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1 l of energy metabolism, ultimately impacting mitochondrial membrane potential.
2 tive oxygen species or depolarization of the mitochondrial membrane potential.
3 ression and, consistent with this, decreased mitochondrial membrane potential.
4 olism, mitochondrial biogenesis and restores mitochondrial membrane potential.
5 tion rate, reserve respiration capacity, and mitochondrial membrane potential.
6 rix into the intermembrane space, sustaining mitochondrial membrane potential.
7 ochondrial dysfunction by inducing a loss of mitochondrial membrane potential.
8 ontributing toward the maintenance of normal mitochondrial membrane potential.
9 ethylrhodamine ethyl ester (TMRE) reports on mitochondrial membrane potential.
10 itosis from the single-cell time-dynamics of mitochondrial membrane potential.
11 to the mitochondria, and parasites retained mitochondrial membrane potential.
12 ells lacking ANT1, despite greater losses of mitochondrial membrane potential.
13 to increased oxidative stress and decreased mitochondrial membrane potential.
14 alizes in mitochondria and also disrupts the mitochondrial membrane potential.
15 c fluorophore intensity during 'flickers' of mitochondrial membrane potential.
16 reased mitochondrial respiration and reduced mitochondrial membrane potential.
17 between higher-order chromatin structure and mitochondrial membrane potential.
18 ntenance of oxidative TCA cycle function and mitochondrial membrane potential.
19 ncrease in the percentage of sperm with high mitochondrial membrane potential.
20 ompared with control cells, but show reduced mitochondrial membrane potential.
21 ase allow for Fo-independent generation of a mitochondrial membrane potential.
22 th excessive cleavage of PINK1 and increased mitochondrial membrane potential.
23 including mitochondrial DNA copy number and mitochondrial membrane potential.
24 ochondrial respiration rate and reduction of mitochondrial membrane potential.
25 ction that is associated with a reduction of mitochondrial membrane potential.
26 s but had significantly reduced lifespan and mitochondrial membrane potential.
27 al mitochondria were used as an indicator of mitochondrial membrane potential.
28 cells after treatment, which showed reduced mitochondrial membrane potential.
29 of pyruvate and its metabolites, and loss of mitochondrial membrane potential.
30 ad4 in trophoblast cells resulted in reduced mitochondrial membrane potential.
31 and motor proteins in addition to changes in mitochondrial membrane potential.
32 ondrial Ca(2+) uptake, without affecting the mitochondrial membrane potential.
33 al reactive oxygen species and protected the mitochondrial membrane potential.
34 rboxylic acid cycle (TCA), and have abnormal mitochondrial membrane potential.
35 oxidative stress and disturbances caused to mitochondrial membrane potential.
36 he parasite by decreasing ATP production and mitochondrial membrane potential.
37 led to decreased ATP synthesis and defective mitochondrial membrane potential.
38 ion gradients, altering plasma membrane and mitochondrial membrane potentials.
39 oes not involve apoptosis or perturbation of mitochondrial membrane potentials.
40 lity, reactive oxygen species generation and mitochondrial membrane potentials.
41 mice had similar respiratory activities and mitochondrial membrane potentials.
42 acrophages overexpressing ACE have increased mitochondrial membrane potential (24% higher), ATP produ
43 s with high concentrations of drug decreased mitochondrial membrane potential, a phenotype that was s
44 metabolic remodeling deficits and decreased mitochondrial membrane potential; a subset had increased
45 in mitochondrial respiration, impairment in mitochondrial membrane potential, aberrant mitochondrial
47 ion identified chemical probes that regulate mitochondrial membrane potential, adenosine 5'-triphosph
48 2.5 mM compound 1 also prevented the loss of mitochondrial membrane potential, adenosine triphosphate
49 etone phosphate:glycerol-3-phosphate ratio), mitochondrial membrane potential, ADP, Ca(2+), 1-monoacy
50 he MB-gCs, in like manner to MB, can restore mitochondrial membrane potential after depolarization wi
51 -induced mild uncoupling is shown to protect mitochondrial membrane potential against FA-induced unco
52 mitochondria relies on maintaining the inner mitochondrial membrane potential (also known as DeltaPsi
53 tive potential in MCF-7 cells, including the mitochondrial membrane potential analysis and the caspas
54 hanistically, AMD1 depletion induced loss of mitochondrial membrane potential and accumulation of rea
55 apoptotic pathway through depolarization of mitochondrial membrane potential and activation of caspa
56 chondrial structural rearrangements, loss of mitochondrial membrane potential and activation of mitop
57 e presence of glucose, showed a higher inner mitochondrial membrane potential and ATP:ADP ratio assoc
59 that Silica NP induces apoptosis via loss of mitochondrial membrane potential and Caspase-3 activatio
61 ced cells displayed an enhanced steady-state mitochondrial membrane potential and consistently showed
62 d, and to a lesser extent Bim; (iii) loss of mitochondrial membrane potential and cytochrome c releas
63 elicited tumor-toxicity through the loss of mitochondrial membrane potential and cytoskeletal breakd
64 ive oxygen species production, and decreased mitochondrial membrane potential and depolarization thre
65 TCA cycle metabolites, as well as decreased mitochondrial membrane potential and deranged mitochondr
66 treatment and was associated with an altered mitochondrial membrane potential and disruption of the p
67 Reproducible distributions of individual mitochondrial membrane potential and electrophoretic mob
68 for simultaneous determination of individual mitochondrial membrane potential and electrophoretic mob
69 energy deficiency, together with compromised mitochondrial membrane potential and elevated oxidative
70 hed cardiomyopathy, restored cardiac myocyte mitochondrial membrane potential and flavoprotein oxidat
71 olic activity was assessed as alterations in mitochondrial membrane potential and flavoprotein oxidat
72 etime becomes progressively shorter, and the mitochondrial membrane potential and glucose uptake beco
76 Activation of PPAR-gamma partially restored mitochondrial membrane potential and IFN-gamma productio
77 itochondrial uncoupling leading to decreased mitochondrial membrane potential and increased mitochond
78 till, both NR and PARP-1 inhibitors restored mitochondrial membrane potential and increased organelle
79 impaired mitochondrial respiration, loss of mitochondrial membrane potential and increased productio
80 tive or oxidative stress, yet exhibited high mitochondrial membrane potential and increased superoxid
81 that PYCR2 loss of function led to decreased mitochondrial membrane potential and increased susceptib
82 2+) channel is unable to induce increases in mitochondrial membrane potential and metabolic activity
83 age-dependent anion channel (VDAC) "rescued" mitochondrial membrane potential and metabolic activity
85 resulted in the increased destabilization of mitochondrial membrane potential and mitochondrial super
87 itochondrial DNA, and a similar reduction in mitochondrial membrane potential and NDUFA9 protein abun
88 le mitochondrial content increases linearly, mitochondrial membrane potential and oxidative phosphory
89 se invertebrate worms significantly improved mitochondrial membrane potential and oxidative stress, w
90 severe mitochondrial damage leads to loss of mitochondrial membrane potential and platelet apoptosis
91 cessive mitochondrial fragmentation, loss of mitochondrial membrane potential and production of react
94 ochthonous lung cancer mouse model had lower mitochondrial membrane potential and reduced mitochondri
95 of cryptolepine was associated with loss of mitochondrial membrane potential and reduced protein exp
96 chondrial unfolded protein response, loss of mitochondrial membrane potential and sensitivity to mito
97 show that, while loss of Ucp2 does increase mitochondrial membrane potential and the production of r
100 hological phenotype in addition to restoring mitochondrial membrane potential and to increasing cells
102 ydrogen), metabolic responsiveness (NAD(P)H, mitochondrial membrane potential), and signal transducti
103 nt mitochondrial fragmentation, reduction in mitochondrial membrane potential, and a significant loss
107 ion, altered mitochondrial motility, reduced mitochondrial membrane potential, and diminished mitocho
108 essed mitochondrial gene expression, reduced mitochondrial membrane potential, and diminished oxygen
109 vities, respiratory responses, redox charge, mitochondrial membrane potential, and electron leak, we
110 ls, promoted mitochondrial fusion, increased mitochondrial membrane potential, and elevated both intr
112 ng dysregulates iron metabolism, depolarizes mitochondrial membrane potential, and induces cell death
113 or alterations in mitochondrial trafficking, mitochondrial membrane potential, and mitochondrial bioe
114 eased oxidative phosphorylation, glycolysis, mitochondrial membrane potential, and mitochondrial biog
115 tes significantly affects energy production, mitochondrial membrane potential, and mitochondrial oxyg
116 is, decreasing PI3K and Akt phosphorylation, mitochondrial membrane potential, and modulating G1-S tr
117 anslocase and uncoupling proteins, decreased mitochondrial membrane potential, and promoted swelling
118 the increase in ROS production, decrease of mitochondrial membrane potential, and proteasome activit
119 active oxygen species generation, undermines mitochondrial membrane potential, and reduces adenosine
120 ced overproduction of ROS and destruction of mitochondrial membrane potential, and resulted in the ir
121 els had elongated mitochondria and increased mitochondrial membrane potential, and RNA-sequencing ana
122 ochondrial dysfunction, restoring dissipated mitochondrial membrane potential, and thus cell energy a
123 tive imaging, bioenergetics measurements and mitochondrial membrane potential- and redox-sensitive dy
124 of intracellular reactive oxygen species and mitochondrial membrane potential as well as microscopy (
125 -state levels of O2(*-), O2 consumption, and mitochondrial membrane potential as well as significantl
126 cells, causing a decrease in respiration and mitochondrial membrane potential, as well as an increase
127 c rat mitochondrial respiration assay, and a mitochondrial membrane potential assay using zebrafish P
128 mitochondrial defects including increases in mitochondrial membrane potential, ATP production, and ca
129 mitochondrial variables such as respiration, mitochondrial membrane potential, buffer calcium, and su
130 coupler FCCP is independent of the effect of mitochondrial membrane potential but dependent on acidif
131 ithdrawal, miR-450a overexpression decreased mitochondrial membrane potential but increased glucose u
133 C isoforms contributed to the maintenance of mitochondrial membrane potential, but only VDAC3 knockdo
135 in cytosolic calcium, prevented the loss of mitochondrial membrane potential (by 70%-80%), and resul
137 cient to initiate mitophagy upon loss of the mitochondrial membrane potential, caused by its (self-)u
138 cal in this quality-control process: loss of mitochondrial membrane potential causes PINK1 to accumul
139 lecule US597 (UA-4) caused depolarization of mitochondrial membrane potential, cell arrest in G0/G1 p
140 ted ROS generation as well as the subsequent mitochondrial membrane potential collapse, chromosome co
141 nate dehydrogenase (SDH) and an elevation of mitochondrial membrane potential combine to drive mitoch
142 production, and recovery from impairment of mitochondrial membrane potential compared with control m
143 e found that ME/CFS CD8+ T cells had reduced mitochondrial membrane potential compared with those fro
146 or of succinate dehydrogenase, Rhes disrupts mitochondrial membrane potential (DeltaPsi (m) ) and pro
149 ndrial mass, and live microscopic imaging of mitochondrial membrane potential (DeltaPsi(m)) and optic
150 owed a reduction in intact cell respiration, mitochondrial membrane potential (DeltaPsi(m)), ROS prod
151 gulate mitochondrial ETC flux and adjust the mitochondrial membrane potential (DeltaPsi(m)), to minim
153 tion, although a direct link between loss of mitochondrial membrane potential (DeltaPsi) and mitophag
159 teries, SMCs show hyperpolarization of their mitochondrial membrane potential (DeltaPsim) and acquire
160 egy enables a light-dependent control of the mitochondrial membrane potential (Deltapsim) and coupled
161 ) overload is thought to dissipate the inner mitochondrial membrane potential (DeltaPsim) and enhance
162 chondrial assessment indicated reduced inner mitochondrial membrane potential (DeltaPsim) and metabol
163 etermine inhibition of toxin-induced loss of mitochondrial membrane potential (DeltaPsim) and necroti
164 Overexpression of full-length Foxg1 enhanced mitochondrial membrane potential (DeltaPsim) and promote
166 on of formyl peptide receptors increases the mitochondrial membrane potential (Deltapsim) and trigger
167 ty transition pore (MPTP) causes loss of the mitochondrial membrane potential (DeltaPsim) and, ultima
168 tion pore (PTP) abruptly opens, resulting in mitochondrial membrane potential (DeltaPsim) dissipation
169 riety of complementary techniques, including mitochondrial membrane potential (DeltaPsim) imaging, hi
170 well as protective effect on cell growth and mitochondrial membrane potential (Deltapsim) in a HL-60
171 cy decreased the oxygen consumption rate and mitochondrial membrane potential (DeltaPsim) indicative
173 chanistically, in the absence of glycolysis, mitochondrial membrane potential (DeltaPsim) of EM cells
174 , sorafenib induces rapid dissipation of the mitochondrial membrane potential (DeltaPsim) that is acc
175 or extra- and intra-mitochondrial Ca(2+) and mitochondrial membrane potential (DeltaPsim) to examine
176 ies established that acute depolarization of mitochondrial membrane potential (Deltapsim) using Delta
178 creased oxidative phosphorylation, a drop in mitochondrial membrane potential (Deltapsim), and the ac
179 drial dysfunction and reflected by decreased mitochondrial membrane potential (DeltaPsim), increased
180 tochondria using depolarization of the inner mitochondrial membrane potential (DeltaPsim), the role o
183 onsive to C12, DKOR MEF): nuclei fragmented; mitochondrial membrane potential (Deltapsimito) depolari
184 ortantly, cancer cells have higher intrinsic mitochondrial membrane potential (Deltapsimt) than norma
185 +) is reduced back to NADPH by activation of mitochondrial membrane potential-dependent nicotinamide
187 ed mitochondrial defects including collapsed mitochondrial membrane potential, dissipated ATP product
188 oxicity, potent inhibition of 6-OHDA-induced mitochondrial membrane potential dissipation and ROS gen
189 re-expression induced apoptosis via loss in mitochondrial membrane potential, down-regulated autopha
190 the cell cycle at S phase, depolarization of mitochondrial membrane potential, down-regulation of Bcl
191 ed CMs, we found that alpha7beta1D preserved mitochondrial membrane potential during hypoxia/reoxygen
193 induced molecular events, such as a loss in mitochondrial membrane potential, externalization of pho
194 it major changes in oxygen consumption rate, mitochondrial membrane potential, F1F0-ATP synthase acti
196 iration, and accelerates the recovery of the mitochondrial membrane potential following mitochondrial
197 ion, decreased ATP production, and increased mitochondrial membrane potential following pathway activ
198 , we demonstrate that the distance-dependent mitochondrial membrane potential gradient exists in vivo
199 chanistically, cysteine deprivation leads to mitochondrial membrane potential hyperpolarization and l
200 e or electron transfer chain (ETC) mitigated mitochondrial membrane potential hyperpolarization, lipi
201 f ATP production despite preservation of the mitochondrial membrane potential; (ii) near-maximal glyc
202 using PET imaging of (18)F-BnTP, we profile mitochondrial membrane potential in autochthonous mouse
203 omena were accompanied by increased synaptic mitochondrial membrane potential in both wt and Tg2576 m
204 ent of mitochondrial transport and protected mitochondrial membrane potential in cultured sensory neu
205 lacking iPLA2-VIA gene function, and restore mitochondrial membrane potential in fibroblasts from pat
207 malized mitochondrial ROS production and the mitochondrial membrane potential in glucose-treated podo
208 mitochondrial respiration and dissipation of mitochondrial membrane potential in HepG2 hepatocarcinom
209 cal regions, (2) identifying regions of high mitochondrial membrane potential in live animals, (3) mo
211 alyzed the mitochondrial redox state and the mitochondrial membrane potential in mice of both sexes w
212 ncreased oxidative stress level and impaired mitochondrial membrane potential in motor neurons affect
213 itochondrial function revealed a decrease in mitochondrial membrane potential in mutant Hsp27 express
215 eased mitochondrial NADH levels and restored mitochondrial membrane potential in p62-deficient cells.
216 also found that PA stimulation decreased the mitochondrial membrane potential in podocytes and induce
217 While the pharmaceutical agents decreased mitochondrial membrane potential in porcine fetal fibrob
218 able to record neuronal Ca(2+) responses and mitochondrial membrane potential in these nerve tissues.
220 ic overexpression of UQCRH in KMRC2 restored mitochondrial membrane potential, increased oxygen consu
221 hibited a lower rate of O(2) uptake, loss of mitochondrial membrane potential, increased reactive oxy
222 that is, they damage nuclear DNA, reduce the mitochondrial membrane potential, induce the epigenetic
223 th increased oxidative stress and decline in mitochondrial membrane potential induced by T-2 toxin an
224 s associated with resistance against loss of mitochondrial membrane potential, induced by oxidative s
225 take was TRPV1-dependent, dissipation of the mitochondrial membrane potential, inhibition of the mito
228 ATP production, assessed through changes in mitochondrial membrane potential, is downregulated in va
229 iratory chain supercomplexes to sustain high mitochondrial membrane potential late during activation
230 on of COX6B2 attenuates OXPHOS and collapses mitochondrial membrane potential leading to cell death o
232 y control pathway, whereby disruption of the mitochondrial membrane potential leads to PINK1 stabiliz
233 The model reveals that reduction in the mitochondrial membrane potential leads to significant de
234 andard chemotherapeutics sensitized cells to mitochondrial membrane potential loss and apoptosis.
235 asmic volume control, absence of significant mitochondrial membrane potential loss, and lack of activ
239 sites was stained with rhodamine 123 (RH), a mitochondrial membrane potential marker, and persisted t
240 in mtPE-deficient cells, and no reduction in mitochondrial membrane potential, mitochondria were exte
242 er glutamate toxicity, including maintaining mitochondrial membrane potential, mitochondrial Ca(2+) h
243 alyses revealed that KO myocytes had a lower mitochondrial membrane potential, mitochondrial Ca(2+) u
244 ilencing of VPS13C was associated with lower mitochondrial membrane potential, mitochondrial fragment
245 x, alpha-tubulin, histone H3, alpha tubulin, mitochondrial membrane potential, mitochondrial mass, ce
246 gen species (ROS) production, dissipation of mitochondrial membrane potential, mitochondrial permeabi
247 reactive oxygen species production, loss of mitochondrial membrane potential, mitochondrial permeabi
248 nd human primary beta-cells, IL-1beta alters mitochondrial membrane potential, mitochondrial permeabi
249 ood materials were tested for improvement of mitochondrial membrane potential (MMP) and ATP level in
252 -cell RNA sequencing (RNA-seq), we show that mitochondrial membrane potential (MMP) distinguishes qui
254 nding on the approach used, and the cell and mitochondrial membrane potentials, more than 1000-fold h
255 ds: Cardiac uptake and response to decreased mitochondrial membrane potential of (18)F-MitoPhos and (
259 ochondrial outer membrane and down-regulated mitochondrial membrane potential, oxygen consumption, an
261 ed the mitochondrial mass but also increased mitochondrial membrane potential per cell in cultured he
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 ROS scavenging assays, wound healing assays, mitochondrial membrane potential readings, corneal fluor
265 ing patients' skin fibroblasts showed slower mitochondrial membrane potential recovery after a mitoch
266 e oxygen species (ROS) activities, increased mitochondrial membrane potential, reduced calcium levels
268 s a V. vulnificus MARTX toxin led to loss of mitochondrial membrane potential, release of cytochrome
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 ranslational modifications: respiration, the mitochondrial membrane potential, ROS, and apoptosis.
275 matrix pH reduction with concomitant loss of mitochondrial membrane potential, SIRT3 dissociates.
276 en consumption, but decreased ATP levels and mitochondrial membrane potential suggesting a mild uncou
277 ssed produces a stable protein which impacts mitochondrial membrane potential, suggesting a potential
278 change in NAD(+)/NADH is caused by increased mitochondrial membrane potential that impairs mitochondr
279 Treated lymphoma cells exhibited a reduced mitochondrial membrane potential that resulted in an irr
280 derived VCP mutant fibroblasts exhibit lower mitochondrial membrane potential, uncoupled respiration,
281 ase, which we propose maintains intermediate mitochondrial membrane potentials under physiologic cond
289 expression in INS1(832/13) cells, changes in mitochondrial membrane potential were unaffected, consis
291 on transport by MSL1 leads to dissipation of mitochondrial membrane potential when it becomes too hig
292 estingly, Abeta-CEL16&28 had depolarized the mitochondrial membrane potential, whereas Abeta-CEL16 ha
293 r membrane that progressively dissipates the mitochondrial membrane potential, which in turn stalls m
294 min treated animals maintained a more normal mitochondrial membrane potential while those isolated fr
295 reactive oxygen species can prevent loss of mitochondrial membrane potential, whilst inhibition of m
296 n, accumulation of complex IV, and increased mitochondrial membrane potential with no change in mitoc
297 ablish a quantitative model to associate the mitochondrial membrane potential with the key pharmacoki
298 2-fold ROS generation, and a 50% decrease in mitochondrial membrane potentials with respect to equiva
299 ll MFGMs treatment significantly reduced the mitochondrial membrane potential (with an order of goat
300 mitochondrial oxidative stress and decreased mitochondrial membrane potential, with higher mtDNA rele