ライフサイエンスコーパス: sodium pump

1 he enzyme operates as a primary electrogenic sodium pump.

2 reduction and the proper functioning of the sodium pump.

3 r pathway recently described for the related sodium pump.

4 A and C in the heart, regulates the cardiac sodium pump.

5 er(18), which may prevent endocytosis of the sodium pump.

6 turnover, and palmitoylated PLM inhibits the sodium pump.

7 A and C in the heart, regulates the cardiac sodium pump.

8 ion may be a universal means to regulate the sodium pump.

9 se led to the intracellular retention of the sodium pump.

10 ptors (DARs) can exist in a complex with the sodium pump.

11 kably similar to those obtained earlier with sodium pump.

12 y lower ( approximately 6-fold) than for the sodium pump.

13 ryl group transfer less efficiently than the sodium pump.

14 s the initial binding of this steroid to the sodium pump.

15 olarization by accelerating the electrogenic sodium pump.

16 in phospholemman (PLM) regulates the cardiac sodium pump, activating the pump when phosphorylated and

17 of neuronal viability is dependent on normal sodium pump activity and establish Drosophila as a usefu

18 Here we demonstrate that changes in sodium pump activity regulate locomotor networks in the

19 Here we demonstrate that changes in sodium pump activity regulate locomotor output in the sp

20 ous studies we postulated that PTH regulates sodium pump activity through isoform-specific PKC-depend

21 Any regulatory effect of PKC on sodium pump activity thus must be lost upon disruption o

22 ere was a transient, significant increase in sodium pump activity while the blastocyst was actively e

23 alpha3, beta1, sodium pump activity, and Na+-Ca++ exchanger levels were

24 transfer ouabain resistance as a measure of sodium pump activity, we identified segments within the

25 e implicated the beta1-subunit in activating sodium pump activity.

26 rylation of the PLM multimer does not change sodium pump activity.

27 surface caveolin-enriched microdomains with sodium pump alpha subunits, despite the lack of caveolin

28 eptide contains only two Cys residues in all sodium pump alpha-subunit sequences and is found in the

29 y seen in Wolfram syndrome via reductions in sodium pump alpha1 and beta1 subunit expression in pancr

30 A chimeric polypeptide consisting of the rat sodium pump alpha3 subunit with the peptide Gln(905)-Val

31 Sodium pumps (alphabeta dimers) with the alpha1 isoform

32 ch as receptors for vasoactive hormones, the sodium pump, and epithelial sodium and water channels.

33 toxin, which interacts specifically with the sodium pump, and lose intracellular K(+) ions.

34 esidency, and that activities of AE1 and the sodium pump are coregulated in kidney.

35 Ubiquitously expressed sodium pumps are best known for maintaining the ionic gr

36 the alpha3 isoform of the Na(+)/K(+) ATPase (sodium pump) are responsible for rapid-onset dystonia pa

37 not all animal cells critically rely on the sodium pump as the unique bioenergizer, but can be repla

38 Our results therefore reveal sodium pumps as dynamic regulators of mammalian spinal m

39 fied the beta1 subunit of Na(+),K(+)-ATPase (sodium pump) as a binding partner for AE1 in the human k

40 ulation by sodium and functions as a primary sodium pump, as reported previously for Na(+)()-NQR from

41 ther CCK receptors nor alpha subunits of the sodium pump, both plasma membrane markers were present o

42 inducible PLM, PLM expression inhibited the sodium pump, but PLM did not inhibit the sodium pump whe

43 ored and dystonia caused by partial block of sodium pumps can be similarly alleviated.

44 This suggests that antiporters or sodium pumps can be utilized interchangeably by S. cerev

45 The Na,K-ATPase or sodium pump carries out the coupled extrusion and uptake

46 The hypothesis of this study is that the sodium pump complex acts as an intracellular signal-tran

47 Understanding how sodium pumps contribute to network regulation and are ta

48 he discovery of the first (to our knowledge) sodium-pumping Cox (Scox), a cbb3 cytochrome from the ex

49 Sodium pump currents were half-maximal when the [Na+]pip

50 Mutations of D586 in the DPPR sequence of sodium pump decrease the enzyme's affinity for inorganic

51 receptor ligand carbachol, which promoted a sodium pump-dependent increase in respiration.

52 receptor-initiated secretion (estimated from sodium pump-dependent increases in oxygen consumption) w

53 0 and 36% of the ATP produced is used by the sodium pump during blastocoel expansion in the human and

54 that Purkinje cells are highly sensitive to sodium pump dysfunction that alters the intrinsic pacema

55 burst firing of cerebellar neurons caused by sodium pump dysfunction underlies dystonia in this model

56 acilitate molecular genetics studies of this sodium-pumping enzyme, a host strain of V. cholerae was

57 t and they demonstrate that atria have fewer sodium pumps, fewer Na+-Ca++ exchangers, and enhanced se

58 fore P(i) implies that both calcium pump and sodium pump form a ternary enzyme.metal.phosphate comple

59 lpha-subunit of sarcolemmal Na+K+-ATPase (or sodium pump) found on most eukaryotic cell membranes, ha

60 riboflavin is a component of the NADH-driven sodium pump from Vibrio cholerae.

61 her with the catalytic alpha1 subunit of the sodium pump) from human kidney membrane fractions.

62 This abnormal firing abates when sodium pump function is restored and dystonia caused by

63 tional change implicated in ion transport by sodium pump has been obtained by measuring the change in

64 onsistent with the physiological role of the sodium pump in burst firing in midbrain dopamine neurons

65 as clinical relevance due to the role of the sodium pump in diseases, including amyotrophic lateral s

66 Phospholemman regulates the plasmalemmal sodium pump in excitable tissues.

67 ed steroid is an endogenous regulator of the sodium pump in humans and, presumably, other mammals.

68 ere we describe a physiological role for the sodium pump in regulating the excitability of mouse neoc

69 h exercise and metabolic stress activate the sodium pump in skeletal muscle.

70 rons into the respiratory chain and the main sodium pump in Vibrio cholerae and many other pathogenic

71 Given the involvement of sodium pumps in movement disorders, such as amyotrophic

72 stion that remains is how partially blocking sodium pumps in the cerebellum induces dystonia.

73 Notably, partially blocking sodium pumps in the cerebellum was necessary and suffici

74 ease the activity of the Na+,K+-ATPase (NKA, sodium pump) in an organ-specific fashion.

75 ion of SERCA, phospholemman exists as both a sodium pump inhibiting monomer and an unassociated oligo

76 thelium of lenses subjected to an episode of sodium pump inhibition.

77 ary to induce cytoplasmic ion alterations by sodium pump inhibition.

78 The ouabain-like sodium pump inhibitor in mammals (so-called "endogenous

79 abain is a highly polar and unusually potent sodium pump inhibitor that possesses uncommon conformati

80 The sodium pump inhibitor, ouabain, increased the frequency

81 Although the sodium pump is intrinsically electrogenic and responsive

82 SIGNIFICANCE STATEMENT: The sodium pump is ubiquitously expressed and responsible fo

83 alyzing structure function relationships for sodium pump isoforms using reverse genetic approaches.

84 ression of kidney AE1 increased cell surface sodium pump levels.

85 Digitalis-like sodium pump ligands (SPLs) effect natriuresis via inhibi

86 We describe a sodium pump-mediated afterhyperpolarization in spinal ne

87 mtr operon, catalyzes the energy-conserving (sodium-pumping) methyl transfer from CH3-H4SPT to CoM du

88 nd in vivo function similar to the mammalian sodium pump (Na(+), K(+)-ATPase).

89 ons across the trophectoderm mediated by the sodium pump (Na+, K+, ATPase) resulting in the vectorial

90 the inhibitory binding site of the membrane sodium pump (Na+, K+-ATPase).

91 rt a positive inotropic effect by inhibiting sodium pump (Na,K-ATPase) activity, decreasing the drivi

92 The sodium pump (Na,K-ATPase) in animal cells is vital for a

93 king an essential transmembrane carrier, the sodium pump (Na,K-ATPase).

94 t for cardenolides, the alpha subunit of the sodium pump, Na(+),K(+)-ATPase (ATPalpha), in 14 species

95 To function as a selective sodium pump, Na(+)-NQR must contain structures that (1)

96 Decreased active K+ uptake via the sodium pump, Na,K-ATPase, contributes to the adjustment.

97 The sodium pump, Na,K-ATPase, is an important protein for ma

98 RprY positively activated the primary sodium pump, NADH : ubiquinone oxidoreductase (NQR), and

99 Measurement of the activity of the sodium pump of human leucocytes was used to test each fr

100 It has generally been assumed that the sodium pump of Na(+)-NQR operates on the basis of thermo

101 ar mechanisms regulating the activity of the sodium pump or Na,K-ATPase during proliferation of hepat

102 the native alpha3 and beta1 subunits of the sodium pump or the alpha3 subunit of the sodium pump tog

103 wo pools of PLM: one not associated with the sodium pump phosphorylated at Ser(63) and one associated

104 The sodium-potassium ATPase (i.e., the "sodium pump") plays a central role in maintaining ionic

105 edox steps that drive these two parts of the sodium pumping process do not have any redox cofactor in

106 ests a highly specific mode of regulation of sodium pump properties in kidney.

107 to be initiated by drug interaction with the sodium pump, reflected by the affinity of the steroid fo

108 NS, suggesting that additional complexity of sodium pump regulation will be found.

109 We studied the growth-promoting effects of 2 sodium pump-selective cardiotonic steroids, ouabain and

110 oxin-induced K(+) efflux is inhibited by the sodium pump-specific inhibitor ouabain and also by the g

111 activation by carbachol and BzATP was due to sodium pump stimulation.

112 e, including the electron transfer pathways, sodium pumping structures, cofactor and subunit composit

113 data are the first indication that cellular sodium pump subunit abundance is modulated by translatio

114 a(1)FLAG to examine regulatory mechanisms of sodium pump subunit expression.

115 rations of ouabain, which do not inhibit the sodium pump sufficiently to perturb the resting cellular

116 activity, we identified segments within the sodium pump that could be replaced with proton pump sequ

117 sruption in the cellular organization of the sodium pump, the sodium/calcium exchanger, and inositol-

118 This respiratory enzyme, which couples sodium pumping to the electron transfer between NADH and

119 the sodium pump or the alpha3 subunit of the sodium pump together with the beta subunit of the gastri

120 as experimentally indistinguishable from the sodium pump value.

121 rs, ion channels, and subunits of proton and sodium pumps variably correlated with drug potency.

122 this study, the biochemical activity of the sodium pump was measured directly in single human and bo

123 An inhibitor of the sodium pump was obtained by this technique in a mass spe

124 onformational change in the unphosphorylated sodium pump was studied as a function of ionic strength

125 hysiological patterns of activity engage the sodium pump, we replayed in vitro a place-specific burst

126 atal cord serum contains an inhibitor of the sodium pump; we attempted to isolate and characterise th

127 the sodium pump, but PLM did not inhibit the sodium pump when palmitoylation was inhibited.

128 be a function of the level of expression of sodium pumps, which are alpha(beta) heterodimers, and of