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1 reatment with a liver-targeted mitochondrial uncoupler.
2 (+/-K(+)) is prevented by the presence of an uncoupler.
3 a2+ uptake was blocked with ruthenium red or uncoupler.
4 fect disappears when PMF is eliminated by an uncoupler.
5 R Ca(2+) ATPase (SERCA) and acts on it as an uncoupler.
6 inyl adenosine synthase, as well as being an uncoupler.
7 affinity modulator, and sarcolipin (SLN), an uncoupler.
8  active against Staphylococcus aureus, is an uncoupler.
9  orally active MEK1/2 inhibitor, acted as an uncoupler.
10 at pH 7.5 in the presence of a protonophoric uncoupler.
11 ugh KPF itself is not a direct mitochondrial uncoupler.
12 or prevented by previous depolarization with uncoupler.
13 omethoxy) phenylylhydrazone, a mitochondrial uncoupler.
14 hondria in the presence of 2,4-dinitrophenol uncoupler.
15 o electron transfer chain inhibitors and ion uncouplers.
16 ial respiratory inhibitors and mitochondrial uncouplers.
17 r than controls not exposed to mitochondrial uncouplers.
18 with ICG and perfused with electromechanical uncouplers.
19 ffected by membrane potential or pH gradient uncouplers.
20 tarved cells or in cells treated with energy uncouplers.
21 is compromised by agents such as alcohols or uncouplers.
22 ced interest in the clinical use of chemical uncouplers.
23 as determined by exposing M. tuberculosis to uncouplers.
24                                 Gap junction uncouplers (1-octanol, carbenoxolone, 18beta-glycyrrheti
25 pressed gap junction genes, and gap junction uncouplers, 18beta-glycyrrhetinic acid (18beta-GA) and o
26 europrotective efficacy of the mitochondrial uncoupler 2,4-dinitrophenol (DNP) in animals receiving s
27                                 The chemical uncoupler 2,4-dinitrophenol (DNP) was an effective and w
28 r Alzheimer's disease, and the mitochondrial uncoupler 2,4-dinitrophenol for obesity.
29                              A mitochondrial uncoupler, 2,4-dinitrophenol (at 1 mmol/L), blocked the
30 cium ionophore, A23187 and the mitochondrial uncoupler, 2,4-dinitrophenol (DNP) as damaging agents.
31 o or in vivo, against the electron transport uncoupler 3-acetylpyridine (3AP).
32             The application of mitochondrial uncouplers (5 microM CCCP or 5 microM FCCP), eliminated
33 or 2,4-dinitrophenol (DNP, the mitochondrial uncoupler, 50 micromol/L) (15.7+/-2.7% versus 40.8+/-5.5
34  most with known antiinfective activity, for uncoupler activity.
35 have a reduced rate of consumption of ATP on uncoupler addition.
36                                              Uncouplers also inhibited a background K+ current and in
37 hlorophenyl hydrazone (CCCP; a mitochondrial uncoupler) alter [Ca2+]i and force transients.
38 ribution was inhibited by proton ionophores (uncouplers), alteration of alpha conformation by illumin
39 heart in the absence of an electromechanical uncoupler and (2) to elucidate the mechanism of verapami
40 Treatment of MDCK cells with a mitochondrial uncoupler and a Ca2+ ionophore led to ATP depletion, nec
41 tential titrated by stepwise additions of an uncoupler and expressed as a function of citrate synthas
42 omyocytes, were eliminated by a gap junction uncoupler and reappeared with its removal.
43                                              Uncouplers and blockers of membrane channels were used t
44 rom the primary site and thus act as symport uncouplers and inhibit transport.
45 t acute administration of DNP (mitochondrial uncoupler) and chronic administration of T(3) decrease e
46    Furthermore, U73122 (Gqalpha-PLC specific uncoupler) and GP2A (Gqalpha specific inhibitor) mirrore
47           Using a combination of inhibitors, uncouplers, and antimycin A, and by following the kineti
48 sitivity of this oxidation to ionophores and uncouplers, and the absence of any delay in the onset of
49 l membrane with visible light results in the uncoupler- and inhibitor-sensitive synthesis of adenosin
50                                Mitochondrial uncouplers are potent stimulants of the carotid body.
51     Treatment with chemical inhibitors or an uncoupler, as well as crosses to mutants known to affect
52    Application of the excitation-contraction uncoupler blebbistatin or the mechanosensitive channel b
53 tabolic insults including treatment with the uncoupler carbonyl cyanide 3-chlorophenylhydrazone (CCCP
54 ere larger in the presence of cyanide or the uncoupler carbonyl cyanide 4-trifluoromethoxyphenylhydra
55  The mitochondrial oxidative phosphorylation uncoupler carbonyl cyanide m-chlorophenyl hydrazone (2 m
56                                 Although the uncoupler carbonyl cyanide m-chlorophenyl hydrazone inhi
57                                          The uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP
58 tapsi(m) conditions, hypersensitivity to the uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP
59                       The electron transport uncoupler carbonyl cyanide m-chlorophenylhydrazone inhib
60 e pH gradient and strongly stimulated by the uncoupler carbonyl cyanide m-chlorophenylhydrazone when
61 phagy after treatment with the mitochondrial uncoupler carbonyl cyanide m-methylhydrazone, because of
62 itochondrial inhibitor NaCN and mitochondria uncoupler carbonyl cyanide p-(trifluoromethoxy) phenyl h
63 r Ca(2+) after addition of the mitochondrial uncoupler carbonyl cyanide p-(trifluoromethoxy)phenyl hy
64 n kinases ERK1 and ERK2 by the mitochondrial uncoupler carbonyl cyanide p-(trifluoromethoxy)phenylhyd
65 -hydroxy-TEMPO (TEMPOL) or the mitochondrial uncoupler carbonyl cyanide p-(trifluoromethoxy)phenylhyd
66  disrupted by treating cells with the proton uncoupler carbonyl cyanide p-chlorophenylhydrazone.
67              However, like the mitochondrial uncoupler carbonyl cyanide p-trifluoromethoxyphenyl hydr
68  of the mitochondrial inhibitor NaCN, or the uncoupler carbonyl cyanide p-trifluoromethoxyphenylhydra
69                       In the presence of the uncouplers carbonyl cyanide m-chlorophenylhydrazone or v
70 endent stress genes by the respiratory chain uncoupler, carbonyl cyanide m-chlorophenyl hydrazine (CC
71  by autophagy) stimulated by a mitochondrial uncoupler, carbonyl cyanide m-chlorophenylhydrazone (CCC
72 cal hypoxia model of mitophagy induced by an uncoupler, carbonyl cyanide m-chlorophenylhydrazone (CCC
73 class through the coronary arteries with the uncoupler, carbonyl cyanide p-trifluoromethoxyphenylhydr
74 ane potential was dissipated by the chemical uncoupler carbonylcyanide m-chlorophenyl hydrazone.
75 in the presence of Zn2+ was abrogated by the uncoupler carbonylcyanide m-chlorophenylhydrazone, sugge
76          It was also inhibited by the proton uncoupler carbonylcyanide m-chlorophenylhydrazone, sugge
77 kainic acid, and NMDA, and the mitochondrial uncoupler carbonylcyanide p-(trifluoromethoxy)phenyl hyd
78                                   The proton uncouplers carbonylcyanide-4-(trifluoromethoxy) phenylhy
79                                   The proton uncouplers carbonylcyanide-4-(trifluoromethoxy)phenylhyd
80 in purple membrane suspensions by the energy-uncoupler CCCP or by lysis of the cells.
81 s TonB independent and was unaffected by the uncouplers CCCP (carbonyl cyanide m-chlorophenylhydrazon
82 yrphostins A9 and AG126 act as mitochondrial uncouplers, collapsing the mitochondrial membrane potent
83 ng respiration and ATP biosynthesis, and are uncouplers, collapsing the pH gradient and membrane pote
84 of electron transport and DeltapH at various uncoupler concentrations or light intensities was obtain
85 tochondrial respiratory chain inhibitors and uncouplers decreased mitochondrial membrane potential le
86 eficial effects of DNP suggest that chemical uncouplers deserve further investigation for the treatme
87 , application of glutamate together with the uncoupler did not prevent the changes in movement or sha
88 emonstrated that their relative potencies as uncouplers differed from their in vitro kinase-inhibitor
89 l CMRO2 in the presence of the mitochondrial uncoupler dinitrophenol (DNP) were compared using 16.4 T
90 ine of these matched proteins induced by the uncoupler dinitrophenol.
91                                Mitochondrial uncouplers dissipate this proton gradient and disrupt nu
92                                     Chemical uncouplers do not induce obvious changes in Cx43-EGFP ju
93 single or repetitive pulses of substrate- or uncoupler-elicited energetic-redox transitions.
94      We have previously used measurements of uncoupler-enforced reverse activity to demonstrate that
95 the formation of a mixed complex between the uncoupler, ETH-129, and Ca(2+) that readily permeates th
96                             We conclude that uncouplers excite the carotid body by inhibiting a backg
97 RN revealed that (1) RN is stimulated by the uncoupler FCCP and high levels of substrates, demonstrat
98  induction of mitophagy by the mitochondrial uncoupler FCCP is independent of the effect of mitochond
99 s were inhibited by hypoxia, cyanide and the uncoupler FCCP, but the greatest sensitivity was seen in
100   On the other hand, mitochondrial metabolic uncoupler FCCP, in the presence of oligomycin (to preven
101 nd mouse HSCs were treated with the chemical uncouplers FCCP and Valinomycin.
102 , however, is to discover safe mitochondrial uncouplers for practical use.
103 hlorophenylhydrazone (CCCP), a mitochondrial uncoupler, found that more than half of the mitochondria
104   The therapeutic potential of mitochondrial uncouplers has been investigated for the treatment of me
105                             The gap-junction uncoupler heptanol had no effect.
106              Treatment with the gap junction uncoupler heptanol significantly reduced the movement of
107  Ca(2+)-free dextran and by the gap junction uncoupler, heptanol, indicated that it was generated by
108 ntally by local perfusion of a mitochondrial uncoupler in a monolayer of cardiac myocytes.
109  characterized as a functional mitochondrial uncoupler in Drosophila.
110           Oleate does not substitute for the uncoupler in either regard.
111 tured hippocampal neurons to a mitochondrial uncoupler in glucose-free medium promotes the formation
112 ed of ATP by incubation with a mitochondrial uncoupler in glucose-free medium.
113 have led to suggestions that they may act as uncouplers in cells.
114 y Cx40-specific and nonspecific gap junction uncouplers in the lungs of wild-type mice and in lungs f
115                                         Both uncouplers increased the expression of mitochondrial gen
116                                              Uncouplers increased trap closure delay and significantl
117 espiration is also inhibited by nigericin or uncoupler, indicating that an acidic matrix pH antagoniz
118  in the presence of a mitochondrial membrane uncoupler, indicating that mitochondria are the main sit
119  inhibited by low concentrations of a proton uncoupler, indicating that PLUTO functions as a proton-s
120       In 60-hour-old biofilms, the extent of uncoupler-induced cell loss was strongly attenuated, ind
121            The capacity for MgATP-dependent, uncoupler-insensitive conjugate transport in vitro stric
122 olated from these cells for MgATP-dependent, uncoupler-insensitive DNP-GS transport.
123  more than 90% impaired for MgATP-dependent, uncoupler-insensitive DNP-GS transport.
124 yl)glutathione (DNP-GS), an MgATP-dependent, uncoupler-insensitive pathway and an electrically driven
125 ae is inferred to encode an MgATP-energized, uncoupler-insensitive vacuolar glutathione S-conjugate t
126 thways identified, only the MgATP-dependent, uncoupler-insensive pathway is subject to inhibition by
127 that Endosidin9 (ES9), a novel mitochondrial uncoupler, is a potent inhibitor of clathrin-mediated en
128 enuated by the presence of the mitochondrial uncoupler M3778 but potentiated by the presence of cobal
129  studies have suggested that a mitochondrial uncoupler might work in a similar manner.
130 I inhibitor), dinitrophenol (a mitochondrial uncoupler), muscle contraction, and sorbitol (producing
131 t blocked mitochondrial Ca(2+) accumulation (uncouplers, nocodazole) eliminated the observed inhibiti
132  in the presence of 0.1 mM dinitrophenol, an uncoupler of ATP synthesis.
133  occurring sVegfr-2 thus acts as a molecular uncoupler of blood and lymphatic vessels; modulation of
134  neurons pretreated with pertussis toxin, an uncoupler of G proteins and MOR.
135 nsmembrane receptors, or pertussis toxin, an uncoupler of G(i) from adenylate cyclase.
136 y increased Ptran (to 0.22) and heptanol, an uncoupler of gap junction channels, significantly decrea
137           The effects of pertussis toxin, an uncoupler of Gi protein from adenylate cyclase, and luzi
138 th application of 2,4-dinitrophenol (DNP, an uncoupler of mitochondrial ATP production) induced an in
139 ort complex II (thenoyltrifluoroacetone), an uncoupler of oxidative phosphorylation (carbonyl cyanide
140  morphology precludes UCP4 from acting as an uncoupler of oxidative phosphorylation but is consistent
141 f electron transport chain complex II, by an uncoupler of oxidative phosphorylation, by uncoupling pr
142     In this study, we found that the classic uncoupler of oxidative phosphorylation, carbonyl cyanide
143 l cyanide m-chlorophenylhydrazone (CCCP), an uncoupler of oxidative phosphorylation, completely preve
144                       It is thought to be an uncoupler of oxidative phosphorylation.
145                        Benzene, an effective uncoupler of oxygen consumption in purified naphthalene
146 us, azide does not appear to act as a simple uncoupler of proton transport and ATP hydrolysis.
147 We recently showed that sarcolipin (SLN), an uncoupler of the sarco(endo)plasmic reticulum Ca(2+) ATP
148  reversed by V-type ATPase inhibitors and by uncouplers of endosomal intralumenal pH, and was correla
149  phosphorylation events were not affected by uncouplers of oxidative respiration, inhibitors of elect
150 tment of cells with metabolic inhibitors and uncouplers of photosynthetic electron transport showed t
151 S) production through use of pharmacological uncouplers of the mitochondrial electron transport chain
152 bind mitochondria and function as endogenous uncouplers of UCP1-independent respiration.
153 pite a widely accepted role of arrestins as "uncouplers" of G protein-coupled receptor (GPCR) signali
154 re control, use of an excitation-contraction uncoupler, optimal vibratome settings and correct handli
155 rial Ca(2+) uptake by either a mitochondrial uncoupler or a Ca(2+) uniporter inhibitor.
156                Treatment of cultures with an uncoupler or blocking ATP synthesis with oligomycin also
157 ed with GSK inhibitors and were treated with uncoupler or cyanide or were made anoxic.
158 nses recorded in the absence and presence of uncoupler or from [Ca2+]c elevations evoked by uncoupler
159 s, inhibiting mitochondrial function with an uncoupler or interrupting the electron transport chain w
160 coupler or from [Ca2+]c elevations evoked by uncoupler or ionophore applied after complete Ca2+ mobil
161  be enhanced by treatment with mitochondrial uncouplers or dissipated by drug-induced disaggregation
162                    Remarkably, mitochondrial uncouplers or Na+ depletion prevent the ability of T cel
163 on mechanism distinct from that triggered by uncouplers or the apoptosis inducer staurosporine.
164 Ca(2+) and is not affected by ruthenium red, uncouplers, or ionophores that perturb transmembrane gra
165 ce of CN(-) or rotenone or the mitochondrial uncoupler p-trifluoromethoxyphenyl hydrazone (FCCP).
166 ted by the CB1R antagonist rimonabant and Gi uncoupler pertussis toxin, and absent in Cnr1(-/-) RGCs.
167 , cells were pretreated with a mitochondrial uncoupler prior to EGF stimulation.
168 revealed by preincubation with mitochondrial uncouplers prior to ATP treatment.
169 as substantially lower in the presence of an uncoupler (Q(10) = 1.61) than its absence (Q(10) = 2.08)
170 mparison, the neuronal-specific gap junction uncouplers quinine (250 microM) and mefloquine (500 nM)
171 DNP)-treated (protonophore and mitochondrial uncoupler) rats.
172                                              Uncouplers reduced pHi by 0.1 unit.
173                                The effect of uncoupler reflects the collapse of an opposing potential
174 will review the small molecule mitochondrial uncouplers reported to date and explore their potential
175 s that target the proton motive force (PMF), uncouplers, represent one possible class of compounds th
176 ucers and blockers can be distinguished from uncouplers, respiratory inhibitors, and blockers of Ca(2
177     ATP depletion induced by a mitochondrial uncoupler resulted in similar alterations even in the pr
178                                          The uncouplers S13 and dinitrophenol showed that NarK2 was n
179 s indicate that the relative contribution of uncoupler-sensitive mitochondrial hydrogen peroxide prod
180  mitochondrial polarization, as indicated by uncoupler-sensitive quenching of the red TMRM fluorescen
181                             Secondly, it was uncoupler-sensitive, and thus triggered by the DeltapH a
182 reas the maximal rate of electron transport (uncoupler-stimulated respiration) was inhibited by appro
183 GFP channels exhibit slow gating by chemical uncouplers such as CO(2) and alkanols.
184 olated rod photoreceptors with the G protein uncoupler suramin or pertussis toxin, which inactivates
185 e, we show that SR4 is a novel mitochondrial uncoupler that causes dose-dependent increase in mitocho
186 onyl cyanide m-chlorophenyl), a protonophore uncoupler that decreases mitochondrial Ca2+ uptake, decr
187          We also show the use of respiratory uncouplers to simulate ischemia in the single myocyte an
188 ve relied on high concentrations of chemical uncouplers to trigger mitochondrial depolarization, a st
189 zone (FCCP), a mitochondrial proton gradient uncoupler, to release mitochondrial free calcium ([Ca2+]
190                 Small molecule mitochondrial uncouplers transport protons from the mitochondrial inne
191                     Possible cytotoxicity by uncoupler treatment was evaluated by caspase 3/7 activit
192 rkin, combined with short-term mitochondrial uncoupler treatment, stimulates widespread mitophagy and
193  (JC-1) in the presence of substrates/ADP or uncouplers (valinomycin/carbonyl cyanide p-(trifluoromet
194 d mitochondria, no stimulation of the MPT by uncoupler was observed in the presence or absence of thi
195  alternative explanations for the effects of uncouplers were evaluated: (a) the 'back-pressure' of th
196    Thus, a new class of V-ATPase inhibitors (uncouplers), which are not simply ionophores, provided n
197                                Mitochondrial uncouplers, which reduce the proton gradient across the
198                      In the latter case, the uncouplers would decrease the RC time constant for membr

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