ライフサイエンスコーパス: ATP depletion

1 (e.g., PARP1 hyperactivation, gammaH2AX, and ATP depletion).

2 ia) and the availability of cellular energy (ATP depletion).

3 in mitochondrial transmembrane potential or ATP depletion.

4 be an off-target activity that was linked to ATP depletion.

5 ctrum in living cells, which disappears upon ATP depletion.

6 inated free 20S particles and was blocked by ATP depletion.

7 efective in cell growth regulation following ATP depletion.

8 ensitive to the temperature and absent after ATP depletion.

9 on via H2O2 and KATP channels, without DA or ATP depletion.

10 reased binding to some V-ATPase mRNAs during ATP depletion.

11 e mobile fraction were reversibly reduced by ATP depletion.

12 This effect can also be mimicked by ATP depletion.

13 inated proteins and the proteasome following ATP depletion.

14 osis, may be primarily driven by chondrocyte ATP depletion.

15 stration buffered ischemia-mediated cerebral ATP depletion.

16 ressing and non-ABCG2-expressing cells or by ATP depletion.

17 m the endoplasmic reticulum because of local ATP depletion.

18 enting caspase-3-mediated degradation during ATP depletion.

19 gnificantly inhibited FAK degradation during ATP depletion.

20 ble in the culture medium within 1 h of mild ATP depletion.

21 i, muramyl dipeptide, and host intracellular ATP depletion.

22 to enhance cell survival by causing partial ATP depletion.

23 illing of spxB mutants was due to more rapid ATP depletion.

24 omal inhibitors but were markedly reduced by ATP depletion.

25 transfectant control G cells but not at 4-h ATP depletion.

26 by hypoxia but were significantly reduced by ATP depletion.

27 n assembly in living epithelial cells during ATP depletion.

28 mbrane potential, superoxide production, and ATP depletion.

29 es may play a role in cellular injury due to ATP depletion.

30 e dehydrogenase leakage without ameliorating ATP depletion.

31 me photosystem I acceptor side limitation or ATP depletion.

32 st protective effects against cell injury by ATP depletion.

33 that promote hepatic lipid accumulation and ATP depletion.

34 were not shed into the luminal space during ATP depletion.

35 did not completely use available PCr to slow ATP depletion.

36 DNA damage causes cell death via NAD(+) and ATP depletion.

37 e-based ATP kit were used to assess cellular ATP depletion.

38 NOS inhibitor, failed to affect MPTP-induced ATP depletion.

39 intensity of E-cadherin staining induced by ATP depletion.

40 anism by which 7-NI counteracts MPTP-induced ATP depletion.

41 conitase inhibition, which results in severe ATP depletion.

42 A similar response is seen in HeLa cells to ATP depletion.

43 akes this kinase complex highly sensitive to ATP depletion.

44 se, resulting in rapid metabolism and marked ATP depletion.

45 and was associated with oxidative stress and ATP depletion.

46 , low levels of DNA hypoploidy, and an early ATP depletion.

47 e) polymerase, resulting in extensive NAD(+)/ATP depletion.

48 responsible for the arc is not sensitive to ATP depletion.

49 ious when reoxygenation followed glucose and ATP depletion.

50 uminescence-based ACCase assay that monitors ATP depletion.

51 B10 conformationally insensitive to cellular ATP depletion.

52 a(+),K(+)-ATPase levels remain unaffected by ATP depletion.

53 lex III activity, suppression of OXPHOS, and ATP depletion.

54 n the absence of JNK/c-Jun overactivation or ATP depletion.

55 multidrug resistance via P-gp inhibition and ATP depletion.

56 oncotic swelling and oncotic death following ATP depletion.

57 the translocon is also strongly inhibited by ATP depletion.

58 ial LLC-PK(1) cells were subjected to either ATP depletion (0.1 microM antimycin A and glucose depriv

59 a,gamma-imido)triphosphate], is abolished by ATP depletion (2 deoxy-D-glucose with oligomycin or perf

60 intracellular Ca(2+) chelation (5 mm EGTA), ATP depletion (4 units/ml apyrase), and the protein kina

61 ATP depletion (5 mm NaCN and 5 mm 2-deoxy-d-glucose in t

62 syncytia, causing mitochondrial failure with ATP depletion, a bioenergetic form of cell death with ne

63 correlated with the extent of intracellular ATP depletion, a hallmark of necrotic cell death.

64 intracellular Ca2+ homeostasis, attenuating ATP depletion, ablating mitochondrial calcium overloadin

65 Inhibition of ISG15 conjugation by ATP depletion abrogated the proteasome inhibitor-depende

66 Pharmacological ATP depletion abrogated VLP production without affecting

67 mitochondrial uptake, probably by enhancing ATP depletion, accounting for the large inhibition of th

68 The degree of ATP depletion after an intravenous (IV) fructose challen

69 pletes hepatic ATP and impairs recovery from ATP depletion after an IV fructose challenge.

70 Whether hypoxia or ATP depletion alone could produce similar activation pat

71 Reduced temperature and ATP depletion also inhibited movement, which is characte

72 including parameters of oxidative stress and ATP depletion, altered redox homeostasis, and impaired r

73 wever, the proteasome inhibitors did prevent ATP depletion, an early effect of LeTx.

74 Hsp27 and F-actin did not change between 2-h ATP depletion and 4-h recovery.

75 t traumatic noise induces transient cellular ATP depletion and activates Rho GTPase pathways, leading

76 nduced altered glutamine metabolism involves ATP depletion and activation of the energy sensor AMP-ac

77 ion of 50 microM H(2)O(2) caused significant ATP depletion and approximately the same amount of cell

78 re chromosome condensation as well as severe ATP depletion and autophagic degeneration, accompanied b

79 yocardial ischemia and reperfusion, in which ATP depletion and Ca(2+) overload occur.

80 stulate that upon mitochondrial dysfunction, ATP depletion and calpain activation contribute to the d

81 tamine oligomerization by Congo red prevents ATP depletion and caspase activation, preserves normal c

82 Further, we observed that 6-ETI induces ATP depletion and cell death accompanied by S phase arre

83 cells from alpha-toxin-induced intracellular ATP depletion and cell death by reducing extracellular A

84 (including itself), resulting in NAD(+) and ATP depletion and cell death.

85 the secondary effects of hypoxia, including ATP depletion and cell injury.

86 Increased temperature worsened the ATP depletion and cell volume shrinkage.

87 (glutamate) release; peroxynitrite-mediated ATP depletion and consequent hypersensitivity of NMDA re

88 This assembly is initiated early during ATP depletion and continues after ATP levels are maximal

89 to support their bioenergetics undergo rapid ATP depletion and death in response to PARP activation.

90 n oxidative phosphorylation are resistant to ATP depletion and death in response to PARP activation.

91 g SM to intact cells (or vesicles) mitigated ATP depletion and Fe- and phospholipase A(2)-induced dam

92 We assessed chondrocytes for ATP depletion and for in situ changes in mitochondrial u

93 K is activated during cardiac stress-induced ATP depletion and functions to stimulate metabolic pathw

94 ose consumption could result in more hepatic ATP depletion and impaired ATP recovery.

95 mitochondrial membrane potential, leading to ATP depletion and necrotic cell death or to cytochrome c

96 marily by metabolic stresses associated with ATP depletion and not by isolated O(2) deprivation.

97 two different mechanisms, cAMP accumulation/ATP depletion and oligomerization/pore formation, contri

98 se predisposes tubular cells to superimposed ATP depletion and oxidant injury.

99 m elevation of [ATP] followed by progressive ATP depletion and Poly ADP Ribose Polymerase cleavage, (

100 o impaired oxidative phosphorylation, muscle ATP depletion and poor exercise capacity.

101 nates a cellular program that limits further ATP depletion and promotes compensatory changes that mai

102 We identified ATP depletion and recovery to energetic homeostasis, alo

103 striatal cells, N-cadherin was decreased by ATP depletion and STHdh(Q111) striatal cells exhibited d

104 ion of inhibitory synapses was unaffected by ATP depletion and the cytoskeletal inhibitors, colchicin

105 t AML differentiation can be induced through ATP depletion and the subsequent activation of DNA damag

106 llular adenylate pools in cellular models of ATP depletion and therefore represent a potential new cl

107 To detect ATP depletion and thus energy deprivation, we measured a

108 intake because of the effect of fructose on ATP depletion and uric acid generation.

109 y restricted in their migration by chilling, ATP depletion and wheatgerm agglutinin and thus moved by

110 Rods induced by ATP-depletion and released from cells by mechanical lysi

111 ate neuroprotection, ameliorating 13-32% of [ATP]-depletion and 19-56% of vital dye uptake at 24 h.

112 ession and STAT3 activation, reduced hepatic ATP depletion, and attenuated oxidative stress.

113 olymerase-1 (PARP-1) hyperactivation, NAD(+)/ATP depletion, and mu-calpain-induced programmed necrosi

114 Ischemia causes AKI as a result of ATP depletion, and rapid recovery of ATP on reperfusion

115 e mitochondrial membrane potential, cellular ATP depletion, and release of mitochondrial cytochrome c

116 nd ROI production, Ca(2+) release, transient ATP depletion, and robust mitochondrial hyperpolarizatio

117 ient elevation of the deltapsim, followed by ATP depletion, and sensitization of normal PBLs to H2O2-

118 Aggregate formation was enhanced by ATP depletion, and upon restoration of metabolic energy,

119 ids, oxidant stress, adenosine triphosphate (ATP) depletion, and mitochondrial dysfunction may be imp

120 ive, and it dramatically predisposed to both ATP depletion- and Fe-mediated attack.

121 Hypoxia-ischemia and ATP depletion are associated with glial swelling and ble

122 rapidly drops to an undetectable level upon ATP depletion as does the availability of RanGTP.

123 equence of acute metabolic perturbation with ATP depletion as occurs in ischemia/reperfusion and acut

124 t on capacitative Ca2+ entry was also due to ATP depletion, as has been suggested recently for its li

125 NK activated at early steps of recovery from ATP depletion, as well as an apoptotic inhibitory protei

126 ps between dietary fructose, UA, and hepatic ATP depletion at baseline and after IV fructose challeng

127 lockade sensitized HK-2 cells to both Fe and ATP depletion attack.

128 However, during stress induced by ATP depletion, AU-rich elements are necessary to maintai

129 Cell lines with a slower rate of ATP depletion (average t(1/2) of 45 h) activate caspase-

130 hese data suggest that recovery from hepatic ATP depletion becomes progressively less efficient as bo

131 srupts axonal energy homeostasis, leading to ATP depletion before physical breakdown of damaged axons

132 e are protected from necrotic cell death and ATP depletion but not from apoptotic death.

133 brefeldin A, glybenclamide, or intracellular ATP depletion but was inhibited in the presence of cytoc

134 ls, a mouse renal proximal tubule cell line, ATP depletion by antimycin A treatment upregulated survi

135 lism that counteract nutrient deficiency and ATP depletion by phosphorylating multiple enzymes and tr

136 in K(ATP) p(open) may arise from submembrane ATP depletion by the Na(+)-K(+) ATPase, as the pump bloc

137 oligomycin, which both induced intracellular ATP depletion (by 50-80%), attenuated collagen and prote

138 e (HK-2) cells after 4 or 18 hours of either ATP depletion/Ca(2+) ionophore- or ferrous ammonium sulf

139 conditions and during superimposed injuries (ATP depletion/Ca2+ ionophore or iron-mediated oxidant st

140 dent increase in HK-2 susceptibility to both ATP-depletion/Ca2+-ionophore- and Fe-mediated attack wit

141 till induces depolarization of mitochondria, ATP depletion, calcium influx, and the accumulation of R

142 ed and involves tissue edema, cell swelling, ATP depletion, calcium toxicity, and oxidative stress.

143 vimentin exchange in ULFs required ATP, and ATP depletion caused a dramatic reduction of the soluble

144 Actin depolymerization or ATP depletion caused a two- to threefold increase in the

145 In addition, ATP depletion caused RME-1 to lose its endosome associat

146 ion of FAO in tubule epithelial cells caused ATP depletion, cell death, dedifferentiation and intrace

147 During 120 minutes of ischemia or ATP depletion, cell viability and tight junctional integ

148 cess and tested this hypothesis by adding an ATP depletion cocktail to cells accumulating unpackaged

149 ombination with comparisons of the effect of ATP depletion, collapse of the proton electrochemical gr

150 ion of catenins observed in MPT cells during ATP depletion contributes to the loss of function of the

151 The exacerbated ATP depletion could not be attributed to impaired glycol

152 bition of GAPDH with iodoacetate exacerbated ATP depletion, cytotoxicity, and necrotic cell death of

153 The MPT then induces ATP depletion-dependent necrosis or caspase-dependent ap

154 way to either caspase-dependent apoptosis or ATP depletion-dependent necrosis.

155 Profound chondrocyte ATP depletion develops in association with heightened NO

156 ATP depletion did not affect Gag membrane binding or mul

157 induced lactate dehydrogenase (LDH) release, ATP depletion, DNA damage, and membrane degradation were

158 procyclic trypanosomes, as a consequence of ATP depletion, due to glycosomal relocation of cytosolic

159 peronin holdase activity is created by rapid ATP depletion during cell lysis.

160 olic dysfunction associated with accelerated ATP depletion during ischemia and diminished regeneratio

161 nstrate severe kidney injury associated with ATP depletion, elevated uric acid, oxidative stress and

162 ed interactions between CIN and hsp90 during ATP depletion enhance CIN-dependent cofilin dephosphoryl

163 Although rotenone caused modest ATP depletion, equivalent ATP loss induced by 2-deoxyglu

164 yte lysate is ATP-dependent, as evidenced by ATP depletion experiments and inhibition with nonhydroly

165 eration rates, and susceptibility to injury (ATP depletion, Fe-mediated oxidant stress) were assessed

166 release of adenosine after fructose-induced ATP depletion, followed by a cAMP response, was demonstr

167 ATP depletion for 30 min increased F-actin content to 14

168 gested cause of Huntington disease (HD), but ATP depletion has not reliably been shown in preclinical

169 After ATP depletion, HSF was rapidly activated (within 30 min)

170 We probe DV volume and pH changes upon ATP depletion, hypo- and hypertonic shock, and rapid wit

171 It is concluded that this in vitro model of ATP depletion in a human proximal tubule cell line repro

172 toskeleton is disrupted by both ischemia and ATP depletion in a site-specific manner.

173 ic mitochondrial membrane depolarization and ATP depletion in a time- and dose-dependent manner; remo

174 xtent of UVA-induced necrotic cell death and ATP depletion in all the cell lines.

175 Finally, ATP depletion in both yeast and mammalian cells further

176 triphosphate (dGTP) accumulation and GTP and ATP depletion in CLL cells was inhibited by MSCs, provid

177 Cellular ATP depletion in diverse cell types results in the net c

178 ion, mitochondrial calcium dysregulation and ATP depletion in melanoma cells but not in normal cells.

179 ted UA level may predict more severe hepatic ATP depletion in response to fructose and hence may be r

180 ssed by chemical cross-linking, we find that ATP depletion in the cell does not measurably alter the

181 with focal adhesions is largely resistant to ATP depletion in these experiments, and, consistent with

182 proximal tubule cells or cells subjected to ATP depletion in vitro induced injury as demonstrated by

183 Mfn2 deficiency were subjected to stress by ATP depletion in vitro.

184 an-dependent nuclear transport observed upon ATP depletion in vivo results from a shortage of RanGTP

185 sport since it was inhibited by chilling and ATP depletion in vivo.

186 in intact liver and adenosine triphosphate (ATP) depletion in cultured cells to model cholangiocyte

187 ment did not reduce F-actin formation during ATP depletion, indicating that it was predominantly not

188 Thus, heat stress and ATP depletion induce distinct patterns of hsp27 redistri

189 ess, DNA damage, proteasomal inhibition, and ATP depletion induce O-GlcNAcylation but not N-linked N,

190 ATP depletion induced by a mitochondrial uncoupler resul

191 st this hypothesis we examined the effect of ATP depletion induced by antimycin A and substrate deple

192 ATP depletion induced by hypoxia or mitochondrial inhibi

193 m cellular stresses such as thapsigargin and ATP depletion induced increased expression of the shorte

194 Recovery from ATP depletion induced increases in Smad 1/5/8 levels; fu

195 Similar to BAK, ATP-depletion (induced by both antimycin-A and hypoxia)

196 Okadaic acid inhibits the ATP depletion-induced association of cPLA(2) with nuclea

197 ATP depletion-induced disruption of Hsp90 chaperone acti

198 of BRG1 by small interfering RNA blocked an ATP depletion-induced increase in TNF-alpha and MCP-1 tr

199 These studies indicate that cholangiocyte ATP depletion induces characteristic, domain-specific ch

200 It is additionally shown that ATP depletion induces nuclear translocation of beta-cate

201 0-100 muM) induced a robust Ca(2+) overload, ATP depletion, inhibited PMCA activity, and consequently

202 ) prevented the POA-induced Ca(2+) overload, ATP depletion, inhibition of the PMCA, and necrosis.

203 t significantly attenuated subsequent severe ATP depletion injury of HK-2 cells.

204 activation protect HK-2 cells against severe ATP depletion injury via distinct signaling pathways.

205 tubule (HK-2) cells were subjected to Fe or ATP depletion injury, followed 1 to 24 hours later by as

206 It shows that loss of the ZA after ATP depletion is associated with the withdrawal of E-cad

207 However, ATP depletion is not the only relevant consequence of me

208 escence actin distribution before and during ATP depletion is quantified and compared with measured A

209 ry neurons, when ATP synthesis is inhibited, ATP depletion is reduced approximately 50% by slowing ac

210 data suggest that the sensitivity of IICR to ATP depletion is regulated by the particular complement

211 tegrity of the junctional complex induced by ATP depletion is related to alterations in tyrosine phos

212 ATP depletion is therefore thought to be an inevitable c

213 While ATP depletion led to cell death, over-acetylated tubulin

214 ry model of Madin-Darby canine kidney cells, ATP depletion led to lactate dehydrogenase release.

215 ically, calcium electroporation caused acute ATP depletion likely due to a combination of increased c

216 G+I, by increasing glycolysis, slowed ATP depletion, maintained lower [P(i)], and maintained a

217 d during intracellular Mg(2+) overload or by ATP depletion, maneuvers that reduce the Ca(2+)-carrying

218 and TCF/LEF-1 to the nucleus indicates that ATP depletion may activate the wnt/wingless signal trans

219 tive potassium (K(ATP)) channels by ischemic ATP depletion may play a role, but little direct evidenc

220 Moreover, the ATP depletion-mediated change from apoptosis to necrosis

221 ic basis of NAMPT inhibition responsible for ATP depletion, metabolic perturbation, and subsequent tu

222 lycolysis block synergized in inducing rapid ATP depletion, mitochondrial damage, and reactive oxygen

223 The two agents synergistically induced ATP depletion, mitochondrial depolarization, oxidative s

224 polymerase (PARP) leads to cellular NAD and ATP depletion, mitochondrial dysfunction, reactive oxyge

225 athway with cellular adenosine triphosphate (ATP) depletion, mitochondrial cytochrome c release, and

226 sugars in its ability to cause intracellular ATP depletion, nucleotide turnover, and the generation o

227 rity of the zonula occludens (ZA) induced by ATP depletion of renal tubular cells.

228 Using adenosine triphosphate (ATP) depletion of cultured normal rat cholangiocytes (NR

229 experimental tool to study the effects of ER ATP depletion on ER function under normal and stress con

230 In this study, the effect of intracellular ATP depletion on the swelling-induced release of D-[3H]a

231 bitory eEF2 phosphorylation occurred without ATP depletion or AMP kinase activation.

232 s cytochrome c release, without ameliorating ATP depletion or Bax translocation, with little or no as

233 nd reoxygenation injury without ameliorating ATP depletion or Bax translocation.

234 nutes after the inhibition of endocytosis by ATP depletion or by hypertonic sucrose.

235 Following either ATP depletion or cisplatin treatment of rat renal tubula

236 R substrates S6K and 4E-BP1 following either ATP depletion or direct activation of the AMP-activated

237 nhibition of proteasome activity, but not by ATP depletion or production of reactive oxygen species.

238 himeras was insensitive to substrate source, ATP depletion, or inhibition of the adenine nucleotide t

239 Nephropathy was attenuated by DC depletion, ATP depletion, or therapeutic IL-1 antagonism.

240 ne (10 nm to 1 microm) caused dose-dependent ATP depletion, oxidative damage, and death.

241 filin, are induced in hippocampal neurons by ATP depletion, oxidative stress, and excess glutamate an

242 that glycolytic inhibition induced profound ATP depletion, PMCA inhibition, [Ca(2+)]i overload, and

243 intestinal epithelial hyperpermeability and ATP depletion, possibly by fostering the formation of pe

244 ATP depletion preconditioning (1 h of antimycin A and 2-

245 It is concluded that ATP depletion preconditioning and A(1) and A(2a) adenosi

246 Cytoprotection by ATP depletion preconditioning or A(1) adenosine receptor

247 nist failed to prevent protection induced by ATP depletion preconditioning.

248 hondrial hyperpolarization and the resultant ATP depletion predispose T-cells to necrosis, thus promo

249 id but glucose deprivation of cells or acute ATP depletion prevented the mTOR-dependent phosphorylati

250 Fructose-induced hepatic ATP depletion prevents TNF-induced apoptosis, whereas it

251 ation of molecular chaperone interactions by ATP depletion produced remarkable DeltaF508-CFTR immobil

252 As ATP depletion progressed with aging in knee chondrocytes

253 vents Abeta-induced mitochondrial damage and ATP depletion) provides superior protection to that deri

254 Thus, ATP depletion, rather than hypoxia per se, was the cause

255 r environmental stress conditions, including ATP depletion, reactive oxygen species, and mitochondria

256 oscopic measurements with 31P showed delayed ATP depletion, reduced acidosis during ischemia, and imp

257 Galpha12 (shGalpha12-MDCK) were subjected to ATP depletion/repletion and H(2)O(2)/catalase as models

258 Third, ATP depletion resulted in microtubule-dependent depletio

259 Induction of injury by ATP depletion resulted in rapid loss of Neph1 and ZO-1 b

260 As expected for an actin-based motor, ATP depletion resulted in significant inhibition of GFP-

261 ATP depletion results in a decrease in soluble cPLA(2) a

262 ATP depletion results in Bax translocation from cytosol

263 P, in the presence of oligomycin (to prevent ATP depletion), reversibly suppressed PF-triggered Ca(2+

264 hibition of anaerobic respiration exacerbate ATP depletion selectively in the proximal tubule after I

265 hondrial hyperpolarization and the resultant ATP depletion sensitize T cells for necrosis, which may

266 The resultant ATP depletion sensitizes T cells for necrosis that may s

267 Instead, labeling of surface proteins after ATP depletion showed a significant decrease in GGT and S

268 drial membrane depolarization, intracellular ATP depletion, specific and unique substrate proteolysis

269 wever, reduced fluctuations on mitosis or on ATP-depletion/stabilization of cortex correlate with inc

270 tion of reactive oxygen species (ROS) during ATP depletion stage.

271 Both ATP depletion studies and heterokaryon analysis demonstr

272 terestingly, PARP activation did not produce ATP depletion, suggesting involvement of a non-energetic

273 rise in GlcN-6-P levels was correlated with ATP depletion, suggesting that ATP loss is caused by pho

274 -deficient mice exhibited more apoptosis and ATP depletion than cells from wild-type mice.

275 anism of action of this compound may involve ATP depletion that leads to growth inhibition and subseq

276 ons, PARP1 hyperactivation, and severe NAD+ /ATP depletion that stimulate Ca2+ -dependent programmed

277 However, upon ATP depletion, they were reversibly segregated into an E

278 -Darby canine kidney cells were subjected to ATP depletion to assess the effects of cellular energy m

279 l line HK-2 was used in an in vitro model of ATP depletion to mimic in vivo renal ischemic injury.

280 Then, we use ATP depletion to show that at 12 hpi, HCMV inhibits deph

281 N-ethylmaleimide or adenosine triphosphate (ATP) depletion to inactivate the flipase did not lead to

282 rivation-induced reactive oxygen species and ATP depletion, two cellular events contributing to the E

283 With anoxia and the concomitant ATP depletion, vesicular storage of NE is impaired, resu

284 Using 31P NMR spectroscopy, we found that ATP depletion was accelerated in TG hearts during no-flo

285 ctroscopy before and after transient hepatic ATP depletion was induced by fructose injection.

286 chment of ezrin from the cytoskeleton during ATP depletion was nearly complete and was not prevented

287 of Na,K-ATPase from the cytoskeleton at 2-h ATP depletion was significantly less in Hsp27 cells comp

288 ct of disrupting Hsp90 chaperone activity by ATP depletion was similar to the effect of the pharmacol

289 mbined with oligomycin (10microM) to prevent ATP depletion, we first identified features of depolariz

290 ate dehydrogenase, morphological damage, and ATP depletion were also significantly less.

291 rgy trapping, the cells become vulnerable to ATP depletion when energy needs increase acutely.

292 glibenclamide prevented cell blebbing after ATP depletion, whereas blebbing was produced by exposure

293 Vanadate mimics this effect of ATP depletion, whereas genistein ameliorates the reducti

294 ials with intracellular calcium overload and ATP depletion, whereas wild-type maintained ionic and en

295 n DNA damage, cells undergo PARP-1-dependent ATP depletion, which is correlated with reduced TAF1 kin

296 receptor P2X7(R) to induce Ca(2+) influx and ATP depletion, which led to necrosis.

297 Mitochondrial dysfunction may lead to ATP depletion, which may contribute to cell death.

298 rce generation are gained from the effect of ATP-depletion, which reduces the rate of retraction but

299 2+)] were unaffected by either extracellular ATP depletion with apyrase or blockade of P2 receptors w

300 but caused mitochondrial depolarization and ATP depletion within primary T cells.