ライフサイエンスコーパス: NCX

1 NCX consists of a transmembrane part and a large intrace

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

3 NCX inactivation occurs in the absence of phosphatidylin

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

5 NCX inhibitors can ameliorate cardiac ischemia-reperfusi

6 NCX is a bidirectional transporter that effluxes (forwar

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

8 NCXs mediate the bidirectional translocation of either N

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

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

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

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

13 Additionally, NCX inhibited lipid peroxidation in an emulsified system

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

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

16 Although NCX Na(+)/Ca(2+) exchangers are classically believed to

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

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

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

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

21 current (I(NaL)), L-type Ca(2+) current, and NCX (Na(+)/Ca(2+) exchanger) current are often measured

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

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

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

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

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

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

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

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

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

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

54 2+) in and Na(+) out) Na(+)-Ca(2+) exchange (NCX).

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

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

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

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

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

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

61 pened upon blocking sodium/calcium exchange (NCX) with KB-R7943 or SEA0400.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 and the activity of Na(+)/Ca(2+) exchanger (NCX) may be altered when the Na(+) gradient is changed.

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

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

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

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

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

85 (2+) implicating the Na(+)/Ca(2+) exchanger (NCX), a major Ca(2+) extrusion mechanism activated with

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

87 luding the mammalian Na(+)/Ca(2+) exchanger (NCX), our study provides a regulatory mechanism for the

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

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

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

95 0%), and increased sodium/calcium exchanger (NCX) activity (~52%).

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 ontractility via a sodium-calcium exchanger (NCX) mediated pathway.

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

104 f the reverse-mode sodium-calcium exchanger (NCX) to these responses during hyperglycemia.

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

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

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

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

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

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

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

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

113 mbrane domain function in cells that express NCX proteins.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

134 +) (Na(i)) that decreases the depolarizing I(NCX) thereby suppressing the action potential plateau an

135 n via accelerating Na(+)/Ca(2+) exchanger (I(NCX))-mediated Ca(2+) efflux from cytosol, thereby reduc

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

137 (2+)](i) and SR Ca(2+) content (integrated I(NCX) during caffeine-induced Ca(2+) transient) were unch

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 igh lipophilicity index and able to increase NCX activity.

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

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

158 Inhibiting NCX with SEA0400 abolished LVDP depression caused by inc

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

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

161 ound in all vertebrate and some invertebrate NCX homologs.

162 Inward NCX current was upregulated at phase 3 of AP in HF when

163 Triggered Ca(2+) waves activate inward NCX and dramatically reduce atrial maximum diastolic pot

164 gnal activating an earlier and larger inward NCX current.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

179 tively, and were insensitive to reverse-mode NCX blockade (KB-R7943).

180 vasoconstrictors by activating reverse-mode NCX.

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

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

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

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

185 tivity of the polyphenolic-NCBR nanocomplex (NCX) was studied.

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

187 However, neither NCX inhibitor nor change of extracellular Na(+) concentr

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

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

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

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

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

201 monstrates that the effect is independent of NCX.

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

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

204 UC5AC secretion was reduced by inhibition of NCX.

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

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

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

208 n 739 within the large intracellular loop of NCX.

209 he distance between the cytoplasmic loops of NCX pairs.

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

211 -6, potent inhibitors of the reverse mode of NCX subtypes 3 (NCX3) and 1 (NCX1), respectively, on the

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

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

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

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

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

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

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

219 1 and 2, had little effect on regulation of NCX by Ca(2+).

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

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

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

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

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

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

226 Genetic suppression of NCX reduces both EADs and DADs.

227 with kinetic properties similar to those of NCX.

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

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

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

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

232 pressed only TRPM4 and all three isoforms of NCXs.

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

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

235 Blocking the activity of TRPM4 or NCX proteins abrogated MUC5AC secretion from NHBE and CF

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

237 -0400 (1 mumol/L) blocked 66+/-3% of outward NCX, 50+/-2% of inward NCX, and 33+/-9% of LTCC current.

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

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

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

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

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

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

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

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

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

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

248 Remaining NCX molecules in the incomplete knockout model likely pr

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

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

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

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

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

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

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

256 which drives calcium import through reverse NCX.

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

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

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

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

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

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

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

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

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

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

267 Altogether, our findings reveal that NCX and TRPM4/TRPM5 are both required for mucin secretio

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

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

270 The NCX kept the original color of PRE (magenta) and release

271 The NCX showed high antioxidant activity, as evidenced by tr

272 th subsequent Na+ accumulation sensed by the NCX.

273 In conclusion, the NCX showed good properties as an antioxidant with potent

274 that NMDA-induced sodium increases drive the NCX into reverse mode, resulting in calcium influx.

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

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

284 This NCX-dependent release was too slow to be involved in cha

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 y KB-R7943, while mRNA expression of venular NCX isoforms was unaltered.

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

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

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

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

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

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

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

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