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

1 and injury via opening of the mitochondrial permeability transition pore.

2 such elusive phenomena as the mitochondrial permeability transition pore.

3 rance to the Ca(2+)-triggered opening of the permeability transition pore.

4 by reversible openings of the mitochondrial permeability transition pore.

5 er formation of the calcium-induced membrane permeability transition pore.

6 etrakis(methochloride)), and blockade of the permeability transition pore.

7 r or monomer, or any component, provides the permeability transition pore.

8 n D (CypD), a component of the mitochondrial permeability transition pore.

9 ctivities to modulation of the mitochondrial permeability transition pore.

10 probability of opening of the mitochondrial permeability transition pore.

11 which inhibits opening of the mitochondrial permeability transition pore.

12 s not caused by opening of the mitochondrial permeability transition pore.

13 lophilin D, a component of the mitochondrial permeability transition pore.

14 tion through modulation of the mitochondrial permeability transition pore.

15 he association of HBx with the mitochondrial permeability transition pore.

16 d Ca(2+) accumulation promote opening of the permeability transition pore.

17 uces cell death by opening the mitochondrial permeability transition pore.

18 tem from direct effects on the mitochondrial permeability transition pore.

19 optosis through opening of the mitochondrial permeability transition pore.

20 abolite flux, and putative components of the permeability transition pore.

21 embrane gradient collapse and opening of the permeability transition pore.

22 mediated pore formation, or upon opening the permeability transition pore.

23 signal via the opening of the mitochondrial permeability transition pore.

24 thout cytochrome c release or opening of the permeability transition pore.

25 itochondrial volume, and does not affect the permeability transition pore.

26 ane, and was unaffected by inhibitors of the permeability transition pore.

27 nd marked sensitization of the mitochondrial permeability transition pore.

28 g resulted from opening of the mitochondrial permeability transition pore.

29 ) response with little contribution from the permeability transition pore.

30 atractyloside, which opens the mitochondria permeability transition pore.

31 ), a putative component of the mitochondrial permeability transition pore.

32 d to isolate components of the mitochondrial permeability transition pore.

33 or of Ca2+ release through the mitochondrial permeability transition pore.

34 ogenases, but below levels that activate the permeability transition pore.

35 a during brief openings of the mitochondrial permeability transition pore.

36 +) overload and opening of the mitochondrial permeability transition pore.

37 and acted as inhibitors of the mitochondrial permeability transition pore.

38 tochondrial matrix through the mitochondrial permeability transition pore.

39 and sensitized the opening of mitochondrial permeability transition pore.

40 in part through opening of the mitochondrial permeability transition pore.

41 be inducing the opening of the mitochondrial permeability transition pore.

42 eactive oxygen species and engagement of the permeability transition pore.

43 involved is the opening of the mitochondrial permeability transition pore, a large conductance pore t

44 oposed to form or regulate the mitochondrial permeability transition pore, a megachannel of high cond

45 The opening of the permeability transition pore, a nonspecific channel in i

46 nd 2) because 2',3'-cAMP opens mitochondrial permeability transition pores, a pro-apoptotic/pro-necro

47 scued by genetic inhibition of mitochondrial permeability transition pore activation.

48 dent of cyclophilin-D-mediated mitochondrial permeability transition pore activity.

49 Components of the mitochondrial permeability transition pore, adenine nucleotide transpo

50 dependent on the opening of a mitochondrial permeability transition pore also blocked TH-ir cell los

51 advances on the nature and regulation of the permeability transition pore, an inner membrane channel

52 ugh a mechanism independent of mitochondrial permeability transition pore and Bax.

53 w matrix [Ca(2+)] and prevent opening of the permeability transition pore and cell death, while meeti

54 and IP3 channels activates the mitochondrial permeability transition pore and contributes to axonal d

55 itochondria, where it induces opening of the permeability transition pore and mitochondrial swelling.

56 tors, including bioenergetics, mitochondrial permeability transition pore and redox-sensing genes.

57 ation of at least two transport systems: the permeability transition pore and the electrogenic H(+) c

58 increased sensitization of the mitochondrial permeability transition pore and the premature induction

59 he data suggest a role for the mitochondrial permeability transition pore and voltage-dependent anion

60 ner mitochondrial membrane known as the PTP (permeability transition pore) and that opening of this p

61 brane permeabilization (MMP), opening of the permeability transition pore, and activation of the mito

62 P-sensitive K(+) channels, the mitochondrial permeability transition pore, and bcl-2 family members.

63 ilize complex I activity, alterations in the permeability transition pore, and compromised inner memb

64 n the mitochondria, opening of mitochondrial permeability transition pore, and loss in mitochondrial

65 ion of Bak, Bcl-2, and Bcl-x(L)), opening of permeability transition pore, and loss of mitochondrial

66 idases, xanthine oxidases, the mitochondrial permeability transition pore, and the mitochondrial ATP-

67 Calpeptin and the mitochondrial permeability transition pore antagonist cyclosporin A al

68 Mitochondrial permeability transition pore antagonists also blocked ca

69 on that was independent of the mitochondrial permeability transition pore, Bcl-2 (B-cell lymphoma 2)

70 ot mediated by blockade of the mitochondrial permeability transition pore, because IGF-I failed to in

71 yclosporin A, a blocker of the mitochondrial permeability transition pore, blocked both the paclitaxe

72 The permeability transition pore blocker cyclosporin A, the

73 ecific antioxidant), and by cyclosporin A (a permeability transition pore blocker).

74 ) was rescued during OGD by cyclosporin A, a permeability transition pore blocker, and (G)N-nitro-arg

75 tiron, and an inhibitor of the mitochondrial permeability transition pore (bongkrekic acid).

76 ess that is independent of the mitochondrial permeability transition pore but regulated by Bcl-2.

77 cytosolic acidification, nitric oxide or the permeability transition pore, but is suppressed when mit

78 agmentation and opening of the mitochondrial permeability transition pore, but no apparent caspase ac

79 oteins bound components of the mitochondrial permeability transition pore, but only risk variant prot

80 f cyclophilin D, which is a component of the permeability transition pore, but was attenuated by geni

81 2O2 promoted activation of the mitochondrial permeability transition pore by Ca2+, but Ca2+-dependent

82 Inhibition of the mitochondrial permeability transition pore by cyclosporin A in wild-ty

83 between Elk-1 protein and the mitochondrial permeability transition pore complex (PTP), a structure

84 antiapoptotic proteins interacting with the permeability transition pore complex that forms at conta

85 bition of GSK-3beta on the end effector, the permeability transition pore complex, to limit MPT induc

86 key regulatory subunit of the mitochondrial permeability transition pore, cyclophilin D (CypD), infl

87 auses mitochondrial alterations through both permeability transition pore-dependent (cytochrome c rel

88 t of the action of Q(0) on the mitochondrial permeability transition pore described previously.

89 piration and swelling data indicate that the permeability transition pore does not open in yeast mito

90 l cyclophilin D, implicated in mitochondrial permeability transition pore formation, and acid sphingo

91 um quenching, inhibitors of calpain, CaMKII, permeability transition pore formation, ryanodine recept

92 mal, and genetic inhibition of mitochondrial permeability transition pore function did not alter mito

93 Mitochondrial permeability transition pore function was normal, and ge

94 pectrometry, and assessment of mitochondrial permeability transition pore function.

95 ls, the outer component of the mitochondrial permeability transition pore, have impairments in learni

96 jor putative components of the mitochondrial permeability transition pore (ie, voltage-dependent anio

97 acid, a known inhibitor of the mitochondrial permeability transition pore in animal cells, was found

98 d in preventing the opening of mitochondrial permeability transition pore in cardiac myocytes under s

99 tional role for mitochondrial porins and the permeability transition pore in learning and synaptic pl

100 to a premature opening of the mitochondrial permeability transition pore in response to repetitive a

101 reveals the importance of the mitochondrial permeability transition pore in the regulation of endoth

102 cyclosporin A, which inhibits mitochondrial permeability transition pores in animal cells.

103 MPT is caused by the opening of permeability transition pores in the inner mitochondrial

104 on pore-dependent (cytochrome c release) and permeability transition pore-independent (mitochondrial

105 ; blocking the activity of the mitochondrial permeability transition pore inhibited HBx activation of

106 in A, an agent that stabilizes mitochondrial permeability transition pore, inhibited BHA-induced loss

107 Third, permeability transition pore inhibition by cyclosporin A

108 The mitochondrial permeability transition pore inhibitor bongkrekic acid (

109 Release was blocked by the mitochondria permeability transition pore inhibitor cyclosporin A (Cs

110 re prevented by pretreatment with either the permeability transition pore inhibitor, cyclosporin A (C

111 eless, cyclosporin A, a direct mitochondrial permeability transition pore inhibitor, reduced infarcti

112 itochondria with TN-Cl and is blocked by the permeability transition pore inhibitors bongkrekic acid

113 Addition of the mitochondrial permeability transition pore inhibitors cyclosporin A an

114 The mitochondrial permeability transition pore is a protein complex locate

115 The mitochondrial permeability transition pore is a recognized drug target

116 The mitochondrial permeability transition pore is a well-known initiator o

117 Thus, the CypD-mediated mitochondrial permeability transition pore is directly linked to the c

118 Inhibition of the mitochondrial permeability transition pore is emerging as a central me

119 lasticity, suggesting that the mitochondrial permeability transition pore is involved in hippocampal

120 ed on recent evidence that the mitochondrial permeability transition pore may be involved in ischemia

121 ells and that differential regulation of the permeability transition pore may underlie the cell-speci

122 mitochondrial depolarization, opening of the permeability transition pore, mitochondrial swelling, an

123 out mice supporting the use of mitochondrial permeability transition pore modifiers as therapeutics i

124 apoptosis involves opening of mitochondrial permeability transition pore (MPTP) and can be prevented

125 that facilitate opening of the mitochondrial permeability transition pore (mPTP) and contribute to th

126 ulated in mitochondria via the mitochondrial permeability transition pore (mPTP) and the new phenomen

127 ines of evidence implicate the mitochondrial permeability transition pore (mPTP) as a key end effecto

128 ht to sensitize opening of the mitochondrial permeability transition pore (mPTP) based on the finding

129 chondrial megachannel (MMC) or mitochondrial permeability transition pore (mPTP) but the oligomeric s

130 ve regulatory component of the mitochondrial permeability transition pore (mPTP) by two research grou

131 KGROUND & AIMS: Opening of the mitochondrial permeability transition pore (MPTP) causes loss of the m

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

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

134 e, we find that closure of the mitochondrial permeability transition pore (mPTP) drives maturation of

135 infarction, but prevention of mitochondrial permeability transition pore (MPTP) formation is crucial

136 s from Ppif(-/-) mice, lacking mitochondrial permeability transition pore (mPTP) formation, agonist-i

137 g fibroblasts A23187 triggered mitochondrial permeability transition pore (MPTP) formation, lactate d

138 Mitochondrial permeability transition pore (mPTP) formation, which is

139 cyclophilin D (CypD)-dependent mitochondrial permeability transition pore (mPTP) in Abeta-impaired ax

140 at represents a novel class of mitochondrial permeability transition pore (mPTP) inhibitors.

141 Mitochondrial permeability transition pore (mPTP) is involved in cardi

142 Opening of the mitochondrial permeability transition pore (MPTP) is thought to be a c

143 ow-conductance) opening of the mitochondrial permeability transition pore (mPTP) may limit mitochondr

144 Carboxyatractyloside (CATR), a mitochondrial permeability transition pore (mPTP) opener, and N-methyl

145 entry causing Ca(2+) overload, mitochondrial permeability transition pore (mPTP) opening and dissipat

146 PP2Cm) that regulates mitochondrial membrane permeability transition pore (MPTP) opening and is essen

147 probability of Ca(2+)-induced mitochondrial permeability transition pore (mPTP) opening in brain mit

148 g evidence suggests persistent mitochondrial permeability transition pore (mPTP) opening is a key pat

149 The mitochondrial permeability transition pore (mPTP) opening plays a crit

150 educing levels of autophagy or mitochondrial permeability transition pore (mPTP) opening restores nor

151 of NCLX-null BAT, triggers the mitochondrial permeability transition pore (mPTP) opening, leading to

152 epolarization waves related to mitochondrial permeability transition pore (MPTP) opening.

153 ial dysfunction resulting from mitochondrial permeability transition pore (mPTP) opening.

154 Long-lasting mitochondrial permeability transition pore (mPTP) openings damage mito

155 epam (4-Cl-DZP) to inhibit the mitochondrial permeability transition pore (mPTP) or the inner membran

156 he threshold of opening of the mitochondrial permeability transition pore (mPTP) such that physiologi

157 d the resultant opening of the mitochondrial permeability transition pore (mPTP) than nonsynaptic mit

158 roduction and induction of the mitochondrial permeability transition pore (MPTP) via cyclophilin D an

159 However, the opening of the mitochondrial permeability transition pore (MPTP) was affected in PS1

160 on conductance consistent with mitochondrial permeability transition pore (mPTP) within the c-subunit

161 pothesis that formation of the mitochondrial permeability transition pore (MPTP), a key signaling eve

162 a structural component of the mitochondrial permeability transition pore (MPTP), decreases its catal

163 desflurane, induces opening of mitochondrial permeability transition pore (mPTP), increase in levels

164 he consequence of opening of a mitochondrial permeability transition pore (mPTP), is a cellular catas

165 t this channel, referred to as Mitochondrial Permeability Transition Pore (MPTP), is formed within th

166 opening of the inner membrane mitochondrial permeability transition pore (mPTP), precipitating mitoc

167 ultimately the opening of the mitochondrial permeability transition pore (mPTP), promoting cell deat

168 rction involves opening of the mitochondrial permeability transition pore (mPTP), resulting in disrup

169 Ca2+ overload and induction of mitochondria permeability transition pore (mPTP)-dependent cell death

170 inhibiting the opening of the mitochondrial permeability transition pore (mPTP).

171 calcium-induced opening of the mitochondrial permeability transition pore (mPTP).

172 ed by oxidative stress and the mitochondrial permeability transition pore (mPTP).

173 ppif ablation, implicating the mitochondrial permeability transition pore (MPTP).

174 own to modulate opening of the mitochondrial permeability transition pore (MPTP).

175 an essential component of the mitochondrial permeability transition pore (MPTP).

176 high-conductance channel: the mitochondrial permeability transition pore (mPTP).

177 he pathological opening of the mitochondrial permeability transition pore (mPTP).

178 ted with the regulation of the mitochondrial permeability transition pore (MPTP).

179 consistent with opening of the mitochondrial permeability transition pore (mPTP).

180 ll death is the opening of the mitochondrial permeability transition pore (MPTP).

181 ochondrial high-conductance and long-lasting permeability transition pores (mPTP) causes respiratory

182 than direct cytoprotection via mitochondria permeability transition pores (MPTP).

183 eltapsi(M)) and the opening of mitochondrial permeability transition pores (mPTP).

184 ygen species (ROS) governed by mitochondrial permeability transition pores (mPTPs) would trigger NLRP

185 ates, as well as the number of mitochondrial permeability transition pores (MPTPs), on the cell respo

186 ,3'-cAMP is a potent opener of mitochondrial permeability transition pores (mPTPs), which can stimula

187 The mitochondrial permeability transition pore (mtPTP) appears to be a key

188 osis through activation of the mitochondrial permeability transition pore (mtPTP) in response to ener

189 of electron transport, ATP synthase, or the permeability transition pore (mtPTP) induced reversible

190 nt defenses, apoptosis via the mitochondrial permeability transition pore (mtPTP), mitochondrial fusi

191 and regulate apoptosis via the mitochondrial permeability transition pore (mtPTP).

192 optosis and is mediated by the mitochondrial permeability transition pore (mtPTP).

193 ne and in the formation of the mitochondrial permeability-transition pore (mtPTP), a nonspecific pore

194 ekic acid, an inhibitor of the mitochondrial permeability transition pore, not only prevented DNA fra

195 ell death, and this process may also involve permeability transition pores on the inner membrane.

196 that reduces mitochondrial Ca(2+) influx and permeability transition pore opening after ischemic inju

197 duced cell death and inhibited mitochondrial permeability transition pore opening after simulated isc

198 and aconitase, thus preventing mitochondrial permeability transition pore opening and cytochrome c re

199 production rates, and enhanced threshold for permeability transition pore opening by Ca(2+).

200 bly converge on suppression of mitochondrial permeability transition pore opening during early reperf

201 imary mouse embryonic fibroblasts to mPT and permeability transition pore opening in a p53- and CypD-

202 um threshold for triggering of mitochondrial permeability transition pore opening in bupivacaine-indu

203 oked cytosolic calcium signals and timing of permeability transition pore opening in response to tert

204 s of mitochondrial proteins, suggesting that permeability transition pore opening may have a function

205 Inhibition of mitochondrial membrane permeability transition pore opening or caspase 9 activi

206 dx diaphragm mitochondria to calcium-induced permeability transition pore opening was restored to nor

207 sensitivity to calcium-induced mitochondrial permeability transition pore opening were significantly

208 Preventing mitochondrial permeability transition pore opening with the cyclophili

209 hondrial membrane potential (an indicator of permeability transition pore opening) and apoptosis (ass

210 uding mitochondrial membrane depolarization, permeability transition pore opening, and cytochrome c r

211 ochondrial membrane potential, mitochondrial permeability transition pore opening, and necrosis.

212 taPsi(m), which is mediated by mitochondrial permeability transition pore opening, as evidenced by th

213 ochondrial membrane potential, mitochondrial permeability transition pore opening, ATP content, and r

214 educed respiration, sensitized mitochondrial permeability transition pore opening, intact electron tr

215 nerated ceramide could prevent mitochondrial permeability transition pore opening, leading to increas

216 tochondrial flash activity and mitochondrial permeability transition pore opening, rejuvenates mitoch

217 perfusion (IR) injury leads to mitochondrial permeability transition pore opening, which contributes

218 l chaperone cyclophilin D (CypD) and trigger permeability transition pore opening, whose role in isch

219 associated with inhibition of mitochondrial permeability transition pore opening.

220 ne nucleotide translocator and mitochondrial permeability transition pore opening.

221 , reactive oxygen species, and mitochondrial permeability transition pore opening.

222 e as cyclosporin A in delaying mitochondrial permeability transition pore opening.

223 reperfusion injury by reducing mitochondrial permeability transition pore opening.

224 reperfusion injury by inducing mitochondrial permeability transition pore opening.

225 s, apoptosis, inflammation, or mitochondrial permeability transition pore opening.

226 waves do not depend on caspase activation or permeability transition pore opening.

227 compromised by opening of the mitochondrial permeability transition pore or by mitochondrial pathway

228 of caspase 3 but not with the mitochondrial permeability transition pore or cytochrome c release fro

229 exceeded, and did not involve the classical permeability transition pore or intracellular Ca2+ overl

230 xygen or nitrogen species, the mitochondrial permeability transition pore, or a variety of signal tra

231 , the threshold for opening of mitochondrial permeability transition pore, oxygen consumption, and me

232 Cyclosporin A blockade of the mitochondrial permeability transition pore partially prevented the los

233 Mitochondrial bioenergetics and permeability transition pore plays a crucial role in thi

234 n is a phenomenon in which the mitochondrial permeability transition pore (PTP) abruptly opens, resul

235 The mitochondrial permeability transition pore (PTP) and associated releas

236 were blocked by inhibiting the mitochondrial permeability transition pore (PTP) and its regulator, BA

237 chondrial membrane potential, opening of the permeability transition pore (PTP) and the release of cy

238 Opening of the permeability transition pore (PTP) has been implicated a

239 m inhibited the opening of the mitochondrial permeability transition pore (PTP) induced by either oxi

240 and blocked completely by the mitochondrial permeability transition pore (PTP) inhibitor cyclosporin

241 e capacity were abolished in the presence of Permeability Transition Pore (PTP) inhibitors.

242 The permeability transition pore (PTP) is an unselective vol

243 The mitochondrial permeability transition pore (PTP) may operate as a phys

244 vity with properties resembling those of the permeability transition pore (PTP) of mammals.

245 take blocker, and lonidamine (100 microm), a permeability transition pore (PTP) opener, inhibited tra

246 f reactive oxygen species (ROS) that induces permeability transition pore (PTP) opening and damages t

247 ochondrial matrix and triggers mitochondrial permeability transition pore (PTP) opening and necrosis

248 Ca(2+) overload-induced mitochondrial permeability transition pore (PTP) opening is accelerate

249 si(m) depolarization caused by mitochondrial permeability transition pore (PTP) opening, and (3) cell

250 ial waves are prevented by Bcl-x(L), involve permeability transition pore (PTP) opening, and yield cy

251 linked to dysregulation of the mitochondrial permeability transition pore (PTP) opening.

252 evidence that MEND depends on mitochondrial permeability transition pore (PTP) openings, followed by

253 n palmitoylation subsequent to mitochondrial permeability transition pore (PTP) openings.

254 sphorylated Bad sensitizes the mitochondrial permeability transition pore (PTP) to Ca2+ through a Bcl

255 ntity of the mitochondrial megachannel (MMC)/permeability transition pore (PTP), a key effector of ce

256 ne the molecular nature of the mitochondrial permeability transition pore (PTP), a key effector of ce

257 yclosporine A, an inhibitor of mitochondrial permeability transition pore (PTP), and ruthenium red, a

258 rane anion channel (IMAC), distinct from the permeability transition pore (PTP), as the first respons

259 ATP-dependent K(+) channels (mito-K(ATP)) or permeability transition pore (PTP), but not by inhibitio

260 (CyPD), a key regulator of the mitochondrial permeability transition pore (PTP), developed EAE, but u

261 ening of a nonspecific channel, known as the permeability transition pore (PTP), in the inner membran

262 ening of a nonspecific channel, known as the permeability transition pore (PTP), in the inner membran

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

264 uptake induced opening of the mitochondrial permeability transition pore (PTP), which was blocked by

265 cell death in many cell types by opening the permeability transition pore (PTP).

266 may include regulation of the mitochondrial permeability transition pore (PTP).

267 Ca(2+)-induced opening of the mitochondrial permeability transition pore (PTP).

268 cyclophilin D (CypD) regulated mitochondrial permeability transition pore (PTP).

269 that has several regulatory features of the permeability transition pore (PTP).

270 ndria are well polarized, and it ceases when permeability transition pores (PTP) open during reperfus

271 A novel population transition and detailed permeability transition pore regulation model were integ

272 We show that the mitochondrial permeability transition pore regulator cyclophilin D (Cy

273 Inhibition of the permeability transition pore rescued these alphaSyn-indu

274 yclosporine A, an inhibitor of mitochondrial permeability transition pore, resulted in inhibition of

275 signaling and specifically the mitochondrial permeability transition pore (SDZ NIM811), also impaired

276 per group; P<0.05), decreased mitochondrial permeability transition pore sensitivity (by 2.4+/-0.5-,

277 d by transient openings of the mitochondrial permeability transition pore stimulating superoxide prod

278 mitochondrial Ca(2+) cycling, mitochondrial permeability transition pore stochastic opening and clos

279 It is concluded that the basic permeability transition pore structure comprises the vol

280 Ca(2+)-mediated opening of the mitochondrial permeability transition pore that determines mitochondri

281 olecules and constitute one component of the permeability transition pore that opens in response to a

282 ant cells require a functional mitochondrial permeability transition pore that regulates pH and thus

283 lophilin D, a regulator of the mitochondrial permeability transition pore that underpins necrosis, bl

284 argeted PPIF, gatekeeper of the mitochondria permeability transition pore, thereby restricting ROS fl

285 hich are larger than previous reports of the permeability transition pore through which cytochrome c

286 h as Bcl2 and Bax, through the mitochondrial permeability transition pore, to ion channels such as mi

287 nner membrane component of the mitochondrial permeability transition pore was detected by immunopreci

288 (VDAC1), a constituent of the mitochondrial permeability transition pore, was down-regulated by miR-

289 ze the calcium dynamics of the mitochondrial permeability transition pore, we used an in vitro assay

290 cing factor, or opening of the mitochondrial permeability transition pore, were not found to play a s

291 y expected for the mitochondrial megachannel/permeability transition pore, whereas dimers obtained at

292 this is because CsA blocks the mitochondrial permeability transition pore which is opened under adver

293 mitochondria is linked to the opening of the permeability transition pore, which in turn causes the l

294 um-dependent regulation of the mitochondrial permeability transition pore, which may account for the

295 if) is an integral part of the mitochondrial permeability transition pore, whose opening leads to cel

296 Inhibiting the opening of the mitochondrial permeability transition pore with cyclosporin A (5 micro

297 r by inhibiting opening of the mitochondrial permeability transition pore with cyclosporin A.

298 transmission and plasticity of blocking the permeability transition pore with low doses of cyclospor

299 elective cellular inhibition of CypD and the permeability transition pore with reduced cellular toxic

300 mental effects such as opening mitochondrial permeability transition pores with resultant release of