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1 on from the mitochondrial matrix through the mitochondrial permeability transition pore.
2 o decrease the probability of opening of the mitochondrial permeability transition pore.
3 yclosporine A, which inhibits opening of the mitochondrial permeability transition pore.
4 cyclophilin D, and sensitized the opening of mitochondrial permeability transition pore.
5 consumption is not caused by opening of the mitochondrial permeability transition pore.
6 ane depolarization through modulation of the mitochondrial permeability transition pore.
7 c calcium to the association of HBx with the mitochondrial permeability transition pore.
8 amily that induces cell death by opening the mitochondrial permeability transition pore.
9 s of FFA can stem from direct effects on the mitochondrial permeability transition pore.
10 tes induces apoptosis through opening of the mitochondrial permeability transition pore.
11 tosolic Ca(2+) signal via the opening of the mitochondrial permeability transition pore.
12 n inhibition and marked sensitization of the mitochondrial permeability transition pore.
13 equent swelling resulted from opening of the mitochondrial permeability transition pore.
14 nslocator (ANT), a putative component of the mitochondrial permeability transition pore.
15 ix was employed to isolate components of the mitochondrial permeability transition pore.
16 A, an inhibitor of Ca2+ release through the mitochondrial permeability transition pore.
17 P production, in part through opening of the mitochondrial permeability transition pore.
18 that OmpU may be inducing the opening of the mitochondrial permeability transition pore.
19 om mitochondria during brief openings of the mitochondrial permeability transition pore.
20 ofiber atrophy and injury via opening of the mitochondrial permeability transition pore.
21 chondrial Ca(2+) overload and opening of the mitochondrial permeability transition pore.
22 autophagy and such elusive phenomena as the mitochondrial permeability transition pore.
23 zations caused by reversible openings of the mitochondrial permeability transition pore.
24 ith cyclophilin D (CypD), a component of the mitochondrial permeability transition pore.
25 peroxidation and acted as inhibitors of the mitochondrial permeability transition pore.
26 ink some HBx activities to modulation of the mitochondrial permeability transition pore.
27 major process involved is the opening of the mitochondrial permeability transition pore, a large cond
28 It is also proposed to form or regulate the mitochondrial permeability transition pore, a megachanne
29 e precursor) and 2) because 2',3'-cAMP opens mitochondrial permeability transition pores, a pro-apopt
30 , which was rescued by genetic inhibition of mitochondrial permeability transition pore activation.
31 it was independent of cyclophilin-D-mediated mitochondrial permeability transition pore activity.
33 of cell death dependent on the opening of a mitochondrial permeability transition pore also blocked
35 ugh ryanodine and IP3 channels activates the mitochondrial permeability transition pore and contribut
36 ng several factors, including bioenergetics, mitochondrial permeability transition pore and redox-sen
37 esulted in an increased sensitization of the mitochondrial permeability transition pore and the prema
39 tochondrial ATP-sensitive K(+) channels, the mitochondrial permeability transition pore, and bcl-2 fa
40 accumulation in the mitochondria, opening of mitochondrial permeability transition pore, and loss in
41 the NAD(P)H oxidases, xanthine oxidases, the mitochondrial permeability transition pore, and the mito
44 l depolarization that was independent of the mitochondrial permeability transition pore, Bcl-2 (B-cel
45 release were not mediated by blockade of the mitochondrial permeability transition pore, because IGF-
47 Z-VDVAD-FMK, tiron, and an inhibitor of the mitochondrial permeability transition pore (bongkrekic a
48 dependent process that is independent of the mitochondrial permeability transition pore but regulated
49 tensive DNA fragmentation and opening of the mitochondrial permeability transition pore, but no appar
50 oth O2*- and H2O2 promoted activation of the mitochondrial permeability transition pore by Ca2+, but
53 an association between Elk-1 protein and the mitochondrial permeability transition pore complex (PTP)
54 deletion of a key regulatory subunit of the mitochondrial permeability transition pore, cyclophilin
55 are reminiscent of the action of Q(0) on the mitochondrial permeability transition pore described pre
56 f mitochondrial cyclophilin D, implicated in mitochondrial permeability transition pore formation, an
57 nction was normal, and genetic inhibition of mitochondrial permeability transition pore function did
59 t anion channels, the outer component of the mitochondrial permeability transition pore, have impairm
60 sion of the major putative components of the mitochondrial permeability transition pore (ie, voltage-
61 th bongkrekic acid, a known inhibitor of the mitochondrial permeability transition pore in animal cel
62 respiration and in preventing the opening of mitochondrial permeability transition pore in cardiac my
63 of Hint2 leads to a premature opening of the mitochondrial permeability transition pore in response t
65 sim and PCD by cyclosporin A, which inhibits mitochondrial permeability transition pores in animal ce
66 ated apoptosis; blocking the activity of the mitochondrial permeability transition pore inhibited HBx
67 with cyclosporin A, an agent that stabilizes mitochondrial permeability transition pore, inhibited BH
76 pal synaptic plasticity, suggesting that the mitochondrial permeability transition pore is involved i
78 ata from knockout mice supporting the use of mitochondrial permeability transition pore modifiers as
79 m 360; and (v) apoptosis involves opening of mitochondrial permeability transition pore (MPTP) and ca
80 nd messengers that facilitate opening of the mitochondrial permeability transition pore (mPTP) and co
81 erated and regulated in mitochondria via the mitochondrial permeability transition pore (mPTP) and th
82 Multiple lines of evidence implicate the mitochondrial permeability transition pore (mPTP) as a k
83 CyPD) is thought to sensitize opening of the mitochondrial permeability transition pore (mPTP) based
88 ion attenuates infarction, but prevention of mitochondrial permeability transition pore (MPTP) format
89 In mouse lung fibroblasts A23187 triggered mitochondrial permeability transition pore (MPTP) format
90 In platelets from Ppif(-/-) mice, lacking mitochondrial permeability transition pore (mPTP) format
92 lored role of cyclophilin D (CypD)-dependent mitochondrial permeability transition pore (mPTP) in Abe
93 ic anilides that represents a novel class of mitochondrial permeability transition pore (mPTP) inhibi
96 Transient (low-conductance) opening of the mitochondrial permeability transition pore (mPTP) may li
99 ncrease in the probability of Ca(2+)-induced mitochondrial permeability transition pore (mPTP) openin
100 ndrial Ca(2+) entry causing Ca(2+) overload, mitochondrial permeability transition pore (mPTP) openin
103 C), and slow depolarization waves related to mitochondrial permeability transition pore (MPTP) openin
104 r 4-chlorodiazepam (4-Cl-DZP) to inhibit the mitochondrial permeability transition pore (mPTP) or the
105 ed ROS lower the threshold of opening of the mitochondrial permeability transition pore (mPTP) such t
106 2+ overload and the resultant opening of the mitochondrial permeability transition pore (mPTP) than n
107 e linked ROS production and induction of the mitochondrial permeability transition pore (MPTP) via cy
108 described an ion conductance consistent with mitochondrial permeability transition pore (mPTP) within
109 tested the hypothesis that formation of the mitochondrial permeability transition pore (MPTP), a key
110 ANT1 protein, a structural component of the mitochondrial permeability transition pore (MPTP), decre
111 rane, but not desflurane, induces opening of mitochondrial permeability transition pore (mPTP), incre
112 y purports that this channel, referred to as Mitochondrial Permeability Transition Pore (MPTP), is fo
113 rosis is early opening of the inner membrane mitochondrial permeability transition pore (mPTP), preci
114 yocardial infarction involves opening of the mitochondrial permeability transition pore (mPTP), resul
125 e potential (Deltapsi(M)) and the opening of mitochondrial permeability transition pores (mPTP).
126 al reactive oxygen species (ROS) governed by mitochondrial permeability transition pores (mPTPs) woul
127 degradation rates, as well as the number of mitochondrial permeability transition pores (MPTPs), on
128 to 2'-AMP; 2',3'-cAMP is a potent opener of mitochondrial permeability transition pores (mPTPs), whi
129 opening of a large proteinaceous pore, the "mitochondrial permeability transition pore" (MTP), is kn
131 initiate apoptosis through activation of the mitochondrial permeability transition pore (mtPTP) in re
132 ism, antioxidant defenses, apoptosis via the mitochondrial permeability transition pore (mtPTP), mito
133 a by-product, and regulate apoptosis via the mitochondrial permeability transition pore (mtPTP).
135 l inner membrane and in the formation of the mitochondrial permeability-transition pore (mtPTP), a no
136 nt with bongkrekic acid, an inhibitor of the mitochondrial permeability transition pore, not only pre
137 inhibitor-1 reduced cell death and inhibited mitochondrial permeability transition pore opening after
138 mplexes II-IV and aconitase, thus preventing mitochondrial permeability transition pore opening and c
139 but they probably converge on suppression of mitochondrial permeability transition pore opening durin
140 tion and calcium threshold for triggering of mitochondrial permeability transition pore opening in bu
141 and increased sensitivity to calcium-induced mitochondrial permeability transition pore opening were
143 n, loss of mitochondrial membrane potential, mitochondrial permeability transition pore opening, and
144 ization of DeltaPsi(m), which is mediated by mitochondrial permeability transition pore opening, as e
145 eta alters mitochondrial membrane potential, mitochondrial permeability transition pore opening, ATP
146 ss, we found reduced respiration, sensitized mitochondrial permeability transition pore opening, inta
147 that CerS6-generated ceramide could prevent mitochondrial permeability transition pore opening, lead
148 Ischemia-reperfusion (IR) injury leads to mitochondrial permeability transition pore opening, whic
149 ll as effective as cyclosporin A in delaying mitochondrial permeability transition pore opening.
150 scue action is associated with inhibition of mitochondrial permeability transition pore opening.
151 olve the adenine nucleotide translocator and mitochondrial permeability transition pore opening.
153 l cells can be compromised by opening of the mitochondrial permeability transition pore or by mitocho
154 sed activation of caspase 3 but not with the mitochondrial permeability transition pore or cytochrome
155 ire reactive oxygen or nitrogen species, the mitochondrial permeability transition pore, or a variety
156 nal shortening, the threshold for opening of mitochondrial permeability transition pore, oxygen consu
158 lity transition is a phenomenon in which the mitochondrial permeability transition pore (PTP) abruptl
160 he uncoupling were blocked by inhibiting the mitochondrial permeability transition pore (PTP) and its
161 delivery system inhibited the opening of the mitochondrial permeability transition pore (PTP) induced
162 were additive and blocked completely by the mitochondrial permeability transition pore (PTP) inhibit
164 demonstrated, linked to dysregulation of the mitochondrial permeability transition pore (PTP) opening
166 e rapid DeltaPsi(m) depolarization caused by mitochondrial permeability transition pore (PTP) opening
167 embrane protein palmitoylation subsequent to mitochondrial permeability transition pore (PTP) opening
168 We present evidence that MEND depends on mitochondrial permeability transition pore (PTP) opening
169 tes in the mitochondrial matrix and triggers mitochondrial permeability transition pore (PTP) opening
171 Here we define the molecular nature of the mitochondrial permeability transition pore (PTP), a key
173 cyclophilin D (CyPD), a key regulator of the mitochondrial permeability transition pore (PTP), develo
174 ondrial Ca(2+) uptake induced opening of the mitochondrial permeability transition pore (PTP), which
175 TSPO has been proposed to play a role in the mitochondrial permeability transition pore (PTP), which
180 III, or with cyclosporine A, an inhibitor of mitochondrial permeability transition pore, resulted in
181 solic calcium signaling and specifically the mitochondrial permeability transition pore (SDZ NIM811),
182 ol: n=80 cells per group; P<0.05), decreased mitochondrial permeability transition pore sensitivity (
183 s are triggered by transient openings of the mitochondrial permeability transition pore stimulating s
184 regulator of Ca(2+)-mediated opening of the mitochondrial permeability transition pore that determin
185 y, loss of cyclophilin D, a regulator of the mitochondrial permeability transition pore that underpin
186 s proteins such as Bcl2 and Bax, through the mitochondrial permeability transition pore, to ion chann
187 ing with the inner membrane component of the mitochondrial permeability transition pore was detected
188 nion channel 1 (VDAC1), a constituent of the mitochondrial permeability transition pore, was down-reg
189 her characterize the calcium dynamics of the mitochondrial permeability transition pore, we used an i
190 apoptosis-inducing factor, or opening of the mitochondrial permeability transition pore, were not fou
191 Possibly, this is because CsA blocks the mitochondrial permeability transition pore which is open
192 ring the calcium-dependent regulation of the mitochondrial permeability transition pore, which may ac
193 encoded by Ppif) is an integral part of the mitochondrial permeability transition pore, whose openin
195 kout of SOD1 or by inhibiting opening of the mitochondrial permeability transition pore with cyclospo
196 hat have detrimental effects such as opening mitochondrial permeability transition pores with resulta
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