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1 putative proton pump) and NDQ type (putative sodium pump).
2 olarization by accelerating the electrogenic sodium pump.
3 he enzyme operates as a primary electrogenic sodium pump.
4 reduction and the proper functioning of the sodium pump.
5 r pathway recently described for the related sodium pump.
6 A and C in the heart, regulates the cardiac sodium pump.
7 er(18), which may prevent endocytosis of the sodium pump.
8 turnover, and palmitoylated PLM inhibits the sodium pump.
9 A and C in the heart, regulates the cardiac sodium pump.
10 ion may be a universal means to regulate the sodium pump.
11 se led to the intracellular retention of the sodium pump.
12 ptors (DARs) can exist in a complex with the sodium pump.
13 kably similar to those obtained earlier with sodium pump.
14 y lower ( approximately 6-fold) than for the sodium pump.
15 ryl group transfer less efficiently than the sodium pump.
16 s the initial binding of this steroid to the sodium pump.
17 in phospholemman (PLM) regulates the cardiac sodium pump, activating the pump when phosphorylated and
18 of neuronal viability is dependent on normal sodium pump activity and establish Drosophila as a usefu
21 ous studies we postulated that PTH regulates sodium pump activity through isoform-specific PKC-depend
23 ere was a transient, significant increase in sodium pump activity while the blastocyst was actively e
25 transfer ouabain resistance as a measure of sodium pump activity, we identified segments within the
28 n almost complete loss of pH sensitivity for sodium-pumping activity, which is in contrast to previou
29 surface caveolin-enriched microdomains with sodium pump alpha subunits, despite the lack of caveolin
30 eptide contains only two Cys residues in all sodium pump alpha-subunit sequences and is found in the
31 y seen in Wolfram syndrome via reductions in sodium pump alpha1 and beta1 subunit expression in pancr
32 A chimeric polypeptide consisting of the rat sodium pump alpha3 subunit with the peptide Gln(905)-Val
34 cations at position S70 removed the residual sodium pumping and greatly enhanced the channel-like act
35 ch as receptors for vasoactive hormones, the sodium pump, and epithelial sodium and water channels.
39 the alpha3 isoform of the Na(+)/K(+) ATPase (sodium pump) are responsible for rapid-onset dystonia pa
40 not all animal cells critically rely on the sodium pump as the unique bioenergizer, but can be repla
42 fied the beta1 subunit of Na(+),K(+)-ATPase (sodium pump) as a binding partner for AE1 in the human k
43 ulation by sodium and functions as a primary sodium pump, as reported previously for Na(+)()-NQR from
44 ther CCK receptors nor alpha subunits of the sodium pump, both plasma membrane markers were present o
45 inducible PLM, PLM expression inhibited the sodium pump, but PLM did not inhibit the sodium pump whe
49 The hypothesis of this study is that the sodium pump complex acts as an intracellular signal-tran
51 he discovery of the first (to our knowledge) sodium-pumping Cox (Scox), a cbb3 cytochrome from the ex
53 Mutations of D586 in the DPPR sequence of sodium pump decrease the enzyme's affinity for inorganic
55 receptor-initiated secretion (estimated from sodium pump-dependent increases in oxygen consumption) w
56 0 and 36% of the ATP produced is used by the sodium pump during blastocoel expansion in the human and
57 that Purkinje cells are highly sensitive to sodium pump dysfunction that alters the intrinsic pacema
58 burst firing of cerebellar neurons caused by sodium pump dysfunction underlies dystonia in this model
59 acilitate molecular genetics studies of this sodium-pumping enzyme, a host strain of V. cholerae was
60 t and they demonstrate that atria have fewer sodium pumps, fewer Na+-Ca++ exchangers, and enhanced se
61 fore P(i) implies that both calcium pump and sodium pump form a ternary enzyme.metal.phosphate comple
62 lpha-subunit of sarcolemmal Na+K+-ATPase (or sodium pump) found on most eukaryotic cell membranes, ha
66 tional change implicated in ion transport by sodium pump has been obtained by measuring the change in
67 onsistent with the physiological role of the sodium pump in burst firing in midbrain dopamine neurons
68 as clinical relevance due to the role of the sodium pump in diseases, including amyotrophic lateral s
70 ed steroid is an endogenous regulator of the sodium pump in humans and, presumably, other mammals.
71 ere we describe a physiological role for the sodium pump in regulating the excitability of mouse neoc
73 rons into the respiratory chain and the main sodium pump in Vibrio cholerae and many other pathogenic
78 ion of SERCA, phospholemman exists as both a sodium pump inhibiting monomer and an unassociated oligo
82 abain is a highly polar and unusually potent sodium pump inhibitor that possesses uncommon conformati
86 alyzing structure function relationships for sodium pump isoforms using reverse genetic approaches.
90 2% of putative gamma motoneurons exhibited a sodium pump-mediated ultra-slow afterhyperpolarization,
91 mtr operon, catalyzes the energy-conserving (sodium-pumping) methyl transfer from CH3-H4SPT to CoM du
93 tions in the alpha-subunit (ATPalpha) of the sodium pump (Na(+)/K(+)-ATPase)(7-11), the physiological
94 ons across the trophectoderm mediated by the sodium pump (Na+, K+, ATPase) resulting in the vectorial
96 rt a positive inotropic effect by inhibiting sodium pump (Na,K-ATPase) activity, decreasing the drivi
99 t for cardenolides, the alpha subunit of the sodium pump, Na(+),K(+)-ATPase (ATPalpha), in 14 species
101 vertebrate and vertebrate species indicate a sodium pump, Na(+)/K(+) ATPase, powers sodium secretion.
109 ar mechanisms regulating the activity of the sodium pump or Na,K-ATPase during proliferation of hepat
110 the native alpha3 and beta1 subunits of the sodium pump or the alpha3 subunit of the sodium pump tog
111 wo pools of PLM: one not associated with the sodium pump phosphorylated at Ser(63) and one associated
113 edox steps that drive these two parts of the sodium pumping process do not have any redox cofactor in
115 to be initiated by drug interaction with the sodium pump, reflected by the affinity of the steroid fo
117 red-shift in the absorption wavelength of a sodium-pump rhodopsin (KR2) by altering dipole moment of
118 We studied the growth-promoting effects of 2 sodium pump-selective cardiotonic steroids, ouabain and
119 oxin-induced K(+) efflux is inhibited by the sodium pump-specific inhibitor ouabain and also by the g
121 e, including the electron transfer pathways, sodium pumping structures, cofactor and subunit composit
122 data are the first indication that cellular sodium pump subunit abundance is modulated by translatio
124 rations of ouabain, which do not inhibit the sodium pump sufficiently to perturb the resting cellular
125 activity, we identified segments within the sodium pump that could be replaced with proton pump sequ
126 sruption in the cellular organization of the sodium pump, the sodium/calcium exchanger, and inositol-
128 the sodium pump or the alpha3 subunit of the sodium pump together with the beta subunit of the gastri
130 rs, ion channels, and subunits of proton and sodium pumps variably correlated with drug potency.
131 this study, the biochemical activity of the sodium pump was measured directly in single human and bo
133 onformational change in the unphosphorylated sodium pump was studied as a function of ionic strength
134 hysiological patterns of activity engage the sodium pump, we replayed in vitro a place-specific burst
135 atal cord serum contains an inhibitor of the sodium pump; we attempted to isolate and characterise th
137 be a function of the level of expression of sodium pumps, which are alpha(beta) heterodimers, and of