ライフサイエンスコーパス: ATP depletion

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

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

3 both glycolytic inhibition and azide-induced ATP depletion.

4 oncotic swelling and oncotic death following ATP depletion.

5 the translocon is also strongly inhibited by ATP depletion.

6 in mitochondrial transmembrane potential or ATP depletion.

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

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

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

10 efective in cell growth regulation following ATP depletion.

11 ensitive to the temperature and absent after ATP depletion.

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

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

14 e mobile fraction were reversibly reduced by ATP depletion.

15 This effect can also be mimicked by ATP depletion.

16 inated proteins and the proteasome following ATP depletion.

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

18 stration buffered ischemia-mediated cerebral ATP depletion.

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

20 m the endoplasmic reticulum because of local ATP depletion.

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

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

23 gnificantly inhibited FAK degradation during ATP depletion.

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

25 to enhance cell survival by causing partial ATP depletion.

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

27 omal inhibitors but were markedly reduced by ATP depletion.

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

29 by hypoxia but were significantly reduced by ATP depletion.

30 n assembly in living epithelial cells during ATP depletion.

31 mbrane potential, superoxide production, and ATP depletion.

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

33 e dehydrogenase leakage without ameliorating ATP depletion.

34 st protective effects against cell injury by ATP depletion.

35 that promote hepatic lipid accumulation and ATP depletion.

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

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

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

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

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

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

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

43 conitase inhibition, which results in severe ATP depletion.

44 me photosystem I acceptor side limitation or ATP depletion.

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

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

47 akes this kinase complex highly sensitive to ATP depletion.

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

49 iated electron transport chain activity, and ATP depletion.

50 and was associated with oxidative stress and ATP depletion.

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

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

53 ious when reoxygenation followed glucose and ATP depletion.

54 uminescence-based ACCase assay that monitors ATP depletion.

55 B10 conformationally insensitive to cellular ATP depletion.

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

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

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

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

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

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

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

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

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

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

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

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

68 Pharmacological ATP depletion abrogated VLP production without affecting

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 pleted autophagy-deficient cells of ATP, and ATP depletion and cell death were prevented by supplemen

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

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

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

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

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

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

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

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

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

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

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

97 ATP depletion and increased mitochondrial mass was ident

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

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

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

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

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

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

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

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

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

107 ATP depletion and succinate accumulation during ischemia

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 Profound chondrocyte ATP depletion develops in association with heightened NO

155 ATP depletion did not affect Gag membrane binding or mul

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

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

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

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

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

161 -sensitivity glucose assay with detection of ATP depletion, enabling 1) quantification of alpha-gluca

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 ATP depletion induced by a mitochondrial uncoupler resul

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

191 ATP depletion induced by hypoxia or mitochondrial inhibi

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

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

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

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

196 ATP depletion-induced disruption of Hsp90 chaperone acti

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

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

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

200 0-100 muM) induced a robust Ca(2+) overload, ATP depletion, inhibited PMCA activity, and consequently

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

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

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

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

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

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

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

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

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

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

211 ATP depletion is therefore thought to be an inevitable c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

238 d that modulation of chromatin compaction by ATP depletion, or treatment with solutions of different

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

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

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

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

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

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

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

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

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

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

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

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

251 As ATP depletion progressed with aging in knee chondrocytes

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

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

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

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

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

257 Third, ATP depletion resulted in microtubule-dependent depletio

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

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

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

261 ATP depletion results in Bax translocation from cytosol

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

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

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

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

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

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

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

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

270 Both ATP depletion studies and heterokaryon analysis demonstr

271 ying either P2X7 deficiency or extracellular ATP depletion suggest that P2X5-dependent anti-L. monocy

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 We used azide-induced ATP depletion to incite cell stress in mouse embryonic f

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

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

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

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

289 After ATP depletion, we observed significant cytosolic compact

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.