ライフサイエンスコーパス: mitochondrial permeability transition

1 AAbs promote excitotoxicity through enhanced mitochondrial permeability transition.

2 FAO regulates the activity of Bak-dependent mitochondrial permeability transition.

3 n iNOS-transgenic hearts, indicating reduced mitochondrial permeability transition.

4 mes are determined largely by Ca(2+)-induced mitochondrial permeability transition.

5 ivation is not dependent on induction of the mitochondrial permeability transition.

6 oleucine-cyclosporin (NIM811) to inhibit the mitochondrial permeability transition.

7 has become clearer with the discovery of the mitochondrial permeability transition.

8 brane potential (Deltapsi(m)) loss caused by mitochondrial permeability transition.

9 acid can reduce apoptosis by minimizing the mitochondrial permeability transition.

10 eam of caspase activation and independent of mitochondrial permeability transition.

11 membrane damage can occur independent of the mitochondrial permeability transition.

12 apoptotic and necrotic cell death involving mitochondrial permeability transition.

13 o TNF caused by ethanol is an induction of a mitochondrial permeability transition.

14 high permeability pathways constituting the mitochondrial permeability transition.

15 by cyclosporine A (CsA), an inhibitor of the mitochondrial permeability transition.

16 in induced a duration-dependent onset of the mitochondrial permeability transition.

17 with necrostatins and compounds that inhibit mitochondrial permeability transition.

18 al cord injury depends on calcium influx and mitochondrial permeability transition.

19 cAMP did not enter the matrix, except during mitochondrial permeability transition.

20 ase 1 (ANT1), a central molecule controlling mitochondrial permeability transition.

21 ased inflammation and improved resistance to mitochondrial permeability transition.

22 d to inhibition or delayed activation of the mitochondrial permeability transition, a key regulator o

23 During the mitochondrial permeability transition, a large channel i

24 east in part, cytochrome c release after the mitochondrial permeability transition activates caspase-

25 least in part, by CO-dependent inhibition of mitochondrial permeability transition and apoptosis.

26 verexpression of Bcl-2 prevented VES-induced mitochondrial permeability transition and apoptosis.

27 ial Ca(2+) uptake and overload, resulting in mitochondrial permeability transition and cell death.

28 s its cytotoxic effects via induction of the mitochondrial permeability transition and changes in int

29 naling or apoptosis, but correlates with the mitochondrial permeability transition and cytochrome c r

30 SHetA2 suppressed mitochondrial permeability transition and enhanced cytoc

31 gliosides and rFasL induced a more extensive mitochondrial permeability transition and greater levels

32 ivated JNK to mitochondria where JNK induces mitochondrial permeability transition and inhibits mitoc

33 cultured mouse hepatocytes, MB prevented the mitochondrial permeability transition and loss of intrac

34 death in brain hypoxia/ischemia by inducing mitochondrial permeability transition and nuclear transl

35 ells and was accompanied by induction of the mitochondrial permeability transition and release of apo

36 itochondrion via induction of a Ca2+-induced mitochondrial permeability transition and that, upon its

37 phogenesis and serves to predispose cells to mitochondrial permeability transition and to trigger cel

38 estrogen starvation-induced BAX activation, mitochondrial permeability transition, and consequent ap

39 reduces mitochondrial Ca(2+) uptake, retards mitochondrial permeability transition, and delays death,

40 ncreased autophagy, blocked the onset of the mitochondrial permeability transition, and suppressed ce

41 Thus, cyclophilin D and the mitochondrial permeability transition are critical regul

42 Thus, cyclophilin D and the mitochondrial permeability transition are required for m

43 mount of cytochrome c released following the mitochondrial permeability transition as a function of m

44 re consistent with greater inhibition of the mitochondrial permeability transition at reperfusion by

45 Inhibitors of caspases 8 and 9, the mitochondrial permeability transition blocker cyclospori

46 An inhibitor of mitochondrial permeability transition, bongkrekic acid,

47 However, alisporivir also inhibits mitochondrial permeability transition by binding to cycl

48 cein localization revealed inhibition of the mitochondrial permeability transition by nicorandil.

49 ng of Hsp60 by siRNA triggers CypD-dependent mitochondrial permeability transition, caspase-dependent

50 When the mitochondrial permeability transition causes severe aden

51 Therefore, Hsp60 is a novel regulator of mitochondrial permeability transition, contributing to a

52 euronal death has been attributed to loss of mitochondrial permeability transition coupled with mitoc

53 etyl-L-cysteine and Tiron) and inhibitors of mitochondrial permeability transition (cyclosporine A an

54 ethanol-pretreated hepatocytes provokes the mitochondrial permeability transition, cytochrome c rele

55 itochondrial function, as shown by increased mitochondrial permeability transition, decline in both r

56 Mitochondrial permeability transition-dependent cell dea

57 h by simultaneously activating apoptotic and mitochondrial permeability transition-dependent necrotic

58 f Mfn-2 is associated with a marked delay in mitochondrial permeability transition downstream of Ca(2

59 use its presumed role in steroidogenesis and mitochondrial permeability transition established using

60 TNF brings about the mitochondrial permeability transition in ethanol-exposed

61 ration, suggesting JNK was directly inducing mitochondrial permeability transition in isolated mitoch

62 ctive oxygen species, and possibly inhibited mitochondrial permeability transition in response to H(2

63 designed to determine the role played by the mitochondrial permeability transition in the pathogenesi

64 signed to determine the role, if any, of the mitochondrial permeability transition in the pathogenesi

65 ffering capacity and are highly sensitive to mitochondrial permeability transition induced by reactiv

66 ity transition in isolated mitochondria, and mitochondrial permeability transition-induced NAD(+) los

67 SP600125 delayed the mitochondrial permeability transition, inhibited cytochr

68 creased in wild-type hearts treated with the mitochondrial permeability transition inhibitor cyclospo

69 is transient, is inhibited by the classical mitochondrial permeability transition inhibitor cyclospo

70 Cyclosporine A (CsA), a mitochondrial permeability transition inhibitor, blocked

71 Mitochondrial permeability transition is a phenomenon in

72 inner mitochondrial membrane, the so-called mitochondrial permeability transition, is a common featu

73 arized as follows: activation of Bax induces mitochondrial permeability transition, leading to releas

74 al injury likely related to induction of the mitochondrial permeability transition may participate in

75 We find that minocycline inhibits mitochondrial permeability-transition-mediated cytochrom

76 Confocal microscopy showed the onset of the mitochondrial permeability transition (MPT) 5 hours afte

77 mitochondrial injury by preventing both the mitochondrial permeability transition (MPT) and cytochro

78 may result from cyclophilin (Cyp)D-mediated mitochondrial permeability transition (MPT) and receptor

79 Here we show that NAD(+) depletion and mitochondrial permeability transition (MPT) are sequenti

80 Our aim was to evaluate the mitochondrial permeability transition (MPT) as a key fac

81 Previous work showed that onset of the mitochondrial permeability transition (MPT) can initiate

82 ctive oxygen species (ROS) threshold for the mitochondrial permeability transition (MPT) in cardiomyo

83 ty results in an increased susceptibility to mitochondrial permeability transition (MPT) induction th

84 Mitochondrial permeability transition (MPT) is a highly

85 The mitochondrial permeability transition (MPT) is a marker

86 The mitochondrial permeability transition (mPT) leads to mit

87 The mitochondrial permeability transition (mPT) may be criti

88 but previous reports had suggested that the mitochondrial permeability transition (mPT) may be invol

89 The mitochondrial permeability transition (MPT) mediates hep

90 strocytes that oxidative stress (OS) and the mitochondrial permeability transition (mPT) play major r

91 The probability of mitochondrial permeability transition (mPT) pore opening

92 otein, but not a wild-type, directly induced mitochondrial permeability transition (MPT) pore opening

93 hemic tissues can trigger the opening of the mitochondrial permeability transition (MPT) pore, result

94 ns inhibit cell death by blocking opening of mitochondrial permeability transition (MPT) pores, mitoc

95 ocked by cyclosporine A [an inhibitor of the mitochondrial permeability transition (MPT) process], z-

96 The induction of the mitochondrial permeability transition (MPT) was document

97 Respiration and the mitochondrial permeability transition (MPT) were assesse

98 Thresholds for mitochondrial permeability transition (mPT) were determi

99 s study investigated whether blockade of the mitochondrial permeability transition (MPT) with N-methy

100 sine triphosphate blocked the Ca(2+)-induced mitochondrial permeability transition (MPT), an effect t

101 ith cyclosporin A (CsA), an inhibitor of the mitochondrial permeability transition (MPT), but not FK5

102 Free Zn2+ in turn induces respiratory block, mitochondrial permeability transition (mPT), cytochrome

103 ative phosphorylation (OXPHOS) and activated mitochondrial permeability transition (mPT), defects whi

104 sanglifehrin A, and Mg2+, inhibitors of the mitochondrial permeability transition (mPT), increased m

105 sis and correlated with moderate increase of mitochondrial permeability transition (MPT), mitochondri

106 ane potential (Deltapsi(m)), indicative of a mitochondrial permeability transition (MPT), on a per ce

107 7 and 143B cells, we detected markers of the mitochondrial permeability transition (MPT), such as mit

108 ted as a central regulatory component of the mitochondrial permeability transition (mPT), triggering

109 acterized by an irreversible increase in the mitochondrial permeability transition (MPT), which is as

110 ), and cytochrome c may then be released via mitochondrial permeability transition (MPT)-dependent or

111 nophilin and a key positive regulator of the mitochondrial permeability transition (MPT).

112 ecedes the major changes associated with the mitochondrial permeability transition (MPT).

113 oke) appears mediated by an event termed the mitochondrial permeability transition (mPT).

114 ased mitochondrial superoxide production and mitochondrial permeability transition (MPT).

115 it mitochondrial dysfunction relating to the mitochondrial permeability transition (MPT).

116 tic cell death as a result of opening of the mitochondrial permeability transition (MPT).

117 are often implicated in the induction of the mitochondrial permeability transition (MPT).

118 e damage to mitochondria in association with mitochondrial permeability transition (MPT).

119 Bax has been attributed to induction of the mitochondrial permeability transition (MPT).

120 release of cytochrome c and the emergence of mitochondrial permeability transition [MPT]).

121 th cyclosporine A, a potent inhibitor of the mitochondrial permeability transition, normalizes mitoch

122 the synaptic mitochondria before undergoing mitochondrial permeability transition, observed as a los

123 and cytochrome c release were independent of mitochondrial permeability transition or caspase activat

124 nd cell death was prevented by inhibition of mitochondrial permeability transition or caspase activit

125 Z-VDVAD-FMK, tiron, and an inhibitor of the mitochondrial permeability transition pore (bongkrekic a

126 sion of the major putative components of the mitochondrial permeability transition pore (ie, voltage-

127 m 360; and (v) apoptosis involves opening of mitochondrial permeability transition pore (MPTP) and ca

128 nd messengers that facilitate opening of the mitochondrial permeability transition pore (mPTP) and co

129 erated and regulated in mitochondria via the mitochondrial permeability transition pore (mPTP) and th

130 Multiple lines of evidence implicate the mitochondrial permeability transition pore (mPTP) as a k

131 CyPD) is thought to sensitize opening of the mitochondrial permeability transition pore (mPTP) based

132 Opening of the mitochondrial permeability transition pore (MPTP) causes

133 Opening of the mitochondrial permeability transition pore (MPTP) causes

134 BACKGROUND & AIMS: Opening of the mitochondrial permeability transition pore (MPTP) causes

135 Here, we find that closure of the mitochondrial permeability transition pore (mPTP) drives

136 ion attenuates infarction, but prevention of mitochondrial permeability transition pore (MPTP) format

137 In mouse lung fibroblasts A23187 triggered mitochondrial permeability transition pore (MPTP) format

138 In platelets from Ppif(-/-) mice, lacking mitochondrial permeability transition pore (mPTP) format

139 Mitochondrial permeability transition pore (mPTP) format

140 lored role of cyclophilin D (CypD)-dependent mitochondrial permeability transition pore (mPTP) in Abe

141 ic anilides that represents a novel class of mitochondrial permeability transition pore (mPTP) inhibi

142 Mitochondrial permeability transition pore (mPTP) is inv

143 Opening of the mitochondrial permeability transition pore (MPTP) is tho

144 Transient (low-conductance) opening of the mitochondrial permeability transition pore (mPTP) may li

145 Carboxyatractyloside (CATR), a mitochondrial permeability transition pore (mPTP) opener

146 C), and slow depolarization waves related to mitochondrial permeability transition pore (MPTP) openin

147 Growing evidence suggests persistent mitochondrial permeability transition pore (mPTP) openin

148 ncrease in the probability of Ca(2+)-induced mitochondrial permeability transition pore (mPTP) openin

149 ndrial Ca(2+) entry causing Ca(2+) overload, mitochondrial permeability transition pore (mPTP) openin

150 Long-lasting mitochondrial permeability transition pore (mPTP) openin

151 The mitochondrial permeability transition pore (mPTP) openin

152 r 4-chlorodiazepam (4-Cl-DZP) to inhibit the mitochondrial permeability transition pore (mPTP) or the

153 ed ROS lower the threshold of opening of the mitochondrial permeability transition pore (mPTP) such t

154 2+ overload and the resultant opening of the mitochondrial permeability transition pore (mPTP) than n

155 e linked ROS production and induction of the mitochondrial permeability transition pore (MPTP) via cy

156 described an ion conductance consistent with mitochondrial permeability transition pore (mPTP) within

157 tested the hypothesis that formation of the mitochondrial permeability transition pore (MPTP), a key

158 rane, but not desflurane, induces opening of mitochondrial permeability transition pore (mPTP), incre

159 y purports that this channel, referred to as Mitochondrial Permeability Transition Pore (MPTP), is fo

160 rosis is early opening of the inner membrane mitochondrial permeability transition pore (mPTP), preci

161 yocardial infarction involves opening of the mitochondrial permeability transition pore (mPTP), resul

162 in D (CypD) is an essential component of the mitochondrial permeability transition pore (MPTP).

163 osporine A or ppif ablation, implicating the mitochondrial permeability transition pore (MPTP).

164 l isomerase known to modulate opening of the mitochondrial permeability transition pore (MPTP).

165 rial membrane, high-conductance channel: the mitochondrial permeability transition pore (mPTP).

166 ted swelling, consistent with opening of the mitochondrial permeability transition pore (mPTP).

167 hemia-based cell death is the opening of the mitochondrial permeability transition pore (MPTP).

168 anism involves inhibiting the opening of the mitochondrial permeability transition pore (mPTP).

169 ociated with the pathological opening of the mitochondrial permeability transition pore (mPTP).

170 cipant in the calcium-induced opening of the mitochondrial permeability transition pore (mPTP).

171 sis is initiated by oxidative stress and the mitochondrial permeability transition pore (mPTP).

172 The mitochondrial permeability transition pore (mtPTP) appea

173 initiate apoptosis through activation of the mitochondrial permeability transition pore (mtPTP) in re

174 ism, antioxidant defenses, apoptosis via the mitochondrial permeability transition pore (mtPTP), mito

175 a by-product, and regulate apoptosis via the mitochondrial permeability transition pore (mtPTP).

176 feature of apoptosis and is mediated by the mitochondrial permeability transition pore (mtPTP).

177 lity transition is a phenomenon in which the mitochondrial permeability transition pore (PTP) abruptl

178 he uncoupling were blocked by inhibiting the mitochondrial permeability transition pore (PTP) and its

179 delivery system inhibited the opening of the mitochondrial permeability transition pore (PTP) induced

180 The mitochondrial permeability transition pore (PTP) may ope

181 demonstrated, linked to dysregulation of the mitochondrial permeability transition pore (PTP) opening

182 Ca(2+) overload-induced mitochondrial permeability transition pore (PTP) opening

183 e rapid DeltaPsi(m) depolarization caused by mitochondrial permeability transition pore (PTP) opening

184 embrane protein palmitoylation subsequent to mitochondrial permeability transition pore (PTP) opening

185 We present evidence that MEND depends on mitochondrial permeability transition pore (PTP) opening

186 tes in the mitochondrial matrix and triggers mitochondrial permeability transition pore (PTP) opening

187 Dephosphorylated Bad sensitizes the mitochondrial permeability transition pore (PTP) to Ca2+

188 Here we define the molecular nature of the mitochondrial permeability transition pore (PTP), a key

189 Cyclosporine A, an inhibitor of mitochondrial permeability transition pore (PTP), and ru

190 cyclophilin D (CyPD), a key regulator of the mitochondrial permeability transition pore (PTP), develo

191 ondrial Ca(2+) uptake induced opening of the mitochondrial permeability transition pore (PTP), which

192 TSPO has been proposed to play a role in the mitochondrial permeability transition pore (PTP), which

193 nthase is the cyclophilin D (CypD) regulated mitochondrial permeability transition pore (PTP).

194 solic calcium signaling and specifically the mitochondrial permeability transition pore (SDZ NIM811),

195 , which was rescued by genetic inhibition of mitochondrial permeability transition pore activation.

196 it was independent of cyclophilin-D-mediated mitochondrial permeability transition pore activity.

197 of cell death dependent on the opening of a mitochondrial permeability transition pore also blocked

198 ugh ryanodine and IP3 channels activates the mitochondrial permeability transition pore and contribut

199 ng several factors, including bioenergetics, mitochondrial permeability transition pore and redox-sen

200 The data suggest a role for the mitochondrial permeability transition pore and voltage-d

201 Calpeptin and the mitochondrial permeability transition pore antagonist cy

202 Mitochondrial permeability transition pore antagonists a

203 an association between Elk-1 protein and the mitochondrial permeability transition pore complex (PTP)

204 are reminiscent of the action of Q(0) on the mitochondrial permeability transition pore described pre

205 f mitochondrial cyclophilin D, implicated in mitochondrial permeability transition pore formation, an

206 nction was normal, and genetic inhibition of mitochondrial permeability transition pore function did

207 Mitochondrial permeability transition pore function was

208 th bongkrekic acid, a known inhibitor of the mitochondrial permeability transition pore in animal cel

209 respiration and in preventing the opening of mitochondrial permeability transition pore in cardiac my

210 of Hint2 leads to a premature opening of the mitochondrial permeability transition pore in response t

211 Our study reveals the importance of the mitochondrial permeability transition pore in the regula

212 ated apoptosis; blocking the activity of the mitochondrial permeability transition pore inhibited HBx

213 The mitochondrial permeability transition pore inhibitor bon

214 Nonetheless, cyclosporin A, a direct mitochondrial permeability transition pore inhibitor, re

215 The mitochondrial permeability transition pore is a protein

216 The mitochondrial permeability transition pore is a recogniz

217 The mitochondrial permeability transition pore is a well-kno

218 Thus, the CypD-mediated mitochondrial permeability transition pore is directly l

219 Inhibition of the mitochondrial permeability transition pore is emerging a

220 pal synaptic plasticity, suggesting that the mitochondrial permeability transition pore is involved i

221 Based on recent evidence that the mitochondrial permeability transition pore may be involv

222 ata from knockout mice supporting the use of mitochondrial permeability transition pore modifiers as

223 inhibitor-1 reduced cell death and inhibited mitochondrial permeability transition pore opening after

224 mplexes II-IV and aconitase, thus preventing mitochondrial permeability transition pore opening and c

225 but they probably converge on suppression of mitochondrial permeability transition pore opening durin

226 tion and calcium threshold for triggering of mitochondrial permeability transition pore opening in bu

227 and increased sensitivity to calcium-induced mitochondrial permeability transition pore opening were

228 Preventing mitochondrial permeability transition pore opening with

229 n, loss of mitochondrial membrane potential, mitochondrial permeability transition pore opening, and

230 ization of DeltaPsi(m), which is mediated by mitochondrial permeability transition pore opening, as e

231 eta alters mitochondrial membrane potential, mitochondrial permeability transition pore opening, ATP

232 ss, we found reduced respiration, sensitized mitochondrial permeability transition pore opening, inta

233 that CerS6-generated ceramide could prevent mitochondrial permeability transition pore opening, lead

234 Ischemia-reperfusion (IR) injury leads to mitochondrial permeability transition pore opening, whic

235 ATP depletion, reactive oxygen species, and mitochondrial permeability transition pore opening.

236 ll as effective as cyclosporin A in delaying mitochondrial permeability transition pore opening.

237 scue action is associated with inhibition of mitochondrial permeability transition pore opening.

238 olve the adenine nucleotide translocator and mitochondrial permeability transition pore opening.

239 l cells can be compromised by opening of the mitochondrial permeability transition pore or by mitocho

240 Cyclosporin A blockade of the mitochondrial permeability transition pore partially pre

241 ol: n=80 cells per group; P<0.05), decreased mitochondrial permeability transition pore sensitivity (

242 s are triggered by transient openings of the mitochondrial permeability transition pore stimulating s

243 regulator of Ca(2+)-mediated opening of the mitochondrial permeability transition pore that determin

244 y, loss of cyclophilin D, a regulator of the mitochondrial permeability transition pore that underpin

245 ing with the inner membrane component of the mitochondrial permeability transition pore was detected

246 kout of SOD1 or by inhibiting opening of the mitochondrial permeability transition pore with cyclospo

247 Inhibiting the opening of the mitochondrial permeability transition pore with cyclospo

248 major process involved is the opening of the mitochondrial permeability transition pore, a large cond

249 It is also proposed to form or regulate the mitochondrial permeability transition pore, a megachanne

250 tochondrial ATP-sensitive K(+) channels, the mitochondrial permeability transition pore, and bcl-2 fa

251 accumulation in the mitochondria, opening of mitochondrial permeability transition pore, and loss in

252 the NAD(P)H oxidases, xanthine oxidases, the mitochondrial permeability transition pore, and the mito

253 l depolarization that was independent of the mitochondrial permeability transition pore, Bcl-2 (B-cel

254 deletion of a key regulatory subunit of the mitochondrial permeability transition pore, cyclophilin

255 t anion channels, the outer component of the mitochondrial permeability transition pore, have impairm

256 ire reactive oxygen or nitrogen species, the mitochondrial permeability transition pore, or a variety

257 nal shortening, the threshold for opening of mitochondrial permeability transition pore, oxygen consu

258 III, or with cyclosporine A, an inhibitor of mitochondrial permeability transition pore, resulted in

259 s proteins such as Bcl2 and Bax, through the mitochondrial permeability transition pore, to ion chann

260 nion channel 1 (VDAC1), a constituent of the mitochondrial permeability transition pore, was down-reg

261 her characterize the calcium dynamics of the mitochondrial permeability transition pore, we used an i

262 apoptosis-inducing factor, or opening of the mitochondrial permeability transition pore, were not fou

263 encoded by Ppif) is an integral part of the mitochondrial permeability transition pore, whose openin

264 peroxidation and acted as inhibitors of the mitochondrial permeability transition pore.

265 ith cyclophilin D (CypD), a component of the mitochondrial permeability transition pore.

266 on from the mitochondrial matrix through the mitochondrial permeability transition pore.

267 ink some HBx activities to modulation of the mitochondrial permeability transition pore.

268 o decrease the probability of opening of the mitochondrial permeability transition pore.

269 cyclophilin D, and sensitized the opening of mitochondrial permeability transition pore.

270 yclosporine A, which inhibits opening of the mitochondrial permeability transition pore.

271 consumption is not caused by opening of the mitochondrial permeability transition pore.

272 ane depolarization through modulation of the mitochondrial permeability transition pore.

273 c calcium to the association of HBx with the mitochondrial permeability transition pore.

274 amily that induces cell death by opening the mitochondrial permeability transition pore.

275 s of FFA can stem from direct effects on the mitochondrial permeability transition pore.

276 tes induces apoptosis through opening of the mitochondrial permeability transition pore.

277 P production, in part through opening of the mitochondrial permeability transition pore.

278 that OmpU may be inducing the opening of the mitochondrial permeability transition pore.

279 om mitochondria during brief openings of the mitochondrial permeability transition pore.

280 chondrial Ca(2+) overload and opening of the mitochondrial permeability transition pore.

281 ofiber atrophy and injury via opening of the mitochondrial permeability transition pore.

282 autophagy and such elusive phenomena as the mitochondrial permeability transition pore.

283 zations caused by reversible openings of the mitochondrial permeability transition pore.

284 l inner membrane and in the formation of the mitochondrial permeability-transition pore (mtPTP), a no

285 al reactive oxygen species (ROS) governed by mitochondrial permeability transition pores (mPTPs) woul

286 degradation rates, as well as the number of mitochondrial permeability transition pores (MPTPs), on

287 to 2'-AMP; 2',3'-cAMP is a potent opener of mitochondrial permeability transition pores (mPTPs), whi

288 sim and PCD by cyclosporin A, which inhibits mitochondrial permeability transition pores in animal ce

289 hat have detrimental effects such as opening mitochondrial permeability transition pores with resulta

290 e precursor) and 2) because 2',3'-cAMP opens mitochondrial permeability transition pores, a pro-apopt

291 Mitochondrial permeability transition (PT) is a phenomen

292 GL and GA were both potent inhibitors of the mitochondrial permeability transition, reactive oxygen s

293 ith cyclosporin A, a potent inhibitor of the mitochondrial permeability transition, reduces the sever

294 In liver, the mitochondrial permeability transition represents a share

295 r-Luciferase NF-kappaB responsive construct, mitochondrial permeability transition using the ApoAlert

296 ition of necrosis by an inhibitory effect on mitochondrial permeability transition via the PGE2 recep

297 In isolated mitochondria, mitochondrial permeability transition was inhibited by H

298 The threshold for calcium-induced mitochondrial permeability transition was substantially

299 s to photosystem II and to components of the mitochondrial permeability transition were also identifi

300 ial membrane damage appears to relate to the mitochondrial permeability transition, whereas outer mit