ライフサイエンスコーパス: NCX

1 NCX activity was stimulated in hypotonic media and inhib

2 NCX consists of a transmembrane part and a large intrace

3 NCX current (I(NCX)) was measured in freshly isolated or

4 NCX current (INCX), measured with whole cell patch clamp

5 NCX inactivation occurs in the absence of phosphatidylin

6 NCX inhibition or detubulation increased Ca(2+) spark ac

7 NCX inhibitors can ameliorate cardiac ischemia-reperfusi

8 NCX is a bidirectional transporter that effluxes (forwar

9 NCX is the main pathway for Ca(2+) extrusion from excita

10 NCX-9 functions in hypodermal seam cells that secrete th

11 NCXs mediate the bidirectional translocation of either N

12 CaCA superfamily includes the Na(+)/Ca(2+) (NCX) and Ca(2+)/H(+) (CAX) antiporters, and in mammals t

13 Partition of 25% NCX in T-space and 75% in M-space provided the best fit

14 s, we propose a model in which GlyT2.PMCA2-3.NCX complex would help Na(+)/K(+)-ATPase in controlling

15 Raising [Na(+)]i activates NCX to operate in a reverse mode, leading to Ca(2+) entr

16 Altered NCX activity modulates the sarcoplastic reticulum Ca(2+)

17 These findings suggest that altered NCX activity may contribute to the pathophysiology of pi

18 ted the Na(+)/Ca(2+)-exchange function of an NCX from Methanococcus jannaschii (NCX_Mj) and report it

19 Na(+) entry to promote Ca(2+) uptake via an NCX to trigger MUC5AC secretion.

20 with NCX3-B as mostly expressed in brain and NCX-AC as predominant in skeletal muscle.

21 ecay stabilize integrals of diastolic Ca and NCX current signals.

22 e data suggest that plasma membrane EAAT and NCX are both involved in Glu-induced ATP synthesis, with

23 hese responses were counteracted by EAAT and NCX blockers, as observed in SH-SY5Y and C6 cells.

24 h responses were again abolished by EAAT and NCX blockers.

25 interplay between the activities of EAAT and NCX, coimmunoprecipitation studies showed a physical int

26 inducible nitric oxide synthase (L-NAME and NCX-4016).

27 Coupled NBC and NCX activities are, therefore, suggested to be responsib

28 ost likely via suppression of both NMDAR and NCX activities.

29 a novel regulatory checkpoint for NMDAR and NCX function based on CRMP2 interaction with these prote

30 We show that endogenous PMCA and NCX activities are necessary for GlyT2 activity and that

31 al cross-talk of Ca(2+) cycling proteins and NCX.

32 lex local cross-talk of Ca pump, release and NCX.

33 aneous Ca(2+) transients and waves in WT and NCX KO cells, respectively.

34 cans of spontaneous Ca(2+) release in WT and NCX KO SAN cells in the presence or absence of an IP3 R

35 cytes isolated from adult wild-type (WT) and NCX knockout (KO) mice.

36 from the monomeric structure of the archaeal NCX homologue (Protein Data Bank entry 3V5U ), we introd

37 Drugs previously classified as NCX or NHE inhibitors are shown to also inhibit hASIC-1.

38 required for synchronous triggering, because NCX is capable of priming the diadic cleft with sufficie

39 Such control of the dyadic [Ca(2+)] by NCX play a critical role in suppressing Ca(2+) sparks du

40 H GABA neurons, and this was also reduced by NCX inhibitors.

41 A currents, to increase Na+ levels sensed by NCX and to increase the Ca2+ transient amplitude.

42 normally-myelinated axons (T-type channels, NCX), others active only when exposed by myelin disrupti

43 Unlike specific inhibition of LTCC, combined NCX and LTCC inhibition has no negative effects on cardi

44 ine NCX1.1 with the 562-679 f-loop deletion (NCX-(Delta562-679)) via adenoviral gene transfer.

45 During NCX-mediated Ca(2+) uptake, a rapid increase in cytosoli

46 n of mitochondrial membrane potential during NCX inhibition completely prevented the rest-dependent [

47 We expanded our studies on EAAT/NCX interplay in the H9c2 cells.

48 on of CBD1, and possibly that for the entire NCX family, is mediated through domain interactions betw

49 We examined NCX Ca(2+) activation in intact rabbit and mouse cardiom

50 For example, NCX and NCKX are important in regulation of cardiac cont

51 ced volume changes on Na(+)-Ca(2+) exchange (NCX) activity in transfected CHO cells.

52 Cardiac Na(+)-Ca(2+) exchange (NCX) activity is regulated by [Ca(2+)]i.

53 ew focuses on cardiac Na(+)/Ca(2+) exchange (NCX) and Na(+)/K(+)-ATPase (NKA).

54 AP) activates reverse Na(+)-Ca(2+) exchange (NCX) and subsequent entry of trigger Ca(2+) is controver

55 the atrial-specific Na(+) /Ca(2+) exchange (NCX) knockout (KO) mouse, a model of cellular Ca(2+) ove

56 cotransport (NBC) or Na(+)/Ca(2+) exchange (NCX), and abolished in Na(+)-free medium or by combined

57 nels and reverse mode Na(+)/Ca(2+) exchange (NCX).

58 2+) in and Na(+) out) Na(+)-Ca(2+) exchange (NCX).

59 Although Na+-Ca2+ exchange (NCX) is essential for Ca2+ extrusion, its participation

60 (the Na+ pump) and, via Na+ / Ca2+ exchange (NCX), exert cardiotonic and vasotonic effects.

61 sex differences of sodium-calcium exchange (NCX) current (INCX).

62 cells, electrogenic sodium-calcium exchange (NCX) is the dominant calcium (Ca) efflux mechanism.

63 ocking reverse mode sodium-calcium exchange (NCX) with KB-R 7943 or SEA-0400 abolished Ca(2+) waves,

64 - to four-fold bigger Na(+)-Ca(2+) exchanger NCX currents (INCX).

65 is known to regulate Na(+)-Ca(2+) exchanger (NCX) activity by binding to two adjacent Ca(2+)-binding

66 the plasma membrane Na(+)/Ca(2+) exchanger (NCX) and the excitatory amino acid transporters (EAATs)

67 influxes through the Na(+)/Ca(2+) exchanger (NCX) and the Na(+)/H(+) exchanger, with the latter exace

68 sh this task are the Na(+)/Ca(2+) exchanger (NCX) and the Na(+)/K(+) pump (NKA).

69 e of the prokaryotic Na(+)/Ca(2+) exchanger (NCX) antiporter NCX_Mj protein from Methanococcus jannas

70 The Na(+)-Ca(2+) exchanger (NCX) appears to play an important role in the regulation

71 te activation of the Na(+)-Ca(2+) exchanger (NCX) as an important player in the generation of EADs.

72 The Na(+)/Ca(2+) exchanger (NCX) has been implied to cause arrhythmias.

73 m channel (LTCC) and Na(+)/Ca(2+) exchanger (NCX) have been implicated in repolarization-dependent ar

74 ns was attenuated by Na(+)-Ca(2+) exchanger (NCX) inhibitors, TRPC channel blockers and the phospholi

75 The Na(+)/Ca(2+) exchanger (NCX) is a membrane protein, which catalyzes the counter

76 Na(+)/Ca(2+) exchanger (NCX) is a plasma membrane transporter that moves Ca(2+)

77 The Na(+)-Ca(2+) exchanger (NCX) is a ubiquitously expressed plasma membrane protein

78 The cardiac Na(+)/Ca(2+) exchanger (NCX) is the major Ca(2+) efflux pathway on the sarcolemm

79 nockout of the three Na(+)/Ca(2+) exchanger (NCX) isoforms, NCX1, NCX2, and NCX3, worsens ischemic br

80 the atrial-specific Na(+) /Ca(2+) exchanger (NCX) knockout mouse, cellular Ca(2+) accumulation during

81 by the plasmalemmal Na(+)/Ca(2+) exchanger (NCX) operating in the reverse mode.

82 the plasma membrane Na(+) /Ca(2+) exchanger (NCX) plays a key role in Ca(2+) influx for triggering Ca

83 Na(+)/Ca(2+) exchanger (NCX) proteins operate through the alternating access mec

84 the plasma membrane Na(+) /Ca(2+) exchanger (NCX) rather than presynaptic depolarization or voltage-a

85 Inhibition of Na(+)-Ca(2+) exchanger (NCX) slowed [Ca(2+)]SR decline during rest by threefold,

86 (2+) implicating the Na(+)/Ca(2+) exchanger (NCX), a major Ca(2+) extrusion mechanism activated with

87 xtruding system, the Na(+)/Ca(2+) exchanger (NCX), in NGF-induced differentiation remains unexplored.

88 and by blocking the Na(+)/Ca(2+) exchanger (NCX), suggesting an important contribution of Ca(2+) inf

89 by inhibition of the Na(+)/Ca(2+) exchanger (NCX).

90 activation of electrogenic Na/Ca exchanger (NCX) during diastole.

91 The electrogenic Na/Ca exchanger (NCX) mediates bidirectional Ca movements that are highly

92 eviously shown to contain a Na/Ca exchanger (NCX) tightly linked to GM1 ganglioside that mediates tra

93 SEA0400, a Na+ / Ca2+ exchanger (NCX) blocker, antagonized the effects of both ouabain an

94 ivate sufficient reverse Na+-Ca2+ exchanger (NCX) to prime the junctional cleft with Ca2+.

95 Na+ level sensed by the Na+, Ca2+ exchanger (NCX).

96 rrent (I(CaL)) and sodium-calcium exchanger (NCX) and may activate ryanodine receptors to initiate a

97 e CaV channels and sodium-calcium exchanger (NCX) as predominant mechanisms of calcium influx.

98 a transport by the sodium-calcium exchanger (NCX) is determined by Vm as well as Na and Ca concentrat

99 of atrial-specific sodium-calcium exchanger (NCX) knockout (KO) SAN cells to study the influence of I

100 In atrial-specific sodium-calcium exchanger (NCX) knockout (KO) SAN cells, where the Ca(2+) clock is

101 suggests that the sodium calcium exchanger (NCX) may contribute to the etiology of pentylenetetrazol

102 The electrogenic sodium/calcium exchanger (NCX) mediates bidirectional calcium transport controlled

103 rting) mode of the sodium-calcium exchanger (NCX) with KB-R7943 partially protected rotenone-treated

104 Na(+)/Ca(2+) exchangers (NCX) constitute a major Ca(2+) export system that facili

105 In eukaryotic Na(+)/Ca(2+) exchangers (NCX) the Ca(2+) binding CBD1 and CBD2 domains form a two

106 Sodium/calcium (Na(+)/Ca(2+)) exchangers (NCX) are membrane transporters that play an essential ro

107 ngers includes both Na(+)/Ca(2+) exchangers (NCXs) and Na(+)/Ca(2+),K(+) exchangers (NCKX) as the fam

108 Na(+)/Ca(2+) exchangers (NCXs) are ubiquitous membrane transporters with a key ro

109 Na(+)/Ca(2+) exchangers (NCXs) promote the extrusion of intracellular Ca(2+) to t

110 pressed full-length Na(+)-Ca(2+) exchangers (NCXs) with mutations in two Ca(2+)-binding domains (CBD1

111 to determine that sodium-calcium exchangers (NCXs) also routinely contribute to the regulation of bas

112 mbrane domain function in cells that express NCX proteins.

113 respectively, whereas in myocytes expressing NCX-(Delta562-679) the response was eliminated (with 100

114 Finally, NCX inhibitors reduced VEGF-induced HUVEC proliferation,

115 ggested that NCX2 and 3 were responsible for NCX activity.

116 itro physiology data supporting the role for NCX-9 in handling calcium exchange at the mitochondrion.

117 ) to those cells containing fully functional NCX/GM1: differentiated NG108-15 and C6 cells.

118 Furthermore, NCX upregulation in the seven-week KO model resulted in

119 el of subcellular Ca cycling, we analyze how NCX strength and distribution alter Ca spark formation.

120 I(NCX) and I(NaK) densities were reduced in atrial versus

121 I(NCX) was recorded by whole-cell patch clamp as the Ni(2+

122 o allow separate measurements of I(Ca) and I(NCX) as a function of J(rel).

123 , increasing [Na+]i and altered I(NaK) and I(NCX) causes rate-dependent atrial AP shortening.

124 The relationship between [Ca(2+)](i) and I(NCX) density revealed I(NCX) upregulation in cAF.

125 udy interactions between J(rel), I(Ca) and I(NCX) in porcine ventricular myocytes.We tested the hypot

126 I(Ca) and I(NCX) were partitioned into subpopulations in the T-space

127 ) and SERCA, and increased I(K1),I(Ks) and I(NCX).

128 ne application protocol; (3) delay between I(NCX) and Ca(m) during Ca(2+)-induced-Ca(2+)-release; (4)

129 cx3 gene prevented the enhancement of both I(NCX) and Ca(2+) content in ER stores, suggesting that NC

130 carried by Na(+)-Ca(2+)-exchange current (I(NCX)) in response to sarcoplasmic reticulum (SR) Ca(2+)

131 minance of inward Na-Ca exchanger current (I(NCX)) over Ca-dependent inactivation of L-type Ca curren

132 NCX current (I(NCX)) was measured in freshly isolated or cultured (up t

133 e an inward Na(+)-Ca(2+) exchange current (I(NCX)), which accelerates diastolic depolarization rate,

134 the antiporter and increased NCX currents (I(NCX)) in the reverse mode of operation.

135 as essential for the Abeta(1-42)-dependent I(NCX) increase.

136 the time of late diastolic depolarization I(NCX) activation.

137 ls (I(Ca)) and the Na(+)/Ca(2+) exchanger (I(NCX)).

138 Insulin (1 microm) increased I(NCX) (at +80 mV) by 110 and 83% in fresh and cultured my

139 (2+)](i) and SR Ca(2+) content (integrated I(NCX) during caffeine-induced Ca(2+) transient) were unch

140 a(2+) release events accompanied by inward I(NCX) currents and delayed afterdepolarizations/triggered

141 investigated (I(Na)(+)/I(CaL)(+)/I(Kr)(+)/I(NCX)(+)/I(f)(+)/I(to)(+)/I(K1)(-)/I(Ks)(-)), we pinpoint

142 horylated RyR2, in combination with larger I(NCX) for a given SR Ca(2+) release and increased diastol

143 nt experimental results: (1) hysteresis of I(NCX) dependence on Ca(m); (2) delay between peak I(NCX)

144 The insulin effect on I(NCX) was not inhibited by wortmannin, a nitric-oxide syn

145 Measured Ca(m) and I(Ca) or I(NCX) were used as input to the model for estimating Ca(t

146 ependence on Ca(m); (2) delay between peak I(NCX) and peak Ca(m) during caffeine application protocol

147 included to suppress any native guinea pig I(NCX)).

148 en [Ca(2+)](i) and I(NCX) density revealed I(NCX) upregulation in cAF.

149 The I(NCX)-based method provided a good estimate for the desce

150 Our data also implicate NCX-9 in a LON-2/heparan sulfate and UNC-6/netrin-mediat

151 Changes in NCX expression and protein were assessed with real-time

152 The time course of the decrease in NCX activity paralleled that of the inflammation-induced

153 An inflammation-induced decrease in NCX activity was observed in a subpopulation of putative

154 s, reducing subsarcolemmal Ca2+ with EGTA in NCX KO mice reveals the dependence of Ca2+ release on NC

155 Ca(2+) transients in WT myocytes but not in NCX KO myocytes.

156 Our results in NCX KO SAN cells also demonstrate that RyRs, but not NCX

157 Ca(2+) clock frequency by IP3 signalling in NCX KO SAN cells demonstrates that the effect is indepen

158 In striking contrast, Ca(2+) transients in NCX KO cardiomyocytes were unaffected by the presence or

159 igh lipophilicity index and able to increase NCX activity.

160 ctional form of the antiporter and increased NCX currents (I(NCX)) in the reverse mode of operation.

161 mogenesis derived from models with increased NCX expression, hypertrophy, and heart failure.

162 hough LTCC inhibition is negative inotropic, NCX inhibition has the opposite effect.

163 he arrhythmic burst pacing pattern of intact NCX KO SAN tissue.

164 ound in all vertebrate and some invertebrate NCX homologs.

165 gnal activating an earlier and larger inward NCX current.

166 ed 66+/-3% of outward NCX, 50+/-2% of inward NCX, and 33+/-9% of LTCC current.

167 P waves on electrocardiograms, and isolated NCX KO SAN cells are quiescent.

168 he archaeal NCX_Mj (Methanococcus jannaschii NCX) system was used to resolve the backbone dynamics in

169 Here we tested two known NCX inhibitors, 2-(2-(4-(4-nitrobenzyloxy)phenyl)ethyl)-

170 as seen in Jurkat cells, which entirely lack NCX.

171 +)-dependent phenotype mirroring full-length NCX but distinct from both CBD1 and CBD2.

172 retaining approximately 20% of control level NCX current) and control mice were similar, suggesting t

173 Specifically, lower NCX expression facilitates Ca(2+)-induced Ca(2+) release

174 Knockdown of NCX1 (the main NCX isoform in HUVECs) by siRNA confirmed the pharmacolo

175 ) scavenger tempol, as well as mitochondrial NCX (mNCX) blocker CGP-37157, inhibited PF-triggered Ca(

176 eticulum is quickly removed via forward mode NCX before Ca-induced Ca release starts, the Ca release

177 pose that Ca(2+) influx through reverse mode NCX is required for the activation and the targeting of

178 Furthermore, inhibitors of reverse mode NCX suppressed the VEGF-induced activation of ERK1/2 in

179 ependent upon Ca(2+) influx via reverse mode NCX.

180 isation by influx of Ca(2+) via reverse mode NCX; (iii) propagation can be maintained by RyRs if they

181 ntribution of Ca(2+) influx via reverse-mode NCX activity.

182 Model NCX fractional activation increased from 0.1 to 1.0 as t

183 At the resting membrane potential if most NCX is localized to the cleft, spontaneous Ca sparks are

184 RT-PCR analysis revealed that multiple NCXs and sodium-calcium-potassium exchangers (NCKXs) are

185 e resting membrane potential (V(m) ~-80 mV), NCX removes Ca from the cell (forward mode).

186 shed in Na(+)-free medium or by combined NBC/NCX blockade.

187 AN cells also demonstrate that RyRs, but not NCX, are required for IP3 to modulate Ca(2+) clock frequ

188 These results indicate the nuclear NCX/GM1 complex acts to gate Ca(2+) transfer from cytoso

189 However, the absence of NCX-mediated depolarization in combination with impaired

190 g with short spark latency in the absence of NCX.

191 CBD1 determines the affinity of NCX for regulatory Ca(2+), although CBD2 is also necessa

192 the Ca(2+)-induced conformational changes of NCX dimers arise from the movement of CBD1.

193 ) counterparts, although the contribution of NCX is unclear.

194 To investigate the contribution of NCX to pacemaking in the SAN, we performed optical volta

195 The contribution of NCX to the inflammation-induced increase in the evoked C

196 light reduced NKA alpha2-mediated control of NCX activity as a possible mechanism underlying triggere

197 ly that residues 562-679 are determinants of NCX inhibition by exchanger inhibitory peptide (XIP).

198 uenced by the cleft/noncleft distribution of NCX, which is unknown.

199 -loop deletion eliminates the enhancement of NCX current by insulin, and we examine the signal pathwa

200 Four cell lines with varying expression of NCX and GM1 in the NE were transfected with cameleon-flu

201 these results indicate that the function of NCX in the regulation of [Ca(2+)]i in putative nocicepti

202 ism for the role of CBD12 in the function of NCX.

203 roterenol, suggesting that the importance of NCX current in fight or flight rate increases is enhance

204 monstrates that the effect is independent of NCX.

205 investigated whether combined inhibition of NCX and LTCC with SEA-0400 is effective against dofetili

206 dy to demonstrate that genetic inhibition of NCX protects against afterdepolarizations and to investi

207 UC5AC secretion was reduced by inhibition of NCX.

208 KB-R7943, an inhibitor of NCX, prevented the ischaemia-induced increases in presyn

209 R was also blocked by KB-R7943, inhibitor of NCX.

210 a murine model with heterozygous knockout of NCX (hetKO) using the patch clamp and Ca(2+) imaging tec

211 n 739 within the large intracellular loop of NCX.

212 The large cytoplasmic domain (f-loop) of NCX is required for regulation by various intracellular

213 he distance between the cytoplasmic loops of NCX pairs.

214 This study reveals a novel mechanism of NCX regulation by cytosolic NADH/NAD(+) redox potential

215 -6, potent inhibitors of the reverse mode of NCX subtypes 3 (NCX3) and 1 (NCX1), respectively, on the

216 Indeed, the forward mode of NCX, evaluated in experiments with ionomycin-induced Ca(

217 edly by inhibiting the Ca(2+) inward mode of NCX.

218 There were two modes of NCX activity: one was evoked in response to relatively l

219 sting that both reverse and forward modes of NCX might be affected.

220 both XIP and receptor-mediated modulation of NCX highlights its important role in acute physiological

221 A panel of NCX inhibitors also significantly reduced VEGF-induced B

222 dy was to (1) characterize the properties of NCX activity in subpopulations of DRG neurons, (2) ident

223 diversity of Ca(2+) regulatory properties of NCX proteins can be achieved by (1) local structure rear

224 Further reduction of NCX expression results in arrhythmia and halt of automat

225 1 and 2, had little effect on regulation of NCX by Ca(2+).

226 inct roles in Ca(2+)-dependent regulation of NCX.

227 f the CBDs in Ca(2+)-dependent regulation of NCX.

228 the elevation of [Na+]i and the reversal of NCX, increasing resting cytosolic and SR Ca2+ content, a

229 However, the role of NCX activity in VEGF signaling and angiogenic functions

230 To date, information on the role of NCX in arrhythmogenesis derived from models with increas

231 Here we further investigated the role of NCX in the etiology of seizures by quantifying the effec

232 However, the role of NCX in the generation of SAN automaticity is controversi

233 To investigate the role of NCX in triggering, we examined Ca2+ sparks in ventricula

234 Genetic suppression of NCX reduces both EADs and DADs.

235 with kinetic properties similar to those of NCX.

236 Using the timing of NCX current reversal as an indicator event for EADs, the

237 was correlated with a shift in the timing of NCX current reversal toward the plateau phase earlier in

238 ever, drugs able to increase the activity of NCXs are not yet available.

239 soforms; whether the regulatory diversity of NCXs is related to structural differences of the pair of

240 ce reveals the dependence of Ca2+ release on NCX.

241 Pharmacological inhibition of either EAAT or NCX counteracted the Glu-induced ATP synthesis.

242 oplasm in exchange for one Ca(2+) moved out, NCX is one of the main Na(+) influx mechanisms in cardio

243 -0400 (1 mumol/L) blocked 66+/-3% of outward NCX, 50+/-2% of inward NCX, and 33+/-9% of LTCC current.

244 -dependent movements detected between paired NCXs were abolished by mutating the Ca(2+) coordination

245 In a major breakthrough, a prokaryotic NCX homolog (NCX_Mj) was recently isolated and its cryst

246 he Caenorhabditis elegans NCLX-type protein, NCX-9, in neural circuit formation.

247 rous skin of adult male Sprague-Dawley rats, NCX activity, as assessed with fura-2-based microfluorim

248 RCX-NCY right harpoon over left harpoon RCY-NCX right harpoon over left harpoon RCY-XCN (X and Y = O

249 f Ca(2+)-dependent ICa inhibition by reduced NCX activity.

250 action potential duration because of reduced NCX activity but also reduced ICa the latter possibly be

251 Depolarized Vm reduces NCX-mediated efflux, elevating [Ca]i, and thus promoting

252 osolic NADH/NAD(+) redox potential regulates NCX activity in adult cardiomyocytes.

253 in HEK 293, whereas the structurally related NCX inhibitor SN-6 does not, suggesting that KB-R7943 di

254 Remaining NCX molecules in the incomplete knockout model likely pr

255 s and INCX amplitudes generated by remaining NCX molecules (only 20% of control) remained almost unch

256 all, these results indicate that during rest NCX effectively competes with SERCA for cytosolic Ca(2+)

257 At rest, NCX deactivated with a time constant typically of 20-40

258 contribution of sodium channels and reverse NCX activity to the degeneration of neurites resulting f

259 We conclude that I(Na) and reverse NCX modulate Ca(2+) release in murine WT cardiomyocytes

260 t blockade of sodium channels and of reverse NCX activity blockade partially protects neurites from i

261 uated TAT-CBD3-induced inhibition of reverse NCX.

262 Ca(2+) activation on a multibeat time scale, NCX might better maintain a stable long-term Ca(2+) bala

263 Vm mediated by the voltage and Ca-sensitive NCX.

264 al [Na(+)]i is higher vs. rabbit, sensitized NCX to self-activation by 0 Na(+) bouts.

265 y properties have been reported with several NCX isoforms; whether the regulatory diversity of NCXs i

266 rial tissue preparation from atrial-specific NCX knockout (KO) mice.

267 ted from wild-type (WT) and cardiac-specific NCX knockout (KO) mice.

268 opagation, and nociceptive behaviour suggest NCX activity has little influence on excitability per se

269 rent (If) blocker ivabradine also suppressed NCX KO SAN automaticity.

270 The authors concluded that NCX is required for increasing sinus rates, but not for

271 Ca(2+) influx efficaciously, indicating that NCX had become active.

272 Western blot analyses suggested that NCX isoforms were differentially distributed within sens

273 epeated for 2-5 min or more, suggesting that NCX was inactive.

274 th subsequent Na+ accumulation sensed by the NCX.

275 SAN cells isolated from the NCX KO exhibited higher SK current than wildtype (WT) an

276 sients and inhibited burst generation in the NCX KO SAN whereas the Ca buffer 1,2-Bis(2-aminophenoxy)

277 de that pacemaker activity is present in the NCX KO SAN, generated by a mechanism that depends upon I

278 on hinders spontaneous depolarization in the NCX KO SAN, possibly by inhibiting L-type Ca currents.

279 )/H(+) (CAX) antiporters, and in mammals the NCX and related proteins constitute families SLC8 and SL

280 Ncx1(-/-)) mice to measure the effect of the NCX current on pacemaking activity in vivo, ex vivo, and

281 The activation of the NCX transport function requires the binding of Ca(2+) to

282 Blockade of the NCX's reverse mode could eliminate these effects.

283 The authors, however, did not simulate the NCX current (INCX), that is, the subject of the study.

284 ed and arrhythmic depolarizations within the NCX KO SAN that failed to propagate into the atria.

285 We incorporated this NCX model into an established ventricular myocyte model,

286 Whereas mRNA encoding all three NCX isoforms (NCX1-3) was detected in putative nocicepti

287 Thus, NCX palmitoylation ubiquitously modulates Ca homeostasis

288 At the same time, NCX total activity increased.

289 he junctional SR that are located closely to NCX in the dyadic cleft.

290 s are induced by I(CaL) with very few due to NCX current.

291 Na(+) accumulation in the SERCA KO due to NCX upregulation and intracellular acidosis potentially

292 rons, (2) identify the isoform(s) underlying NCX activity, and (3) begin to assess the function of th

293 This was reversed when Ca(2+) influx via NCX was increased by reducing [Na(+)]o to 13 mm.

294 Ca(2+)]i transients due to Ca(2+) influx via NCX.

295 Ca(2+) uptake via NCX underlies the ischaemia-induced Ca(2+) rise and the

296 een Na(+) accumulation and Ca(2+) uptake via NCX underlies the ischaemia-induced Ca(2+) rise and the

297 Furthermore, the exact mechanism by which NCX exerts its potentially proarrhythmic effect, ie, by

298 esults demonstrate that CRMP2 interacts with NCX and NMDAR and that TAT-CBD3 protects against glutama

299 involved in Glu-induced ATP synthesis, with NCX playing a pivotal role.

300 Myocytes from young NCX KO mice are known to exhibit normal resting cytosoli