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1 ased inflammation and improved resistance to mitochondrial permeability transition.
2 AAbs promote excitotoxicity through enhanced mitochondrial permeability transition.
3 m loads from near zero to levels approaching mitochondrial permeability transition.
4 FAO regulates the activity of Bak-dependent mitochondrial permeability transition.
5 gered cell necrosis involving PPIF-dependent mitochondrial permeability transition.
6 n iNOS-transgenic hearts, indicating reduced mitochondrial permeability transition.
7 with mitochondrial changes characteristic of mitochondrial permeability transition.
8 mes are determined largely by Ca(2+)-induced mitochondrial permeability transition.
9 ivation is not dependent on induction of the mitochondrial permeability transition.
10 oleucine-cyclosporin (NIM811) to inhibit the mitochondrial permeability transition.
11 has become clearer with the discovery of the mitochondrial permeability transition.
12 brane potential (Deltapsi(m)) loss caused by mitochondrial permeability transition.
13 acid can reduce apoptosis by minimizing the mitochondrial permeability transition.
14 eam of caspase activation and independent of mitochondrial permeability transition.
15 membrane damage can occur independent of the mitochondrial permeability transition.
16 apoptotic and necrotic cell death involving mitochondrial permeability transition.
17 o TNF caused by ethanol is an induction of a mitochondrial permeability transition.
18 xpression, inner membrane potentials, or the mitochondrial permeability transition.
19 high permeability pathways constituting the mitochondrial permeability transition.
20 ase 1 (ANT1), a central molecule controlling mitochondrial permeability transition.
21 with necrostatins and compounds that inhibit mitochondrial permeability transition.
22 al cord injury depends on calcium influx and mitochondrial permeability transition.
23 cAMP did not enter the matrix, except during mitochondrial permeability transition.
24 d to inhibition or delayed activation of the mitochondrial permeability transition, a key regulator o
26 least in part, by CO-dependent inhibition of mitochondrial permeability transition and apoptosis.
27 verexpression of Bcl-2 prevented VES-induced mitochondrial permeability transition and apoptosis.
28 ial Ca(2+) uptake and overload, resulting in mitochondrial permeability transition and cell death.
29 s its cytotoxic effects via induction of the mitochondrial permeability transition and changes in int
30 naling or apoptosis, but correlates with the mitochondrial permeability transition and cytochrome c r
32 gliosides and rFasL induced a more extensive mitochondrial permeability transition and greater levels
33 ivated JNK to mitochondria where JNK induces mitochondrial permeability transition and inhibits mitoc
34 cultured mouse hepatocytes, MB prevented the mitochondrial permeability transition and loss of intrac
35 death in brain hypoxia/ischemia by inducing mitochondrial permeability transition and nuclear transl
36 ells and was accompanied by induction of the mitochondrial permeability transition and release of apo
37 itochondrion via induction of a Ca2+-induced mitochondrial permeability transition and that, upon its
38 phogenesis and serves to predispose cells to mitochondrial permeability transition and to trigger cel
39 estrogen starvation-induced BAX activation, mitochondrial permeability transition, and consequent ap
40 reduces mitochondrial Ca(2+) uptake, retards mitochondrial permeability transition, and delays death,
41 ncreased autophagy, blocked the onset of the mitochondrial permeability transition, and suppressed ce
44 mount of cytochrome c released following the mitochondrial permeability transition as a function of m
46 re consistent with greater inhibition of the mitochondrial permeability transition at reperfusion by
49 ng of Hsp60 by siRNA triggers CypD-dependent mitochondrial permeability transition, caspase-dependent
50 Therefore, Hsp60 is a novel regulator of mitochondrial permeability transition, contributing to a
51 euronal death has been attributed to loss of mitochondrial permeability transition coupled with mitoc
52 itochondrial function, as shown by increased mitochondrial permeability transition, decline in both r
54 h by simultaneously activating apoptotic and mitochondrial permeability transition-dependent necrotic
55 acking Ppif or Mlkl or given an inhibitor of mitochondrial permeability transition displayed attenuat
56 f Mfn-2 is associated with a marked delay in mitochondrial permeability transition downstream of Ca(2
57 otein similar to BAK and BAX, regulating the mitochondrial permeability transition during apoptosis.
58 use its presumed role in steroidogenesis and mitochondrial permeability transition established using
60 ration, suggesting JNK was directly inducing mitochondrial permeability transition in isolated mitoch
61 ctive oxygen species, and possibly inhibited mitochondrial permeability transition in response to H(2
62 designed to determine the role played by the mitochondrial permeability transition in the pathogenesi
63 ffering capacity and are highly sensitive to mitochondrial permeability transition induced by reactiv
64 ity transition in isolated mitochondria, and mitochondrial permeability transition-induced NAD(+) los
66 creased in wild-type hearts treated with the mitochondrial permeability transition inhibitor cyclospo
67 is transient, is inhibited by the classical mitochondrial permeability transition inhibitor cyclospo
70 inner mitochondrial membrane, the so-called mitochondrial permeability transition, is a common featu
71 may result from cyclophilin (Cyp)D-mediated mitochondrial permeability transition (MPT) and receptor
74 ctive oxygen species (ROS) threshold for the mitochondrial permeability transition (MPT) in cardiomyo
75 ty results in an increased susceptibility to mitochondrial permeability transition (MPT) induction th
80 but previous reports had suggested that the mitochondrial permeability transition (mPT) may be invol
82 strocytes that oxidative stress (OS) and the mitochondrial permeability transition (mPT) play major r
83 otein, but not a wild-type, directly induced mitochondrial permeability transition (MPT) pore opening
85 hemic tissues can trigger the opening of the mitochondrial permeability transition (MPT) pore, result
86 ns inhibit cell death by blocking opening of mitochondrial permeability transition (MPT) pores, mitoc
87 ocked by cyclosporine A [an inhibitor of the mitochondrial permeability transition (MPT) process], z-
90 s study investigated whether blockade of the mitochondrial permeability transition (MPT) with N-methy
91 sine triphosphate blocked the Ca(2+)-induced mitochondrial permeability transition (MPT), an effect t
92 ith cyclosporin A (CsA), an inhibitor of the mitochondrial permeability transition (MPT), but not FK5
93 Free Zn2+ in turn induces respiratory block, mitochondrial permeability transition (mPT), cytochrome
94 ative phosphorylation (OXPHOS) and activated mitochondrial permeability transition (mPT), defects whi
95 sanglifehrin A, and Mg2+, inhibitors of the mitochondrial permeability transition (mPT), increased m
96 ane potential (Deltapsi(m)), indicative of a mitochondrial permeability transition (MPT), on a per ce
97 7 and 143B cells, we detected markers of the mitochondrial permeability transition (MPT), such as mit
98 ted as a central regulatory component of the mitochondrial permeability transition (mPT), triggering
99 acterized by an irreversible increase in the mitochondrial permeability transition (MPT), which is as
100 itochondria and consequent triggering of the mitochondrial permeability transition (mPT), which is es
101 ), and cytochrome c may then be released via mitochondrial permeability transition (MPT)-dependent or
110 th cyclosporine A, a potent inhibitor of the mitochondrial permeability transition, normalizes mitoch
111 the synaptic mitochondria before undergoing mitochondrial permeability transition, observed as a los
112 and cytochrome c release were independent of mitochondrial permeability transition or caspase activat
113 nd cell death was prevented by inhibition of mitochondrial permeability transition or caspase activit
114 Z-VDVAD-FMK, tiron, and an inhibitor of the mitochondrial permeability transition pore (bongkrekic a
115 sion of the major putative components of the mitochondrial permeability transition pore (ie, voltage-
116 m 360; and (v) apoptosis involves opening of mitochondrial permeability transition pore (MPTP) and ca
117 nd messengers that facilitate opening of the mitochondrial permeability transition pore (mPTP) and co
118 erated and regulated in mitochondria via the mitochondrial permeability transition pore (mPTP) and th
119 Multiple lines of evidence implicate the mitochondrial permeability transition pore (mPTP) as a k
120 o that of mitochondrial megachannel (MMC) or mitochondrial permeability transition pore (mPTP) but th
121 tive or positive regulatory component of the mitochondrial permeability transition pore (mPTP) by two
127 ion attenuates infarction, but prevention of mitochondrial permeability transition pore (MPTP) format
128 In mouse lung fibroblasts A23187 triggered mitochondrial permeability transition pore (MPTP) format
129 In platelets from Ppif(-/-) mice, lacking mitochondrial permeability transition pore (mPTP) format
130 lored role of cyclophilin D (CypD)-dependent mitochondrial permeability transition pore (mPTP) in Abe
131 ic anilides that represents a novel class of mitochondrial permeability transition pore (mPTP) inhibi
133 Transient (low-conductance) opening of the mitochondrial permeability transition pore (mPTP) may li
135 k-1 mutants, reducing levels of autophagy or mitochondrial permeability transition pore (mPTP) openin
136 ndrial Ca(2+) entry causing Ca(2+) overload, mitochondrial permeability transition pore (mPTP) openin
139 C), and slow depolarization waves related to mitochondrial permeability transition pore (MPTP) openin
140 ves mitochondrial dysfunction resulting from mitochondrial permeability transition pore (mPTP) openin
142 ncrease in the probability of Ca(2+)-induced mitochondrial permeability transition pore (mPTP) openin
143 c stimulation of NCLX-null BAT, triggers the mitochondrial permeability transition pore (mPTP) openin
144 r 4-chlorodiazepam (4-Cl-DZP) to inhibit the mitochondrial permeability transition pore (mPTP) or the
145 ed ROS lower the threshold of opening of the mitochondrial permeability transition pore (mPTP) such t
146 2+ overload and the resultant opening of the mitochondrial permeability transition pore (mPTP) than n
147 e linked ROS production and induction of the mitochondrial permeability transition pore (MPTP) via cy
149 described an ion conductance consistent with mitochondrial permeability transition pore (mPTP) within
150 tested the hypothesis that formation of the mitochondrial permeability transition pore (MPTP), a key
151 rane, but not desflurane, induces opening of mitochondrial permeability transition pore (mPTP), incre
152 ansition, as the consequence of opening of a mitochondrial permeability transition pore (mPTP), is a
153 y purports that this channel, referred to as Mitochondrial Permeability Transition Pore (MPTP), is fo
154 rosis is early opening of the inner membrane mitochondrial permeability transition pore (mPTP), preci
155 ) overload and ultimately the opening of the mitochondrial permeability transition pore (mPTP), promo
156 yocardial infarction involves opening of the mitochondrial permeability transition pore (mPTP), resul
169 initiate apoptosis through activation of the mitochondrial permeability transition pore (mtPTP) in re
170 ism, antioxidant defenses, apoptosis via the mitochondrial permeability transition pore (mtPTP), mito
171 a by-product, and regulate apoptosis via the mitochondrial permeability transition pore (mtPTP).
173 lity transition is a phenomenon in which the mitochondrial permeability transition pore (PTP) abruptl
174 he uncoupling were blocked by inhibiting the mitochondrial permeability transition pore (PTP) and its
175 delivery system inhibited the opening of the mitochondrial permeability transition pore (PTP) induced
176 tes in the mitochondrial matrix and triggers mitochondrial permeability transition pore (PTP) opening
177 demonstrated, linked to dysregulation of the mitochondrial permeability transition pore (PTP) opening
179 embrane protein palmitoylation subsequent to mitochondrial permeability transition pore (PTP) opening
180 We present evidence that MEND depends on mitochondrial permeability transition pore (PTP) opening
182 Here we define the molecular nature of the mitochondrial permeability transition pore (PTP), a key
184 cyclophilin D (CyPD), a key regulator of the mitochondrial permeability transition pore (PTP), develo
185 ondrial Ca(2+) uptake induced opening of the mitochondrial permeability transition pore (PTP), which
186 TSPO has been proposed to play a role in the mitochondrial permeability transition pore (PTP), which
188 solic calcium signaling and specifically the mitochondrial permeability transition pore (SDZ NIM811),
189 , which was rescued by genetic inhibition of mitochondrial permeability transition pore activation.
190 it was independent of cyclophilin-D-mediated mitochondrial permeability transition pore activity.
191 of cell death dependent on the opening of a mitochondrial permeability transition pore also blocked
192 ugh ryanodine and IP3 channels activates the mitochondrial permeability transition pore and contribut
193 ng several factors, including bioenergetics, mitochondrial permeability transition pore and redox-sen
197 an association between Elk-1 protein and the mitochondrial permeability transition pore complex (PTP)
198 are reminiscent of the action of Q(0) on the mitochondrial permeability transition pore described pre
199 f mitochondrial cyclophilin D, implicated in mitochondrial permeability transition pore formation, an
200 nction was normal, and genetic inhibition of mitochondrial permeability transition pore function did
202 e PAGE, mass spectrometry, and assessment of mitochondrial permeability transition pore function.
203 respiration and in preventing the opening of mitochondrial permeability transition pore in cardiac my
204 of Hint2 leads to a premature opening of the mitochondrial permeability transition pore in response t
205 Our study reveals the importance of the mitochondrial permeability transition pore in the regula
206 ated apoptosis; blocking the activity of the mitochondrial permeability transition pore inhibited HBx
214 ata from knockout mice supporting the use of mitochondrial permeability transition pore modifiers as
215 inhibitor-1 reduced cell death and inhibited mitochondrial permeability transition pore opening after
216 mplexes II-IV and aconitase, thus preventing mitochondrial permeability transition pore opening and c
217 but they probably converge on suppression of mitochondrial permeability transition pore opening durin
218 tion and calcium threshold for triggering of mitochondrial permeability transition pore opening in bu
219 and increased sensitivity to calcium-induced mitochondrial permeability transition pore opening were
221 n, loss of mitochondrial membrane potential, mitochondrial permeability transition pore opening, and
222 ization of DeltaPsi(m), which is mediated by mitochondrial permeability transition pore opening, as e
223 eta alters mitochondrial membrane potential, mitochondrial permeability transition pore opening, ATP
224 ss, we found reduced respiration, sensitized mitochondrial permeability transition pore opening, inta
225 that CerS6-generated ceramide could prevent mitochondrial permeability transition pore opening, lead
226 creases the mitochondrial flash activity and mitochondrial permeability transition pore opening, reju
227 Ischemia-reperfusion (IR) injury leads to mitochondrial permeability transition pore opening, whic
228 from ischemia-reperfusion injury by reducing mitochondrial permeability transition pore opening.
229 scue action is associated with inhibition of mitochondrial permeability transition pore opening.
230 olve the adenine nucleotide translocator and mitochondrial permeability transition pore opening.
232 ll as effective as cyclosporin A in delaying mitochondrial permeability transition pore opening.
233 ring ischemia-reperfusion injury by inducing mitochondrial permeability transition pore opening.
234 ardial necrosis, apoptosis, inflammation, or mitochondrial permeability transition pore opening.
235 l cells can be compromised by opening of the mitochondrial permeability transition pore or by mitocho
238 ol: n=80 cells per group; P<0.05), decreased mitochondrial permeability transition pore sensitivity (
239 s are triggered by transient openings of the mitochondrial permeability transition pore stimulating s
240 ane potential, mitochondrial Ca(2+) cycling, mitochondrial permeability transition pore stochastic op
241 regulator of Ca(2+)-mediated opening of the mitochondrial permeability transition pore that determin
242 Gboxin-resistant cells require a functional mitochondrial permeability transition pore that regulate
243 y, loss of cyclophilin D, a regulator of the mitochondrial permeability transition pore that underpin
244 ing with the inner membrane component of the mitochondrial permeability transition pore was detected
245 kout of SOD1 or by inhibiting opening of the mitochondrial permeability transition pore with cyclospo
247 major process involved is the opening of the mitochondrial permeability transition pore, a large cond
248 It is also proposed to form or regulate the mitochondrial permeability transition pore, a megachanne
249 tochondrial ATP-sensitive K(+) channels, the mitochondrial permeability transition pore, and bcl-2 fa
250 accumulation in the mitochondria, opening of mitochondrial permeability transition pore, and loss in
251 the NAD(P)H oxidases, xanthine oxidases, the mitochondrial permeability transition pore, and the mito
252 l depolarization that was independent of the mitochondrial permeability transition pore, Bcl-2 (B-cel
253 isk variant proteins bound components of the mitochondrial permeability transition pore, but only ris
254 deletion of a key regulatory subunit of the mitochondrial permeability transition pore, cyclophilin
255 ire reactive oxygen or nitrogen species, the mitochondrial permeability transition pore, or a variety
256 nal shortening, the threshold for opening of mitochondrial permeability transition pore, oxygen consu
257 III, or with cyclosporine A, an inhibitor of mitochondrial permeability transition pore, resulted in
258 s proteins such as Bcl2 and Bax, through the mitochondrial permeability transition pore, to ion chann
259 nion channel 1 (VDAC1), a constituent of the mitochondrial permeability transition pore, was down-reg
260 her characterize the calcium dynamics of the mitochondrial permeability transition pore, we used an i
261 apoptosis-inducing factor, or opening of the mitochondrial permeability transition pore, were not fou
262 encoded by Ppif) is an integral part of the mitochondrial permeability transition pore, whose openin
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
292 GL and GA were both potent inhibitors of the mitochondrial permeability transition, reactive oxygen s
294 ide and are more sensitive to Ca(2+)-induced mitochondrial permeability transition, suggesting that S
296 ition of necrosis by an inhibitory effect on mitochondrial permeability transition via the PGE2 recep
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