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1 ompared with control cells, but show reduced mitochondrial membrane potential.
2 ase allow for Fo-independent generation of a mitochondrial membrane potential.
3 th excessive cleavage of PINK1 and increased mitochondrial membrane potential.
4 including mitochondrial DNA copy number and mitochondrial membrane potential.
5 ochondrial respiration rate and reduction of mitochondrial membrane potential.
6 l of energy metabolism, ultimately impacting mitochondrial membrane potential.
7 ction that is associated with a reduction of mitochondrial membrane potential.
8 s but had significantly reduced lifespan and mitochondrial membrane potential.
9 al mitochondria were used as an indicator of mitochondrial membrane potential.
10 cells after treatment, which showed reduced mitochondrial membrane potential.
11 of pyruvate and its metabolites, and loss of mitochondrial membrane potential.
12 ad4 in trophoblast cells resulted in reduced mitochondrial membrane potential.
13 and motor proteins in addition to changes in mitochondrial membrane potential.
14 tive oxygen species or depolarization of the mitochondrial membrane potential.
15 dent mitochondrial fragmentation and loss of mitochondrial membrane potential.
16 was removed by the SERCA and depended on the mitochondrial membrane potential.
17 ondria biogenesis while negatively impacting mitochondrial membrane potential.
18 In addition, there was a loss of mitochondrial membrane potential.
19 eating heart and to be necessary to maintain mitochondrial membrane potential.
20 causes mitochondrial aggregation and loss of mitochondrial membrane potential.
21 respectively) in islet Ca(2+), NAD(P)H, and mitochondrial membrane potential.
22 olism, mitochondrial biogenesis and restores mitochondrial membrane potential.
23 lar reactive oxygen species that can disrupt mitochondrial membrane potential.
24 loop, intrinsic catalytic activity, and the mitochondrial membrane potential.
25 creased mitochondrial density, and defective mitochondrial membrane potential.
26 rial DNA content, mitochondrial activity and mitochondrial membrane potential.
27 tion rate, reserve respiration capacity, and mitochondrial membrane potential.
28 f ATP biogenesis and eventual dissipation of mitochondrial membrane potential.
29 rix into the intermembrane space, sustaining mitochondrial membrane potential.
30 ochondrial dysfunction by inducing a loss of mitochondrial membrane potential.
31 ethylrhodamine ethyl ester (TMRE) reports on mitochondrial membrane potential.
32 to the mitochondria, and parasites retained mitochondrial membrane potential.
33 ells lacking ANT1, despite greater losses of mitochondrial membrane potential.
34 to increased oxidative stress and decreased mitochondrial membrane potential.
35 alizes in mitochondria and also disrupts the mitochondrial membrane potential.
36 c fluorophore intensity during 'flickers' of mitochondrial membrane potential.
37 reased mitochondrial respiration and reduced mitochondrial membrane potential.
38 between higher-order chromatin structure and mitochondrial membrane potential.
39 ntenance of oxidative TCA cycle function and mitochondrial membrane potential.
40 ncrease in the percentage of sperm with high mitochondrial membrane potential.
41 oes not involve apoptosis or perturbation of mitochondrial membrane potentials.
42 ion gradients, altering plasma membrane and mitochondrial membrane potentials.
43 proportion of mitochondria exhibited loss of mitochondrial membrane potential, abnormal structure, an
45 055 and ABT-737 cooperate to trigger loss of mitochondrial membrane potential, activation of caspases
46 2.5 mM compound 1 also prevented the loss of mitochondrial membrane potential, adenosine triphosphate
47 etone phosphate:glycerol-3-phosphate ratio), mitochondrial membrane potential, ADP, Ca(2+), 1-monoacy
48 Mitochondrial fragmentation and decreased mitochondrial membrane potential also accompany the incr
49 tive potential in MCF-7 cells, including the mitochondrial membrane potential analysis and the caspas
50 apoptotic pathway through depolarization of mitochondrial membrane potential and activation of caspa
51 ctive oxygen species, reduction in levels of mitochondrial membrane potential and adenosine-5'-tripho
52 e presence of glucose, showed a higher inner mitochondrial membrane potential and ATP:ADP ratio assoc
53 that Silica NP induces apoptosis via loss of mitochondrial membrane potential and Caspase-3 activatio
56 ced cells displayed an enhanced steady-state mitochondrial membrane potential and consistently showed
57 d, and to a lesser extent Bim; (iii) loss of mitochondrial membrane potential and cytochrome c releas
58 elicited tumor-toxicity through the loss of mitochondrial membrane potential and cytoskeletal breakd
59 ssing either PDK1 or LDHA maintained a lower mitochondrial membrane potential and decreased ROS produ
60 TCA cycle metabolites, as well as decreased mitochondrial membrane potential and deranged mitochondr
61 treatment and was associated with an altered mitochondrial membrane potential and disruption of the p
62 esent study, we show that Rac2 GTPase alters mitochondrial membrane potential and electron flow throu
63 Reproducible distributions of individual mitochondrial membrane potential and electrophoretic mob
64 for simultaneous determination of individual mitochondrial membrane potential and electrophoretic mob
67 reased nicotinamide adenine dinucleotide and mitochondrial membrane potential and increased cell deat
68 itochondrial uncoupling leading to decreased mitochondrial membrane potential and increased mitochond
69 erability, an effect associated with loss of mitochondrial membrane potential and increased mitochond
70 till, both NR and PARP-1 inhibitors restored mitochondrial membrane potential and increased organelle
72 that PYCR2 loss of function led to decreased mitochondrial membrane potential and increased susceptib
73 tes and neutrophils exhibit enhanced loss of mitochondrial membrane potential and increased susceptib
74 These responses were further correlated to mitochondrial membrane potential and insulin secretion.
75 ammed necrosis by triggering the collapse of mitochondrial membrane potential and large-scale loss of
77 2+) channel is unable to induce increases in mitochondrial membrane potential and metabolic activity
78 age-dependent anion channel (VDAC) "rescued" mitochondrial membrane potential and metabolic activity
80 resulted in the increased destabilization of mitochondrial membrane potential and mitochondrial super
81 le mitochondrial content increases linearly, mitochondrial membrane potential and oxidative phosphory
82 severe mitochondrial damage leads to loss of mitochondrial membrane potential and platelet apoptosis
83 cessive mitochondrial fragmentation, loss of mitochondrial membrane potential and production of react
85 of cryptolepine was associated with loss of mitochondrial membrane potential and reduced protein exp
86 chondrial unfolded protein response, loss of mitochondrial membrane potential and sensitivity to mito
87 c apoptotic cascade beginning with a loss of mitochondrial membrane potential and terminating in oxid
90 hological phenotype in addition to restoring mitochondrial membrane potential and to increasing cells
93 ydrogen), metabolic responsiveness (NAD(P)H, mitochondrial membrane potential), and signal transducti
94 severe respiratory chain deficiency, loss of mitochondrial membrane potential, and a disturbance of t
95 nt mitochondrial fragmentation, reduction in mitochondrial membrane potential, and a significant loss
98 f MCJ leads to increased complex I activity, mitochondrial membrane potential, and ATP production.
100 externalization, caspase activation, loss of mitochondrial membrane potential, and BAX translocation
101 eactive oxygen species production, decreased mitochondrial membrane potential, and cytochrome c relea
102 ent and rounding of PN mitochondria, reduces mitochondrial membrane potential, and damages plasma mem
103 induce lateral condensation of actin, impair mitochondrial membrane potential, and degrade Bcl-x(L) p
104 ion, altered mitochondrial motility, reduced mitochondrial membrane potential, and diminished mitocho
105 ls, promoted mitochondrial fusion, increased mitochondrial membrane potential, and elevated both intr
106 wing diminished NAD(P)H, mitochondrial NADH, mitochondrial membrane potential, and insulin secretion.
107 se, decreased lipid oxidation, reduced inner mitochondrial membrane potential, and mitochondrial ATP
108 or alterations in mitochondrial trafficking, mitochondrial membrane potential, and mitochondrial bioe
109 eased oxidative phosphorylation, glycolysis, mitochondrial membrane potential, and mitochondrial biog
110 tes significantly affects energy production, mitochondrial membrane potential, and mitochondrial oxyg
111 f effector cells, and caused senescence, low mitochondrial membrane potential, and poorly protective
112 anslocase and uncoupling proteins, decreased mitochondrial membrane potential, and promoted swelling
113 active oxygen species generation, undermines mitochondrial membrane potential, and reduces adenosine
114 ced overproduction of ROS and destruction of mitochondrial membrane potential, and resulted in the ir
115 els had elongated mitochondria and increased mitochondrial membrane potential, and RNA-sequencing ana
116 stress, the percentage of cells with altered mitochondrial membrane potential, and the induced expres
117 ochondrial dysfunction, restoring dissipated mitochondrial membrane potential, and thus cell energy a
118 activation of caspase-8, -9, and -3; loss of mitochondrial membrane potential; and apoptosis upon tre
119 activation of caspase-8, -9, and -3; loss of mitochondrial membrane potential; and caspase-dependent
120 e, uncoupling and ATP synthesis, and loss of mitochondrial membrane potential are evident in KO cells
121 -state levels of O2(*-), O2 consumption, and mitochondrial membrane potential as well as significantl
122 cells, causing a decrease in respiration and mitochondrial membrane potential, as well as an increase
123 c rat mitochondrial respiration assay, and a mitochondrial membrane potential assay using zebrafish P
124 ion and apoptosis were examined by assessing mitochondrial membrane potential, ATP levels, and cytoch
125 mitochondrial defects including increases in mitochondrial membrane potential, ATP production, and ca
126 he effects of alpha-MSH on caspase activity, mitochondrial membrane potential, Bcl2 to BAX expression
127 ction was independent of oxidative stress or mitochondrial membrane potential but appeared to involve
128 coupler FCCP is independent of the effect of mitochondrial membrane potential but dependent on acidif
129 to uptake persisted after dissipation of the mitochondrial membrane potential but was absent in mitop
130 tochondrial Ca(2+) uptake (despite unchanged mitochondrial membrane potential) but increased steady-s
131 C isoforms contributed to the maintenance of mitochondrial membrane potential, but only VDAC3 knockdo
136 cient to initiate mitophagy upon loss of the mitochondrial membrane potential, caused by its (self-)u
137 lecule US597 (UA-4) caused depolarization of mitochondrial membrane potential, cell arrest in G0/G1 p
139 ted ROS generation as well as the subsequent mitochondrial membrane potential collapse, chromosome co
142 nate dehydrogenase (SDH) and an elevation of mitochondrial membrane potential combine to drive mitoch
143 production, and recovery from impairment of mitochondrial membrane potential compared with control m
146 ron transport chain and, conversely, loss of mitochondrial membrane potential correlated with diminis
147 orate (TMRM) to evaluate the kinetics of the mitochondrial membrane potential (Deltapsi (m)) during t
148 d production of reactive species and loss of mitochondrial membrane potential (Deltapsi(m)) in them.
149 homeostasis, a persistent depolarization of mitochondrial membrane potential (Deltapsi(m)), and inse
150 y of caspases 3 and 9 and leads to a loss of mitochondrial membrane potential (DeltaPsi(m)), indicati
151 rs of cytoplasmic free Ca(2+) ([Ca(2+)](c)), mitochondrial membrane potential (Deltapsi(m)), matrix A
152 tion, although a direct link between loss of mitochondrial membrane potential (DeltaPsi) and mitophag
153 ulation of UCP2 was critical for controlling mitochondrial membrane potential (Deltapsi) and superoxi
155 tential, various ion currents (patch-clamp), mitochondrial membrane potential (DeltaPsi), and cytosol
157 gen species (ROS) at clamped levels of inner mitochondrial membrane potential (DeltaPsi), enabling mo
159 V paralleled a decrease in depolarization of mitochondrial membrane potential (DeltaPsi, monitored by
161 teries, SMCs show hyperpolarization of their mitochondrial membrane potential (DeltaPsim) and acquire
162 egy enables a light-dependent control of the mitochondrial membrane potential (Deltapsim) and coupled
163 ) overload is thought to dissipate the inner mitochondrial membrane potential (DeltaPsim) and enhance
164 etermine inhibition of toxin-induced loss of mitochondrial membrane potential (DeltaPsim) and necroti
165 Overexpression of full-length Foxg1 enhanced mitochondrial membrane potential (DeltaPsim) and promote
167 on of formyl peptide receptors increases the mitochondrial membrane potential (Deltapsim) and trigger
168 ty transition pore (MPTP) causes loss of the mitochondrial membrane potential (DeltaPsim) and, ultima
169 ty transition pore (MPTP) causes loss of the mitochondrial membrane potential (DeltaPsim) and, ultima
170 b and sorafenib, axitinib did not affect the mitochondrial membrane potential (Deltapsim) but resulte
171 tion pore (PTP) abruptly opens, resulting in mitochondrial membrane potential (DeltaPsim) dissipation
172 lar mechanism of PINK1 in dissipation of the mitochondrial membrane potential (DeltaPsim) has not bee
173 riety of complementary techniques, including mitochondrial membrane potential (DeltaPsim) imaging, hi
174 well as protective effect on cell growth and mitochondrial membrane potential (Deltapsim) in a HL-60
175 cy decreased the oxygen consumption rate and mitochondrial membrane potential (DeltaPsim) indicative
177 chanistically, in the absence of glycolysis, mitochondrial membrane potential (DeltaPsim) of EM cells
178 , sorafenib induces rapid dissipation of the mitochondrial membrane potential (DeltaPsim) that is acc
179 or extra- and intra-mitochondrial Ca(2+) and mitochondrial membrane potential (DeltaPsim) to examine
180 ies established that acute depolarization of mitochondrial membrane potential (Deltapsim) using Delta
183 4-hydroxy-2-nonnenal-modified proteins, and mitochondrial membrane potential (Deltapsim) were measur
184 creased oxidative phosphorylation, a drop in mitochondrial membrane potential (Deltapsim), and the ac
185 drial dysfunction and reflected by decreased mitochondrial membrane potential (DeltaPsim), increased
186 tochondria using depolarization of the inner mitochondrial membrane potential (DeltaPsim), the role o
187 onsive to C12, DKOR MEF): nuclei fragmented; mitochondrial membrane potential (Deltapsimito) depolari
188 ortantly, cancer cells have higher intrinsic mitochondrial membrane potential (Deltapsimt) than norma
191 PV sera also caused dramatic changes in the mitochondrial membrane potential detected with the JC-1
192 nhibition was associated with maintenance of mitochondrial membrane potential, diminished caspase-3 a
193 f this enzyme results in the collapse of the mitochondrial membrane potential, disruption of pyrimidi
194 oxicity, potent inhibition of 6-OHDA-induced mitochondrial membrane potential dissipation and ROS gen
195 re-expression induced apoptosis via loss in mitochondrial membrane potential, down-regulated autopha
196 ulation of CD133(+) cells that exhibits high mitochondrial membrane potential (DPsim(hi)) were enrich
197 ed CMs, we found that alpha7beta1D preserved mitochondrial membrane potential during hypoxia/reoxygen
199 to mitochondria resulting in dissipation of mitochondrial membrane potential during virus infection
200 induced molecular events, such as a loss in mitochondrial membrane potential, externalization of pho
201 it major changes in oxygen consumption rate, mitochondrial membrane potential, F1F0-ATP synthase acti
202 iration, and accelerates the recovery of the mitochondrial membrane potential following mitochondrial
203 ion, decreased ATP production, and increased mitochondrial membrane potential following pathway activ
204 f ATP production despite preservation of the mitochondrial membrane potential; (ii) near-maximal glyc
205 loid exposure caused the progressive loss of mitochondrial membrane potential in astrocytes, accompan
206 omena were accompanied by increased synaptic mitochondrial membrane potential in both wt and Tg2576 m
207 reactive oxygen species and prevents loss of mitochondrial membrane potential in cells expressing mut
208 ve oxygen species (ROS) and eventual loss of mitochondrial membrane potential in cells lacking the NF
209 lacking iPLA2-VIA gene function, and restore mitochondrial membrane potential in fibroblasts from pat
211 malized mitochondrial ROS production and the mitochondrial membrane potential in glucose-treated podo
213 mitochondrial respiration and dissipation of mitochondrial membrane potential in HepG2 hepatocarcinom
214 cal regions, (2) identifying regions of high mitochondrial membrane potential in live animals, (3) mo
215 ncreased oxidative stress level and impaired mitochondrial membrane potential in motor neurons affect
216 itochondrial function revealed a decrease in mitochondrial membrane potential in mutant Hsp27 express
217 eased mitochondrial NADH levels and restored mitochondrial membrane potential in p62-deficient cells.
218 condensation, DNA fragmentation, and loss of mitochondrial membrane potential in Plasmodium falciparu
219 also found that PA stimulation decreased the mitochondrial membrane potential in podocytes and induce
220 se changes occur without significant loss of mitochondrial membrane potential in retina and optic ner
221 able to record neuronal Ca(2+) responses and mitochondrial membrane potential in these nerve tissues.
222 Donor T-cells exhibited a hyperpolarized mitochondrial membrane potential, increased superoxide p
224 th increased oxidative stress and decline in mitochondrial membrane potential induced by T-2 toxin an
225 s associated with resistance against loss of mitochondrial membrane potential, induced by oxidative s
226 take was TRPV1-dependent, dissipation of the mitochondrial membrane potential, inhibition of the mito
227 ticancer potential by studying its effect on mitochondrial membrane potential, intracellular calcium
230 ATP production, assessed through changes in mitochondrial membrane potential, is downregulated in va
231 iratory chain supercomplexes to sustain high mitochondrial membrane potential late during activation
233 and selective depolarization of the parasite mitochondrial membrane potential, leading to a disruptio
234 y control pathway, whereby disruption of the mitochondrial membrane potential leads to PINK1 stabiliz
237 sites was stained with rhodamine 123 (RH), a mitochondrial membrane potential marker, and persisted t
238 in mtPE-deficient cells, and no reduction in mitochondrial membrane potential, mitochondria were exte
239 er glutamate toxicity, including maintaining mitochondrial membrane potential, mitochondrial Ca(2+) h
240 alyses revealed that KO myocytes had a lower mitochondrial membrane potential, mitochondrial Ca(2+) u
241 ilencing of VPS13C was associated with lower mitochondrial membrane potential, mitochondrial fragment
242 x, alpha-tubulin, histone H3, alpha tubulin, mitochondrial membrane potential, mitochondrial mass, ce
243 gen species (ROS) production, dissipation of mitochondrial membrane potential, mitochondrial permeabi
244 reactive oxygen species production, loss of mitochondrial membrane potential, mitochondrial permeabi
245 nd human primary beta-cells, IL-1beta alters mitochondrial membrane potential, mitochondrial permeabi
246 ood materials were tested for improvement of mitochondrial membrane potential (MMP) and ATP level in
250 nding on the approach used, and the cell and mitochondrial membrane potentials, more than 1000-fold h
254 ed decrease of cell respiration, collapse of mitochondrial membrane potential, overproduction of reac
255 ochondrial outer membrane and down-regulated mitochondrial membrane potential, oxygen consumption, an
256 y removes UCP2 and paradoxically reduces the mitochondrial membrane potential, oxygen consumption, an
257 rous noninvasive approaches monitoring NADH, mitochondrial membrane potential, oxygen consumption, an
258 are to determine the effects of glutamate on mitochondrial membrane potential, oxygen consumption, mi
260 ed the mitochondrial mass but also increased mitochondrial membrane potential per cell in cultured he
261 getics, ALKBH7-depleted cells maintain their mitochondrial membrane potential, plasma membrane integr
262 MSL1 function is not directly implicated in mitochondrial membrane potential pulsing, but is complem
263 ed bleomycin-induced cardiolipin remodeling, mitochondrial membrane potential, reactive oxygen specie
264 ing patients' skin fibroblasts showed slower mitochondrial membrane potential recovery after a mitoch
266 s a V. vulnificus MARTX toxin led to loss of mitochondrial membrane potential, release of cytochrome
267 l calcium overload and resulted in a loss of mitochondrial membrane potential, release of cytochrome
270 the latter showed the most severe defects in mitochondrial membrane potential, response to calcium, a
271 In contrast, genetic reconstitution of the mitochondrial membrane potential restored ROS, which wer
272 ation, oxidative TCA cycle function, and the mitochondrial membrane potential, resulting in diminishe
273 at OmpU treatment leads to the disruption of mitochondrial membrane potential, resulting in the relea
274 matrix pH reduction with concomitant loss of mitochondrial membrane potential, SIRT3 dissociates.
275 , unlike CL biosynthesis, dissipation of the mitochondrial membrane potential stimulates CL remodelin
276 en consumption, but decreased ATP levels and mitochondrial membrane potential suggesting a mild uncou
277 1 (Opa1), despite inducing a decrease in the mitochondrial membrane potential, suggesting a unique Dr
278 nerable plaques by targeting the collapse of mitochondrial membrane potential that occurs during apop
280 Treated lymphoma cells exhibited a reduced mitochondrial membrane potential that resulted in an irr
281 derived VCP mutant fibroblasts exhibit lower mitochondrial membrane potential, uncoupled respiration,
285 aller due to continued fatty acid oxidation, mitochondrial membrane potential was increased in FGF21-
288 mbrane protein Ucp2, which acts to lower the mitochondrial membrane potential, was upregulated in pha
289 with measurements of oxygen consumption and mitochondrial membrane potential, was used to evaluate t
290 eased intracellular glutathione, and altered mitochondrial membrane potential were found in monocytes
291 effects of cytoplasmic Ca(2+) overloading on mitochondrial membrane potential were significantly redu
292 expression in INS1(832/13) cells, changes in mitochondrial membrane potential were unaffected, consis
294 neurons revealed large fluctuations in inner mitochondrial membrane potential when Bcl-x(L) was genet
295 on transport by MSL1 leads to dissipation of mitochondrial membrane potential when it becomes too hig
296 r membrane that progressively dissipates the mitochondrial membrane potential, which in turn stalls m
297 reactive oxygen species can prevent loss of mitochondrial membrane potential, whilst inhibition of m
299 by showing FO-independent generation of the mitochondrial membrane potential with increased dependen
300 se development, respectively, while boosting mitochondrial membrane potential with l-carnitine-foster
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