ライフサイエンスコーパス: Na Ca2 exchanger

1 studies, we also constructed a cysteineless Na+-Ca2+ exchanger.

2 pecies in the roles played by the SR and the Na+-Ca2+ exchanger.

3 tion is not altered by overexpression of the Na+-Ca2+ exchanger.

4 e binding motif (P-loop) in the frog cardiac Na+-Ca2+ exchanger.

5 th an acceleration of Ba2+ entry through the Na+-Ca2+ exchanger.

6 lanced by efflux mediated by the sarcolemmal Na+-Ca2+ exchanger.

7 ow concentrations even in the absence of any Na+-Ca2+ exchanger.

8 teristics to tissue-specific isoforms of the Na+-Ca2+ exchanger.

9 d favors extrusion of cytosolic Ca2+ via the Na+-Ca2+ exchanger.

10 m Ca2+-adenosine triphosphatase (ATPase) and Na+-Ca2+ exchanger.

11 be prevented by inhibiting the mitochondrial Na+/Ca2+ exchanger.

12 driving force of calcium efflux through the Na+/Ca2+ exchanger.

13 with a mechanism based on activation of the Na+/Ca2+ exchanger.

14 A receptors and fast local extrusion via the Na+/Ca2+ exchanger.

15 channel, cardiac L-type calcium channel, and Na+/Ca2+ exchanger.

16 from activity changes of the plasma membrane Na+/Ca2+ exchanger.

17 LO blocks both the PTP and the mitochondrial Na+/Ca2+ exchanger.

18 ed from mitochondria through the PTP and the Na+/Ca2+ exchanger.

19 resence of Na+, suggesting the presence of a Na+ -Ca2+ exchanger.

20 similarity, which are highly conserved among Na+-Ca2+ exchangers.

21 oltage-clamped snail neurones, which have no Na+-Ca2+ exchangers.

22 rotein product shows similarity to mammalian Na+/Ca2+ exchangers.

23 olar H+/Ca2+ exchanger related to vertebrate Na+/Ca2+ exchangers.

24 de of voltage-sensitive Na+ channels and the Na+/--Ca2+ exchanger.

25 Na+/Ca2+ exchangers, a high-capacity Ca2+ extrusion syst

26 The Na+-Ca2+ exchanger acted to remove cytoplasmic Ca2+ thro

27 wo-electrode voltage clamp method to measure Na+-Ca2+ exchanger activity.

28 Instead, Na+/Ca2+ exchanger activity was found to be enhanced in

29 abyrinth in a pattern similar to that of the Na(+)-Ca2+ exchanger and kallikrein, marker proteins exp

30 emonstrated overlapping distributions of the Na(+)-Ca2+ exchanger and ryanodine receptors (RyR2) in A

31 fflux from the cell can be maintained by the Na(+)-Ca2+ exchanger and that other Ca2+ removal mechani

32 Na+-Ca2+ exchanger and Ca2+ channel are two major sarcol

33 However, if the sarcolemmal Na+-Ca2+ exchanger and Ca2+-ATPase were inhibited then r

34 ndria occurs primarily via the mitochondrial Na+-Ca2+ exchanger and helps to sustain post-tetanic tra

35 genic (TG) mouse myocytes overexpressing the Na+-Ca2+ exchanger and in wild-type (WT) myocytes.

36 transient fall, decay was abolished when the Na+-Ca2+ exchanger and sarcolemmal Ca2+-ATPase were inhi

37 se in intracellular Ca2+ via reversal of the Na+-Ca2+ exchanger and subsequently to the initiation of

38 via the ion current (INaCa) produced by the Na+/Ca2+ exchanger and constitutes an important determin

39 likely occurs via an L-type Ca2+ channel and Na(+)-Ca2+ exchanger, and (3) PKC plays a crucial role i

40 Ca2+ channels, the protective effect of the Na+-Ca2+ exchanger, and the lack of significant Ca2+ rel

41 ac actions of genistein on the SR Ca2+ load, Na+/Ca2+ exchanger, and myofilament Ca2+ sensitivity, wh

42 X1 expresses tissue-specific isoforms of the Na+/Ca2+ exchanger, and the isoforms have been examined

43 that plasma membrane Ca2+ pumps (PMCAs) and Na+/Ca2+ exchangers are the major Ca2+ extrusion pathway

44 The role of the Na+-Ca2+ exchanger as a major determinant of cell Ca2+ i

45 tion of the myocardium to the absence of the Na+-Ca2+ exchanger as measured by both immunoblots and m

46 extracellular Na+ with Tris, by Ni2+ or the Na+/Ca2+ exchanger blocker KB-R7943, or with BAPTA in th

47 Blockade of Ca2+ release from mitochondrial Na(+)-Ca2+ exchanger, but not from ER Ca2+ stores, also

48 that depends on Na+ influx and mitochondrial Na(+)-Ca2+ exchanger, but not on Ca2+ influx.

49 1.4 cells because Ba2+ is transported by the Na+-Ca2+ exchanger, but it enters these cells only poorl

50 Inhibition of the mitochondrial Na+-Ca2+ exchanger by CGP-37157 (25 microM) decreased ka

51 to functionally adapt to the absence of the Na+-Ca2+ exchanger by limiting Ca2+ influx.

52 membrane segments of the cardiac sarcolemmal Na+-Ca2+ exchanger by site-directed mutagenesis.

53 essed by disruption or overexpression of the Na+/Ca2+ exchanger, CalX, respectively.

54 of a neuronal (but not glial) isoform of the Na+/Ca2+ exchanger can be altered by the activation of t

55 /reperfusion injury by overexpression of the Na+/Ca2+ exchanger can be overcome partially by female-s

56 tif, we constructed a full-length frog heart Na+-Ca2+ exchanger cDNA (fNCX1a) containing this exon.

57 nd a specific inhibitor of the mitochondrial Na+/Ca2+ exchanger, CGP-37157, we have demonstrated that

58 er ovary cells expressing the bovine cardiac Na+-Ca2+ exchanger (CK1.4 cells) and vector-transfected

59 Split Na+/Ca2+ exchangers consisting of N- or C-terminal domai

60 The current topological model of the Na+-Ca2+ exchanger consists of 11 transmembrane segments

61 The Na(+)-Ca2+ exchanger contains internal regions of sequen

62 the phase and size of LCRs and the resultant Na(+)-Ca2+ exchanger current and is crucial for both bas

63 en in the basal state and activate an inward Na(+)-Ca2+ exchanger current that affects spontaneous be

64 l's inactivation kinetics without changes in Na+-Ca2+ exchanger current density.

65 ent of Ca2+ current, ICa, and suppression of Na+-Ca2+ exchanger current, INa-Ca would enable the myoc

66 range from -88 to +72 mV, consistent with a Na+-Ca2+ exchanger current.

67 ed EADs, whereas a peptide antagonist of the Na+/Ca2+ exchanger current, also hypothesized to support

68 ne-induced Ca2+ transients and the resultant Na+-Ca2+ exchanger currents were increased 10-fold in tr

69 CGP37157, an inhibitor of the mitochondria Na+/Ca2+ exchanger, decreased K+off when added alone but

70 ochondrial Ca2+ uptake, or inhibition of the Na+-Ca2+ exchanger did not measurably alter the amplitud

71 a2+ dynamics predicts that Ca2+ flux via the Na(+)-Ca2+ exchanger during an action potential can acco

72 of submembrane [Ca2+] and activation of the Na+-Ca2+ exchanger during diastolic depolarization (DD)

73 buffer and release Ca2+ through the PTP and Na+/Ca2+ exchanger during physiological Ca2+ signalling.

74 assess whether the reversal potential of the Na+-Ca2+ exchanger (ENa-Ca) was different in transgenic

75 ced SR Ca2+-ATPase expression, and increased Na+-Ca2+ exchanger explain the reduced diastolic [Ca2+]i

76 of accelerated protein synthesis or enhanced Na+-Ca2+ exchanger expression pathways can be differenti

77 t the activity of the Na+-K+ pump influences Na+-Ca2+ exchanger function in the absence of changes in

78 ring relaxation, indicating enhanced forward Na+-Ca2+ exchanger function.

79 a2+ transient, implying impaired sarcolemmal Na+/Ca2+ exchanger function.

80 of accelerated protein synthesis or enhanced Na+-Ca2+ exchanger gene expression in cardiocytes; howev

81 The transcript of the Na+-Ca2+ exchanger gene NCX1 undergoes alternative splic

82 The Na+/Ca2+ exchanger gene NCX1 expresses tissue-specific i

83 changer superfamily includes three mammalian Na(+)-Ca2+ exchanger genes and a number of alternative s

84 Pacemaking current is carried by the Na+-Ca2+ exchanger, I(NaCa), which depends on the intrac

85 esigned this study to assess the role of the Na(+)-Ca2+ exchanger in excitation-contraction coupling

86 2+ exchange current (INa-Ca) produced by the Na(+)-Ca2+ exchanger in response to the intracellular Ca

87 s the activity of the cardiac isoform of the Na+-Ca2+ exchanger in oocytes was confirmed in adult rat

88 nder these conditions, overexpression of the Na+-Ca2+ exchanger in TG myocytes accelerates the declin

89 We directly tested the role of the Na+-Ca2+ exchanger in the action of the glycoside ouabai

90 difference in the reversal potential of the Na+-Ca2+ exchanger in transgenic and control myocytes.

91 phosphate calcium channels (IP3) but not the Na+/Ca2+ exchanger in both the mature and aged heart, su

92 s of the sarcoplasmic reticulum (SR) and the Na+/Ca2+ exchanger in the small, slowly decaying Ca2+ tr

93 ed, but the mRNA levels of phospholamban and Na+/Ca2+ exchanger increased 1.4-fold and 1.8-fold, resp

94 r myocytes, isoproterenol down-regulates the Na+-Ca2+ exchanger, independent of intracellular Ca2+ an

95 (TRP) channel proteins (TRPC4 and TRPC5) and Na+/Ca2+ exchanger, indicating that intracellular store

96 inhibitor, Ru-360, but not influenced by an Na+/Ca2+ exchanger inhibitor or ROS scavengers.

97 le for Iti, because Iti was inhibited by the Na+/Ca2+ exchanger inhibitory peptide XIP (10 micromol/L

98 The Na(+)-Ca2+ exchanger is inhibited by 5 mM nickel.

99 onclude that in embryonic mouse myocytes the Na+-Ca2+ exchanger is absolutely required for the effect

100 myocytes, indicating that the overexpressed Na+-Ca2+ exchanger is functionally active.

101 Na+-Ca2+ exchanger is one of the major sarcolemmal Ca2+

102 The Na+/Ca2+ exchanger is a major transporter of Ca2+ in neu

103 The Na+/Ca2+ exchanger is a plasma membrane protein that reg

104 and suggest that coexpression of Nav1.6 and Na+/Ca2+ exchanger is associated with axonal degeneratio

105 ions derived from modelling suggest that the Na+-Ca2+ exchanger itself could be involved.

106 om control mouse embryos or embryos with the Na+-Ca2+ exchanger knocked out.

107 Heart tubes isolated from homozygous Na+-Ca2+ exchanger knockout mice (NCX-/-) display surpri

108 in the action of the glycoside ouabain using Na+-Ca2+ exchanger knockout mice.

109 nant with LIGA 20-induced restoration of the Na+/Ca2+ exchanger located at the inner membrane of the

110 e infarcted heart, increased activity of the Na(+)-Ca2+ exchanger may promote Ca2+ entry or decrease

111 Modulation of subsarcolemmal Ca2+ by the Na+-Ca2+ exchanger may be an important regulator of exci

112 and energy metabolites, indicating that the Na+/Ca2+ exchanger may play a role in ischemia/reperfusi

113 CU) and extrude it through the mitochondrial Na+/Ca2+ exchanger (mNCE).

114 M, n =12), an inhibitor of the mitochondrial Na+/Ca2+ exchanger (mNCX), (2) Ruthenium Red (40 muM, n

115 n female LVH compared with control rats, and Na+-Ca2+ exchanger mRNA levels were increased similarly

116 to load was examined by assessing c-fos and Na+-Ca2+ exchanger mRNA levels, because there are rapidl

117 The increase in phospholamban or Na+/Ca2+ exchanger mRNAs did not, however, result in cha

118 ggested that reversal of the plasma membrane Na+/Ca2+ exchanger (NCE) may account in part for the ris

119 Inhibition of the plasma membrane Na+ -Ca2+ exchanger (NCX) and of SERCA had a small but s

120 SEA0400, a Na+ / Ca2+ exchanger (NCX) blocker, antagonized the effe

121 on and increased the Na+ level sensed by the Na+, Ca2+ exchanger (NCX).

122 regional variations in the expression of the Na+-Ca2+ exchanger (NCX) have been examined qualitativel

123 The Na+-Ca2+ exchanger (NCX) is a key linker, through Ca2+ s

124 The sarcolemmal Na+-Ca2+ exchanger (NCX) is the main Ca2+ extrusion mech

125 Cardiac-specific Na+-Ca2+ exchanger (NCX) knockout (KO) mice surprisingly

126 is reduced in myocytes from cardiac-specific Na+-Ca2+ exchanger (NCX) knockout (KO) mice.

127 Na+-Ca2+ exchanger (NCX) protein levels and activity wer

128 within couplons activate sufficient reverse Na+-Ca2+ exchanger (NCX) to prime the junctional cleft w

129 storage and release, Ca2+ transport via the Na+-Ca2+ exchanger (NCX), and Ca2+ buffering in the alte

130 ises in submembrane [Na+] ([Na+]sm) local to Na+-Ca2+ exchangers (NCX) could enhance Ca2+ influx via

131 , we previously proposed the hypothesis that Na+/Ca2 + exchanger (NCX) may be involved in inside-out

132 that the effect of[Na+]i accumulation on the Na+/Ca2+ exchanger (NCX) can potentially account for thi

133 ban are decreased on average by 28% and that Na+/Ca2+ exchanger (NCX) protein is increased on average

134 ttenuated by pharmacological blockade of the Na+/Ca2+ exchanger (NCX), intermediate Ca2+-activated K+

135 bsequently affect Ca2+ signaling through the Na+/Ca2+ exchanger (NCX).

136 The cardiac Na+, Ca2+ exchanger (NCX1) is thought to achieve a high

137 The cardiac sarcolemmal Na+-Ca2+ exchanger (NCX1) influences cardiac contractili

138 The cardiac Na+-Ca2+ exchanger (NCX1) is a membrane protein that ext

139 The cardiac Na+-Ca2+ exchanger (NCX1) is one of the major sarcolemma

140 The cardiac Na+-Ca2+ exchanger (NCX1) is the principal Ca2+ efflux m

141 The Na+-Ca2+ exchanger (NCX1) is up-regulated in hypertrophy

142 The Na+-Ca2+ exchanger (NCX1) plays a major role in calcium

143 ude calcium from intracellular space via the Na+/Ca2+ exchanger (NCX1) or sequester it into the sarco

144 l ion transport regulators, inhibits cardiac Na+/Ca2+ exchanger (NCX1).

145 olemmal phosphoprotein, inhibits the cardiac Na+/Ca2+ exchanger (NCX1).

146 mice with a cardiac-specific knockout of the Na+-Ca2+ exchanger, NCX1.

147 The cardiac Na+/Ca2+ exchanger, NCX1, has been modeled to consist of

148 elease was not mediated by the mitochondrial Na+/Ca2+ exchanger or by reversal of the uniporter respo

149 onal cell death, interventions that increase Na+/Ca2+ exchanger or decrease TRP function have the pot

150 o changes in protein level of calsequestrin, Na+/Ca2+ exchanger or phospholamban (PLB), but with both

151 In contrast, inhibition of the Na+/Ca2+exchanger or the plasma membrane Ca2+ ATPase had

152 conclusion, in males, overexpression of the Na+/Ca2+ exchanger reduced postischemic recovery of both

153 (10 mM), had no effect) or inhibition of the Na+-Ca2+ exchanger (replacing extracellular Na+ with N-m

154 rotein levels of SERCA2a, phospholamban, and Na+/Ca2+ exchanger revealed a pattern of changes qualita

155 of Ca2+, by inhibition of the mitochondrial Na+/ Ca2+ exchanger, reversibly hastens final recovery o

156 y, we found that Ca2+ extrusion via PMCA and Na+/Ca2+ exchangers slows in an activity-dependent manne

157 Although Na+-Ca2+ exchanger, store-operated Ca2+ channels and pla

158 gh the reverse mode operation of presynaptic Na+/Ca2+ exchangers that are activated by an LTF-inducin

159 m transgenic mice overexpressing the cardiac Na+-Ca2+ exchanger the time to peak and relaxation of tw

160 ractile Ca2+ is transported primarily by the Na+-Ca2+ exchanger, the beta-agonists' simultaneous enha

161 Overexpression of the cardiac Na+/Ca2+ exchanger therefore may increase susceptibility

162 NCX3 is the third isoform of a mammalian Na+-Ca2+ exchanger to be cloned.

163 ution of the sarcoplasmic reticulum (SR) and Na+-Ca2+ exchanger to intracellular Ca2+ regulation in m

164 f Na+-K+ pump activity on the ability of the Na+-Ca2+ exchanger to remove Ca2+ was investigated in is

165 g was followed by increased transcription of Na+/Ca2+ exchanger, TRPC4, TRPC5, and related transcript

166 were dialyzed with Ca2+ buffers or after the Na+-Ca2+ exchanger was blocked by Li+.

167 Activity of the Na+-Ca2+ exchanger was monitored during release of Ca2+

168 t difference in the transmural expression of Na+-Ca2+ exchanger was observed.

169 However Ca2+ flux via the Na+-Ca2+ exchanger was slower when the Na+-K+ pump was i

170 The Na+/Ca2+ exchanger was likely responsible for Iti, becau

171 te and GABAA receptors, K+ channels, and the Na+-Ca2+ exchanger were blocked or by application of the

172 produce a persistent sodium current, and the Na+/Ca2+ exchanger, which can be driven by persistent so

173 levels of the sarcolemmal Ca(2+)-ATPase and Na+/Ca2+ exchanger, which move Ca2+ across the cell memb

174 Inhibition of the mitochondrial Na+-Ca2+ exchanger with CGP-37157 (50 microM) dramatical

175 conditions favoring reverse operation of the Na+-Ca2+ exchanger, Zn2+ application induced a slow incr