ca2+ pumping activity in maintaining cytosolic Ca2+, gen
29 preparation indicated a 3-4-fold increase in Ca2+ pumping activity in the transfected cells, and the
33 table cells (consisting of a plasma membrane Ca2+ pump and channel; Ca2+ store with pump and channel;
34 1cnb1) lacks a Golgi and a vacuolar membrane Ca2+ pump and grows very poorly on Ca2+-depleted medium.
35 action on the cardiac sarcoplasmic reticulum Ca2+ pump and myocardial relaxation, may prove valuable
36 ived the most attention because it expresses Ca2+ pumps and Ca2+ channels, thus endowing it with the
38 ma membrane (PMCA) and intracellular (SERCA) Ca2+ pumps and characterizing their role in initiation a
41 concentration of sarcoplasmic reticulum (SR)-Ca2+ pumps and parvalbumin, (b) fast off-rate of Ca2+ fr
42 xpected, the relative proportions used by SR-Ca2+ pumps and the crossbridges were similar to other mu
44 SERCA2a, the cardiac sarcoplasmic reticulum Ca2+ pump, and SERCA2b, which is expressed in all tissue
45 co/endoplasmic reticulum Ca2+-ATPase (SERCA) Ca2+ pumps, and additionally increases ion leakage acros
47 dephosphorylation cycles regulating IP3R and Ca2+ pumps are a controlling factor for sustained Ca2+ o
49 ises a synthetic, light-driven transmembrane Ca2+ pump based on a redox-sensitive, lipophilic Ca2+-bi
51 pletion of Ca2+ pools using the irreversible Ca2+ pump blocker, thapsigargin, induces DDT1MF-2 smooth
54 he concept of vectorial Ca2+ efflux in which Ca2+ pumping by SERCA reduces [Ca2+]c after stimulation.
55 iated with inhibition of the plasma membrane Ca2+ pump (by 29 +/- 3 %, P < 0.01) and increased Ca2+ s
58 lts revealed that the thapsigargin-resistant Ca2+ pump does maintain physiological Ca2+ levels, is ab
59 these complexes include: (a) binding of the Ca2+-pump domain to only the C-terminal part of CaM (b)
63 es in the EC50 of the sarcoplasmic reticulum Ca2+ pump for CA2+ and increases in the contractile para
64 finity of the cardiac sarcoplasmic reticulum Ca2+ pump for Ca2+, represses both the rates of relaxati
65 )plasmic reticulum Ca2+-ATPase 1 (SERCA1), a Ca2+ pump found in the muscle sarcoplasmic reticulum (SR
68 C of isoform 4a of the human plasma membrane Ca2+ pump (hPMCA4a) was studied using the COS cell expre
71 ts suggest that PLB is a regulator of the SR Ca2+ pump in mouse aorta and plays a regulatory role in
72 There appear to be three different types of Ca2+ pumps in mammalian tissues: the sarco(endo)plasmic
73 tructure, role, and regulation of individual Ca2+ pumps in plants, we have used yeast as a heterologo
74 with sarco/endoplasmic reticulum Ca2+ ATPase Ca2+ pumps in the internal stores can give rise to eithe
76 psigargin (and cyclopiazonic acid)-sensitive Ca2+-pump in cooperation with a H+-dependent Ca2+ transp
77 of animal sarcoplasmic/endoplasmic reticulum Ca2+ pumps, inhibited the formation of the phosphoprotei
78 ating that the pentamer is not essential for Ca2+ pump inhibition and that the monomer is the more ac
81 ow depletion of the ER by exposure to the ER Ca2+ pump inhibitor cyclopiazonic acid resulted in a del
85 n and thapsigargin, an endoplasmic reticulum Ca2+-pump inhibitor, were effective inducers of apoptosi
86 al [Ca2+]i, while endoplasmic reticulum (ER) Ca2+ pump inhibitors and release channel activators (tha
87 esting that the dissociation of PLB from the Ca2+ pump is complete, not partial, when the pump binds
89 odine receptor and Ca2+ re-uptake via the SR Ca2+ pump) is controlled, is the change in the Ca2+ conc
90 boxyl-terminal region of the plasma membrane Ca2+ pump isoform 4b contains two autoinhibitory regions
91 ata demonstrate a direct physical binding of Ca2+ pump isoform 4b to MAGUKs via their PDZ domains and
92 C termini of alternatively spliced "b"-type Ca2+ pump isoforms resemble those of K+ channels and N-m
96 whether, and to what extent, alterations in Ca2+ pump numbers can affect contraction and relaxation
97 und that extrusion through the ATP-dependent Ca2+ pump of the plasma membrane is the dominant form of
99 uate the effects of overexpression of the SR Ca2+ pump on cardiac contractility, we used the isolated
102 t CA1 pyramidal neurons that plasma membrane Ca2+ pumps (PMCAs) and Na+/Ca2+ exchangers are the major
104 Ca2+ pump (pmr1) or both Golgi and vacuolar Ca2+ pumps (pmr1 pmc1 cnb1) were sensitive to growth on
111 id-induced recovery of bradykinin-releasable Ca2+-pumping pools, whereas cyclooxygenase and lipoxygen
112 igh (20%) serum treatment, which induces new Ca2+ pump protein, return of Ca2+ pools, and reentry of
114 ression in a yeast strain lacking endogenous Ca2+ pumps reveals further functional differences from h
115 n by varying the level of activity of the ER Ca2+ pump (SERCA), CICR and release-activated Ca2+ trans
120 mains of phospholamban (PLB) and the cardiac Ca2+ pump (SERCA2a) have been investigated by chemical c
121 Ca2+ ATPase isoform 3 (SERCA3) is one of two Ca2+ pumps serving intracellular Ca2+ signaling pools in
122 y both thapsigargin-sensitive and -resistant Ca2+ pumps; since these pumps accumulate Ca2+ in distinc
123 drugs that inhibit the endoplasmic reticulum Ca2+ pump (thapsigargin, cyclopiazonic acid, and tert-bu
125 TPase isoform 2 (SERCA2) is an intracellular Ca2+ pump that replenishes ER Ca2+, and it seems likely
126 get domains derived from the plasma membrane Ca2+-pump, the Ca2+-activated K+-channel, the Ca2+/CaM-d
127 cific inhibitor of the endoplasmic reticulum Ca2+ pump, to analyse the effects of Ca2+ released from
128 2+-saturated Ca2+ extrusion rate through the Ca2+ pump (Vmax) of parasitised red cells was marginally
129 tribution of the sarcoplasmic reticulum (SR) Ca2+ pump (vs. diffusion) to the kinetics of [Ca24]i dec
130 ' of the Ca2+ sparks was longest when the SR Ca2+ pump was blocked, intermediate in control and short
131 out in human red cells whose plasma membrane Ca2+ pump was inhibited either by depleting the cells of
132 full Ca2+ equilibration, the plasma membrane Ca2+ pump was inhibited either by depleting the cells of
136 To identify and characterize individual Ca2+ pumps, we have expressed an Arabidopsis ECA1 gene e
137 e-operated Ca2+ channels and plasma membrane Ca2+ pump were present and functional in hCPCs, they had
140 Finally, we inhibited sarcoplasmic reticulum Ca2+ pumping with cyclopiazonic acid (CPA), an inhibitor
142 bsequent block of the sarcoplasmic reticulum Ca2+ pump (with cyclopiazonic acid) abolished Ca2+ oscil
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