ライフサイエンスコーパス: transmembrane potential

1 ger conductance is observed under a positive transmembrane potential).

2 oupling and ATP synthesis, Ca(2+) uptake and transmembrane potential.

3 nt flowing through the pore under an applied transmembrane potential.

4 charged residues in response to a change in transmembrane potential.

5 ATP coincident with a loss of mitochondrial transmembrane potential.

6 tween the inner and outer bath establishes a transmembrane potential.

7 H(2)O(2) depends on the mitochondrial inner transmembrane potential.

8 a2+] gradient, and strongly dependent on the transmembrane potential.

9 s Bak and Bax, and reduces the mitochondrial transmembrane potential.

10 microscopy was used to verify mitochondrial transmembrane potential.

11 st H2O2-mediated disruption of mitochondrial transmembrane potential.

12 to open and close in response to changes in transmembrane potential.

13 pha-hydroxyryanodine complex is sensitive to transmembrane potential.

14 dissociation of the ligand are sensitive to transmembrane potential.

15 molecule photoactivatable optical sensors of transmembrane potential.

16 Occlusion was dependent upon a cis-negative transmembrane potential.

17 ocaspases 8 and 3, and loss of mitochondrial transmembrane potential.

18 efront and perpendicular to gradients in the transmembrane potential.

19 net current flows along the gradient in the transmembrane potential.

20 rs to originate from a reduced mitochondrial transmembrane potential.

21 ex environment, which includes a substantial transmembrane potential.

22 nalization and collapse of the mitochondrial transmembrane potential.

23 duced changes in intramembrane potential and transmembrane potential.

24 s H(2)O(2)-induced loss of the mitochondrial transmembrane potential.

25 , like As(2)O(3), disrupts the mitochondrial transmembrane potential.

26 pecies production, and drop in mitochondrial transmembrane potential.

27 iated with ROS-induced loss of mitochondrial transmembrane potential.

28 brane permeability changes, or mitochondrial transmembrane potential.

29 ng that the ions decreased the mitochondrial transmembrane potential.

30 a cells leads to alteration of mitochondrial transmembrane potential.

31 volved the early disruption of mitochondrial transmembrane potential.

32 betaCD complex varies continuously with the transmembrane potential.

33 ase and delay but do not prevent the loss of transmembrane potential.

34 ne externalization and loss of mitochondrial transmembrane potential.

35 rs to be preceded by a loss of mitochondrial transmembrane potential.

36 l cardiolipin, and loss of the mitochondrial transmembrane potential.

37 electrical low-pass filtering of the cell's transmembrane potential.

38 tio of OHC displacement to the change in its transmembrane potential.

39 give large and fast responses to changes in transmembrane potential.

40 ich is then able to record the intracellular transmembrane potential.

41 chondrial network with varying mitochondrial transmembrane potential.

42 er the cell, inducing a fast upstroke of the transmembrane potential.

43 of their modification rates by Ag(+) to the transmembrane potential.

44 larization by using fluorescent reporters of transmembrane potential.

45 ionic strength of the aqueous phase, and the transmembrane potential.

46 he pore will compromise the integrity of the transmembrane potential.

47 nditions could induce VDAC closure at <10 mV transmembrane potentials.

48 frequent and prolonged closures, even at low transmembrane potentials.

49 mparison reveals the existence of a critical transmembrane potential above which delivery with the se

50 of electroporation is related to the maximum transmembrane potential achieved.

51 The dependence of the maximum transmembrane potential across the cell membrane on cell

52 By focusing the transmembrane potential across the selectivity filter, t

53 Free energy calculations of the fractional transmembrane potential, acting upon key charged residue

54 ma membrane asymmetry, loss of mitochondrial transmembrane potential, activation of caspase-3, and in

55 (DN) Akt-1 resulted in loss of mitochondrial transmembrane potential, activation of caspases-9 and -3

56 uncouple channel opening from changes in the transmembrane potential, allowing current activation at

57 cal current injected into the cochlea induce transmembrane potential along the outer hair cell (OHC)

58 oppositely charged, a combination of a large transmembrane potential and a large nanotube diameter ca

59 This in turn changes the resting transmembrane potential and affects the excitability of

60 IN cells undergo a decrease in mitochondrial transmembrane potential and an increase in annexin V bin

61 TPCs are activated by a decrease in transmembrane potential and an increase in cytosolic cal

62 open or close in response to changes in the transmembrane potential and are essential for generating

63 asmic cytochrome c to maintain mitochondrial transmembrane potential and ATP production.

64 l plasma membrane is a sigmoidal function of transmembrane potential and bathing media osmolality.

65 sis was defined by the loss of mitochondrial transmembrane potential and by DNA fragmentation.

66 Simultaneous optical mapping of transmembrane potential and Ca(2+) transients was perfor

67 Mitochondrial transmembrane potential and Ca2+ fluxing were assessed b

68 lide antibiotic that regulates mitochondrial transmembrane potential and Ca2+ fluxing, has been used

69 idate this model, we used optical mapping of transmembrane potential and calcium transients.

70 IAP-2; and induced loss of the mitochondrial transmembrane potential and caspase-independent, calpain

71 y in Rb cells leads to loss of mitochondrial transmembrane potential and caspase-independent, calpain

72 ed H(2)O(2)-induced changes in mitochondrial transmembrane potential and cell death.

73 r domains in these channels sense changes in transmembrane potential and control ion flux across memb

74 alysis, theory, and mathematical modeling of transmembrane potential and currents have been an integr

75 o blocks depolarization of the mitochondrial transmembrane potential and cytochrome c release.

76 athway of apoptosis, as evidenced by loss of transmembrane potential and cytoplasmic release of cytoc

77 SMCs through depolarization of mitochondrial transmembrane potential and down-regulated PH-PASMC prol

78 ition state; this includes a decrease in the transmembrane potential and elevated generation of react

79 In vivo, TCL1 stabilizes the mitochondrial transmembrane potential and enhances cell proliferation

80 uced a substantial drop in the mitochondrial transmembrane potential and increases in cytosolic heme

81 Disruption of the CcO complex caused loss of transmembrane potential and induction of Ca2+/Calcineuri

82 ent with the disruption of the mitochondrial transmembrane potential and induction of cytochrome c re

83 er the influence of acidic pH and a positive transmembrane potential and initiates translocation in a

84 We simultaneously mapped transmembrane potential and intracellular Ca in Langendo

85 Optical mapping of transmembrane potential and intracellular Ca(2+) was per

86 lated by two distinct physiological signals, transmembrane potential and intracellular Ca(2+), each a

87 is not associated with loss of mitochondrial transmembrane potential and is blocked by overexpression

88 We studied the transmembrane potential and magnetic fields from electri

89 Mitochondrial transmembrane potential and mTOR were assessed by flow c

90 In addition to transmembrane potential and nanotube diameter, solution

91 preceded the reduction of the mitochondrial transmembrane potential and nuclear chromatin condensati

92 evaluation of the effects on the cytoplasmic transmembrane potential and on the respiration of isolat

93 related with protection of the mitochondrial transmembrane potential and prevention of cytochrome c r

94 -Darpp expression enforces the mitochondrial transmembrane potential and protects against ceramide-in

95 Bid and caspase-3, decrease in mitochondrial transmembrane potential and release of cytochrome c from

96 ding Bid cleavage, decrease in mitochondrial transmembrane potential and release of cytochrome c from

97 The model enables calculation of the transmembrane potential and the fraction of the cell mem

98 he ionic current passing through a pore in a transmembrane potential and thereby provides both the co

99 p-32 and t-Darpp preserved the mitochondrial transmembrane potential and was associated with increase

100 d that glutamate binding is dependent on the transmembrane potential and, thus, is electrogenic.

101 ocardium using high-speed optical mapping of transmembrane potentials and calcium concentrations in t

102 induced NAD depletion, loss of mitochondrial transmembrane potential, and cell death, demonstrating a

103 from mitochondria, decrease in mitochondrial transmembrane potential, and cleavage of poly(ADP-ribose

104 Basal mitochondrial respiration, transmembrane potential, and electron transport system e

105 the mycobacterial membrane, equilibrates the transmembrane potential, and is localized within both th

106 ectron transport chain function, collapse of transmembrane potential, and loss of dehydrogenase activ

107 poptotic protein Noxa, loss of mitochondrial transmembrane potential, and release of cytochrome c in

108 truct also allows the measurement of E. coli transmembrane potential, and the determination of the pr

109 m an alpha-helix, dissipated the cytoplasmic transmembrane potential, and uncoupled the respiration o

110 f NaCl on polarization of interfacial water, transmembrane potentials, and mechanisms for ion transpo

111 Frequency-dependent transmembrane potentials are modeled for spherical, weak

112 Without the transmembrane potential as a countermeasure, water will

113 Membranes flex with changes in transmembrane potential as a result of changes in interf

114 We have also found that a transmembrane potential as small as 20 mV strongly biase

115 ed by loss of cytochrome c and mitochondrial transmembrane potential as well as by induction of caspa

116 vents loss of cytochrome c and mitochondrial transmembrane potential as well as caspase activation an

117 abilization which, in turn, are modulated by transmembrane potential, as well as peptide concentratio

118 izing Jurkat cells with 7-ns pulses produces transmembrane potentials associated with increased membr

119 tify the influence of synaptic inputs on the transmembrane potential at the axon initial segment.

120 of shock-induced activation depended on the transmembrane potential at the end of the shock.

121 The binding is enhanced at increased transmembrane potentials, because the free energy contri

122 els attenuated the loss of the mitochondrial transmembrane potential, blocked mitochondrial fission,

123 the cytosol; (b) reduction in mitochondrial transmembrane potential; (c) proteolytic processing of c

124 inhibits ara-C-induced loss of mitochondrial transmembrane potential, caspase-3 activation, and apopt

125 of intracellular ATP, loss of mitochondrial transmembrane potential, caspase-3/7 activation, and LDH

126 ociated with the loss of mitochondrial inner transmembrane potential, caspases activation, the transl

127 y observed negative bias in the asymmetry of transmembrane potential changes (DeltaVm) induced by str

128 es that can simultaneously respond to pH and transmembrane potential changes.

129 ane were marked by 160 min and mitochondrial transmembrane potential collapsed over roughly the same

130 water pores is then seen; it discharges the transmembrane potential, considerably reduces the size o

131 on pathway, leading to loss of mitochondrial transmembrane potential, cytochrome c release and activa

132 tion of caspase-8; (c) loss of mitochondrial transmembrane potential; (d) release of cytochrome c; an

133 xicity of Fe + AA, because the mitochondrial transmembrane potential decreased early in the process,

134 Mitochondria rapidly lose their transmembrane potential (Delta Psi m) and generate react

135 t sHA 14-1 triggered a loss of mitochondrial transmembrane potential (Delta psi m) and weak caspase-9

136 sociated with elevation of the mitochondrial transmembrane potential (Delta psi(m)) and increased pro

137 Bid processing, dissipation of mitochondrial transmembrane potential (Delta Psi(m)), and cytochrome c

138 characterized by rapid loss of mitochondrial transmembrane potential (delta psi(m)), caspase-dependen

139 channel (VDAC3) and alter the mitochondrial transmembrane potential (Delta Psi(m)).

140 principally exhibit increased mitochondrial transmembrane potential (DeltaPsi(m)) and altered metabo

141 duced a time-dependent loss of mitochondrial transmembrane potential (DeltaPsi(m)) and DNA fragmentat

142 d macrophages, we investigated mitochondrial transmembrane potential (DeltaPsi(m)) and the mitochondr

143 A loss of mitochondrial transmembrane potential (Deltapsi(m)) beginning at 24 h

144 eactive oxygen species (ROS) and disrupt the transmembrane potential (DeltaPsi(m)) but does not perme

145 and chemically induced loss of mitochondrial transmembrane potential (Deltapsi(m)) caused recruitment

146 in resulted in a rapid loss of mitochondrial transmembrane potential (Deltapsi(m)) in a subpopulation

147 species (ROS) and lowering of mitochondrial transmembrane potential (DeltaPsi(m)) in in vitro HCV-in

148 lent H37Rv induces significant mitochondrial transmembrane potential (Deltapsi(m)) loss caused by mit

149 ymphocytes is regulated by the mitochondrial transmembrane potential (Deltapsi(m)) through controllin

150 with BHA also induced loss of mitochondrial transmembrane potential (Deltapsi(m)), cytochrome c, and

151 e victorin-induced collapse in mitochondrial transmembrane potential (Deltapsi(m)), indicative of a m

152 thin the mitochondrial compartment preserved transmembrane potential (DeltaPsi(m)), NAD(+) content, a

153 ation of caspases, the loss of mitochondrial transmembrane potential (Deltapsi(m)), the cleavage of B

154 depends on maintenance of the mitochondrial transmembrane potential (Deltapsi(m)), which is generate

155 rylation, and increases in the mitochondrial transmembrane potential (deltaPsi(m)), which were preced

156 t to contribute to the loss of mitochondrial transmembrane potential (Deltapsi(m)).

157 ly member, A1, and the loss of mitochondrial transmembrane potential (Deltapsi(m)).

158 st, both these agents decrease mitochondrial transmembrane potential (Deltapsi(m)).

159 gradient, which underlies the mitochondrial transmembrane potential (DeltaPsi(mem)), is harnessed fo

160 oxic side by a gradual rise of mitochondrial transmembrane potential (Deltapsi) and reactive oxygen s

161 rations (1 to 3 M), coupled with its loss of transmembrane potential (DeltaPsi) during postexponentia

162 nes based upon negative charge, disrupts the transmembrane potential (Deltapsi) in mitochondria, and

163 e model was tested by estimating the pHi and transmembrane potential (DeltaPsi) of cells acid stresse

164 nce vs absence of pH gradients (DeltapH) and transmembrane potentials (DeltaPsi).

165 ctivities, followed by reduced mitochondrial transmembrane potential, DeltaPsi(M).

166 hich also served to report the mitochondrial transmembrane potential, DeltaPsi.

167 which can be regulated through mitochondrial transmembrane potential (Deltapsim) and mammalian target

168 y biochemical checkpoints, the mitochondrial transmembrane potential (deltapsim) and production of re

169 vels, apoptosis, ER tress and, mitochondrial transmembrane potential (DeltaPsim) decline.

170 Mitochondrial transmembrane potential (DeltaPsim) was measured as a fu

171 tion of caspase 8, the loss of mitochondrial transmembrane potential (DeltaPsim), and apoptotic cell

172 of electron transport, loss of mitochondrial transmembrane potential (DeltaPsim), decline in ATP leve

173 roteases and disruption of the mitochondrial transmembrane potential (Deltapsim).

174 rillation is due to shock-induced changes of transmembrane potential (DeltaV(m)) in the bulk of ventr

175 n shocks induce complex nonlinear changes of transmembrane potential (DeltaV(m)).

176 rillation shocks induce nonlinear changes of transmembrane potential (DeltaVm) that determine the out

177 ion of charges at the membrane surfaces; the transmembrane potential, determined by imbalance of char

178 esults are compatible with the proposal that transmembrane potentials, determined mainly by extracell

179 l division, was independent of the organelle transmembrane potential, did not require the chaperone H

180 etween two electrolyte solutions, applying a transmembrane potential difference, and measuring the re

181 ctance of ion channels can be modulated by a transmembrane potential difference, due to alterations o

182 ondrial dysfunction, as indicated by loss of transmembrane potential, diminished mitochondrial mass,

183 ial), which is the sum of contributions from transmembrane potential, dipole potential, and the diffe

184 n apoptosis, causing mitochondrial swelling, transmembrane potential dissipation, membrane blebbing,

185 Numerical simulation of the initial transmembrane potential distribution and propidium iodid

186 at with low ac frequencies (10Hz-10kHz), the transmembrane potential does not vary with the frequency

187 currently eliminated the depolarizing sag of transmembrane potential during hyperpolarizing current i

188 p confers drug resistance through changes in transmembrane potential (E(m)) or ion conductance, we st

189 Microelectrodes were used to record transmembrane potentials from isolated epicardial and en

190 brane conductance regulator, which shunt the transmembrane potential generated by movement of protons

191 hannel in the AM also functions to shunt the transmembrane potential generated by proton pumping and

192 gnetic action field and optically imaged the transmembrane potentials generated by planar wavefronts

193 e area for postshock propagation but smaller transmembrane potential gradients to initiate new wavefr

194 how that under the condition of high applied transmembrane potential (>100 mV) and low ionic strength

195 spectral shift associated with the change in transmembrane potential has been used for continuous mem

196 UC1 attenuated (i) the loss of mitochondrial transmembrane potential, (ii) mitochondrial cytochrome c

197 2C12 cells with TCDD disrupted mitochondrial transmembrane potential in a time-dependent fashion and

198 is elaborated to account for the effect of a transmembrane potential in computer simulations.

199 fluorescent protein 2.3 (VSFP2.3) to monitor transmembrane potential in either myocytes or nonmyocyte

200 al shift response can be used to measure the transmembrane potential in single cells.

201 multisite high-resolution optical mapping of transmembrane potential in strands of cells of mixed Cx4

202 igh-frequency cut-off of the outer hair cell transmembrane potential in vivo may be necessary for coc

203 A fragmentation, and decreased mitochondrial transmembrane potential in VSMC while decreasing PP1cgam

204 Applied DC electric fields change transmembrane potentials in CA3 pyramidal cell somata by

205 ict that at short cell-to-tip distances, the transmembrane potential increases significantly while th

206 nnexin V binding and a drop in mitochondrial transmembrane potential indicative of apoptotic cell dea

207 udy, we investigated the distribution of OHC transmembrane potential induced along the cell perimeter

208 The OHC transmembrane potential induced by the EEF is shown to b

209 Mitochondrial dysfunction and altered transmembrane potential initiate a mitochondrial respira

210 h gives successive values of the prestimulus transmembrane potential instead of successive values of

211 However, the transmembrane potential is an incomplete metric.

212 of the action potential foot, even when the transmembrane potential is measured 150 microm below the

213 foot with propagation direction, even if the transmembrane potential is measured 150 microm below the

214 At the microscopic level, the transmembrane potential is thought to decay nonlinearly

215 simulations at different concentrations and transmembrane potentials is presented.

216 TOR), which is a sensor of the mitochondrial transmembrane potential, is increased in lupus T cells.

217 in reactive oxygen species and mitochondrial transmembrane potential loss, but does not cleave bid or

218 hydrolyzes ATP to maintain the mitochondrial transmembrane potential (mdeltapsi).

219 and capacitance, the EEF-induced nonuniform transmembrane potential measured in this study suggests

220 Mitochondrial transmembrane potential (MTP) was measured by a cationic

221 ecording steady-state and dynamic changes in transmembrane potential noninvasively across an intact c

222 The model determines transmembrane potential, number of pores, and distributi

223 mmetric conductance upon the polarity of the transmembrane potential observed experimentally is repro

224 ilter that defines the region over which the transmembrane potential occurs.

225 at rates from 10 V/s to 1 kV/s, to a maximum transmembrane potential of +/-1000 mV.

226 M (aggregate of the three transporters) at a transmembrane potential of -61 mV.

227 s a proton flux of 3100 +/- 500 H+/s/FO at a transmembrane potential of 106 mV (25 degrees C and pH 6

228 with the model's prediction that a critical transmembrane potential of 250 mV is achieved when the c

229 t broad-spectrum antibiotic that reduces the transmembrane potential of Gram-positive and Gram-negati

230 In the last assay the mitochondrial transmembrane potential of Jkt cells was measured with t

231 ed cells were resistant to a decrease in the transmembrane potential of mitochondria induced by staur

232 pecifically, we determine the sensitivity to transmembrane potential of second harmonic generation by

233 The resulting changes in the transmembrane potential of the cell initiates a process

234 for PEGs with 15 to 45 monomers, at applied transmembrane potentials of -40 to -80 mV and for three

235 DOPC mixed bilayers in 1 M KCl solution with transmembrane potentials of 0, +/-25, +/-50, +/-75, and

236 energy that is modified by the action of the transmembrane potential on dipole moments held by the do

237 be inside diameter, solution pH, and applied transmembrane potential on the rate and selectivity of p

238 The patterns of transmembrane potential on the whole heart during and im

239 onsists of a simple difference of the sum of transmembrane potentials on one side of a tissue sheet a

240 IL-1beta to cause a decline in mitochondrial transmembrane potential or ATP depletion.

241 vage, and DNA fragmentation, but not loss of transmembrane potential or viability, indicating that ce

242 ular wire to create a Berkeley Red Sensor of Transmembrane potential, or BeRST 1 ("burst").

243 For ion channels, the transmembrane potential plays a critical role by acting

244 r changes that include loss of mitochondrial transmembrane potential, production of reactive oxygen s

245 Transmembrane potential recordings (n = 5) at the PM rev

246 Potassium concentration and transmembrane potential recordings showed that AC stimul

247 e propagation using the ionic current versus transmembrane potential relationship fit from the experi

248 DIM #34 induced loss of mitochondrial inner transmembrane potential, release of cytochrome c into th

249 Transmembrane potential responses of single cardiac cell

250 translocation is driven only by the negative transmembrane potential resulting from the asymmetric bi

251 Furthermore, increasing the transmembrane potential results in a decrease in the abi

252 rchitecture and dissipation of mitochondrial transmembrane potential revealed a functional link betwe

253 in this study we experimentally explore the transmembrane potential's distribution across the open p

254 electrostatic computations indicate that the transmembrane potential sensed by the charged residues i

255 a 4-h exposure to CDDO, mitochondrial inner transmembrane potential-sensitive dyes revealed mitochon

256 idal electric fields have smaller effects on transmembrane potentials: sensitivity drops as an expone

257 resulted in a 50% decrease in mitochondrial transmembrane potential, sequential activation of caspas

258 single cells in response to step changes in transmembrane potentials set with a patch electrode, usi

259 cantly even at high atrial rates because the transmembrane potential spends little time at voltages a

260 m, varied linearly with the amplitude of the transmembrane potential step between -80 and +60 mV.

261 hia coli has been suggested to dissipate the transmembrane potential, such that the depletion of ATP

262 cell membrane, with subsequent alteration of transmembrane potential that is a function of cell bioph

263 es can be described by three parameters: the transmembrane potential, the membrane surface potential,

264 In contrast, at zero transmembrane potential, the peptides bind weakly to the

265 NaSal resulted in the loss of mitochondrial transmembrane potential, the release of cytochrome c and

266 At high transmembrane potentials, the alanine-based peptides, wh

267 of cell membrane integrity and mitochondrial transmembrane potential through unknown mechanisms.

268 ition pore, which in turn causes the loss of transmembrane potential, thus initiating apoptotic degra

269 Many approaches for studying the transmembrane potential (TMP) induced during the treatme

270 As K(+) channels, they drive the transmembrane potential toward E(K) when open and thus d

271 turn, was followed by loss of mitochondrial transmembrane potential, translocation of cytochrome c t

272 agocytic clearance, and retain mitochondrial transmembrane potential until constitutive platelet deat

273 Previous measurements of transmembrane potential using the electrochromic probe d

274 of shock strength and rest potential on the transmembrane potential V(m) and pore density N around t

275 ectroporation current predicts that both the transmembrane potential V(m) and the pore density N are

276 When spatial maps of transmembrane potential (V(m)) are available, pECG can b

277 y use of optical recordings of shock-induced transmembrane potential (V(m)) changes (DeltaV(m)) measu

278 e and the relationship with local changes of transmembrane potential (V(m)) were determined in geomet

279 ernal electrodes to induce sustained VT, and transmembrane potentials (V(m)) were compared with synth

280 cteristics of ventricular fibrillation (VF), transmembrane potentials (V(m)) were recorded from multi

281 ted parameters (e.g., ion concentrations and transmembrane potential, V(m)) drift in time, never atta

282 ew the effects of electrical currents on the transmembrane potential, V(m), as a shock is applied to

283 In our experiments, the transmembrane potential, V(m), was first measured optica

284 We tested the responses of plasma transmembrane potential (Vm) depolarization, voltage gat

285 We tested the responses of plasma transmembrane potential (Vm) depolarization, voltage gat

286 The lack of transmembrane potential (Vm) distribution data makes it

287 h involved recording high-fidelity (200 kHz) transmembrane potential (Vm) signals with glass microele

288 ; disruption of this spatial gradient of the transmembrane potential (Vmem) diminishes or eliminates

289 s effects, we show that hyperpolarization of transmembrane potential (Vmem) in ventral cells outside

290 treatment with bFGF, a loss of mitochondrial transmembrane potential was accompanied by down-regulati

291 A transmembrane potential was applied across a single nano

292 A loss of mitochondrial transmembrane potential was detected in vivo, although n

293 Mitochondrial transmembrane potential was determined by JC-1 fluoresce

294 lthough no mitochondrial swelling or loss of transmembrane potential was observed in isolated mitocho

295 Transmembrane potentials were recorded from right ventri

296 er respiratory inhibitors, which perturb the transmembrane potential, were equally efficient in induc

297 lds were applied to this system to model the transmembrane potential, which proved to be important.

298 uses a rapid depolarization of mitochondrial transmembrane potential, which recovers to original leve

299 atment induced the collapse of mitochondrial transmembrane potential within 2 h, indicating a MPT.

300 of events: dissipation of the mitochondrial transmembrane potential within 30 min, release of mitoch