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

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

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

3 ctivities to modulation of the mitochondrial permeability transition pore.

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

5 probability of opening of the mitochondrial permeability transition pore.

6 which inhibits opening of the mitochondrial permeability transition pore.

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

8 tochondrial matrix through the mitochondrial permeability transition pore.

9 tion through modulation of the mitochondrial permeability transition pore.

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

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

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

13 and sensitized the opening of mitochondrial permeability transition pore.

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

15 optosis through opening of the mitochondrial permeability transition pore.

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

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

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

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

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

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

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

23 nd marked sensitization of the mitochondrial permeability transition pore.

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

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

26 atractyloside, which opens the mitochondria permeability transition pore.

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

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

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

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

31 chondrial KATP channel or the Ca2+-dependent permeability transition pore.

32 ensitive, indicating a probable role for the permeability transition pore.

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

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

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

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

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

38 such elusive phenomena as the mitochondrial permeability transition pore.

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

40 by reversible openings of the mitochondrial permeability transition pore.

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

42 er formation of the calcium-induced membrane 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 nd 2) because 2',3'-cAMP opens mitochondrial permeability transition pores, a pro-apoptotic/pro-necro

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

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

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

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

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

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

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

53 Opening of the permeability transition pore and disruption of the mitoc

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

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

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

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

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

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

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

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

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

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

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

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

66 Mitochondrial permeability transition pore antagonists also blocked ca

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

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

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

70 The permeability transition pore blocker cyclosporin A, the

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

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

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

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

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

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

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

78 2O2 promoted activation of the mitochondrial permeability transition pore by Ca2+, but Ca2+-dependent

79 Blockade of the mitochondrial permeability transition pore by cyclosporin A allows com

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

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

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

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

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

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

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

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

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

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

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

91 Mitochondrial permeability transition pore function was normal, and ge

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

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

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

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

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

97 ese properties are identical to those of the permeability transition pore in mitochondria.

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

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

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

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

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

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

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

105 Third, permeability transition pore inhibition by cyclosporin A

106 The mitochondrial permeability transition pore inhibitor bongkrekic acid (

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

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

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

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

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

112 The mitochondrial permeability transition pore is a protein complex locate

113 The mitochondrial permeability transition pore is a recognized drug target

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 ,3'-cAMP is a potent opener of mitochondrial permeability transition pores (mPTPs), which can stimula

175 large proteinaceous pore, the "mitochondrial permeability transition pore" (MTP), is known to occur u

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

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

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

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

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

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

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

183 concluded that cyclophilin D binding to the permeability transition pore must occur at the inner fac

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

185 oth cases and is comparable in size with the permeability transition pore of heart and liver mitochon

186 The permeability transition pore of rat liver mitochondria c

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

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

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

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

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

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

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

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

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

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

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

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

199 Preventing mitochondrial permeability transition pore opening with the cyclophili

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

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

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

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

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

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

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

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

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

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

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

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

212 associated with inhibition of mitochondrial permeability transition pore opening.

213 ne nucleotide translocator and mitochondrial permeability transition pore opening.

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

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

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

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

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

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

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

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

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

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

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

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

226 otential (delta psiM) causing opening of the permeability transition pore (PTP) in mitochondrial memb

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

255 ed, recombinant Bax opened the mitochondrial permeability transition pore (PTP).

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

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

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

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

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

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

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

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

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

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

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

267 cells, cyclophilin D, is a component of the permeability transition pore that is formed by the adeni

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

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

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

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

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

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

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

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

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

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

278 hondria (Saccharomyces cerevisiae) contain a permeability transition pore which is regulated differen

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

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

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

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

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

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

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

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