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1 retained a normal KCNQ4 current and resting membrane potential.
2 ed voltages and increased I (NaP) at resting membrane potential.
3 glutamate into synaptic vesicles, driven by membrane potential.
4 ative phosphorylation coupling efficiency or membrane potential.
5 ubsequent step involving the electrochemical membrane potential.
6 h signalling through their effects on plasma membrane potential.
7 ATPase (NKA), the ion channel that maintains membrane potential.
8 ptake, but rather directly from dysregulated membrane potential.
9 uptake, without affecting the mitochondrial membrane potential.
10 e lipid II flippase activity that depends on membrane potential.
11 ygen species and protected the mitochondrial membrane potential.
12 cycle (TCA), and have abnormal mitochondrial membrane potential.
13 in real-time (every 50 us) based on myocyte membrane potential.
14 ssociated EET current leads to more negative membrane potential.
15 nces governing the dynamics of sub-threshold membrane potential.
16 nse dynamics are due to the shift in resting membrane potential.
17 signal cascade is direct action on the cell membrane potential.
18 ess and disturbances caused to mitochondrial membrane potential.
19 dent ion channels in response to a change in membrane potential.
20 burst when depolarized from a hyperpolarized membrane potential.
21 ples changes in intracellular nucleotides to membrane potential.
22 onsistent with this, decreased mitochondrial membrane potential.
23 ward the maintenance of normal mitochondrial membrane potential.
24 e single-cell time-dynamics of mitochondrial membrane potential.
25 ation and move at slower timescales than the membrane potential.
26 et, inserting into a membrane and disrupting membrane potential.
27 varying voltages 0-80 mV positive to resting membrane potential.
28 lectivity of the hair cell by modulating its membrane potential.
29 nner consistent with a temperature dependent membrane potential.
30 oxygen species generation and mitochondrial membrane potentials.
31 lar respiratory activities and mitochondrial membrane potentials.
32 esterol concentration and intrinsic electric membrane potentials.
33 xpectedly enhanced LTCC opening at polarized membrane potentials.
34 a(v) activity is shifted to more-depolarized membrane potentials.
36 rexpressing ACE have increased mitochondrial membrane potential (24% higher), ATP production rates (2
37 urrents activate at unprecedentedly negative membrane potentials (-60 mV) even in the absence of intr
38 ncentrations of drug decreased mitochondrial membrane potential, a phenotype that was stably altered
39 de of tonic current generated at depolarized membrane potential-a property associated with outward re
40 odeling deficits and decreased mitochondrial membrane potential; a subset had increased resting mitoc
42 epolarization conducts to SMCs, depolarizing membrane potential, activating L-type Ca(2+) channels an
43 f voltage-gated Ca(2+) channels near resting membrane potentials, activation of NMDA receptors in the
44 chemical probes that regulate mitochondrial membrane potential, adenosine 5'-triphosphate contents,
45 like manner to MB, can restore mitochondrial membrane potential after depolarization with rotenone.
47 etically favourable in TbAQP2, driven by the membrane potential, although aquaporins are normally str
48 ncreased Ca(2+) influx closer to the resting membrane potential, an effect recapitulated by Abeta(1-4
49 ase (NKA) complex is the master regulator of membrane potential and a target for anti-cancer therapie
50 lasma membrane permeability, reduced resting membrane potential and accelerated protein catabolism.
51 AMD1 depletion induced loss of mitochondrial membrane potential and accumulation of reactive oxygen s
52 not significant, differences in the resting membrane potential and action potential characteristics
54 n velocity primarily by altering the resting membrane potential and are associated with significant m
56 ative strategy that merges ultrafast optical membrane potential and Ca(2+) measurements, pharmacologi
57 ent DNA nanodevice that reports the absolute membrane potential and can be targeted to organelles in
61 ncy, together with compromised mitochondrial membrane potential and elevated oxidative stress, result
62 loop that restrains the excitatory effect on membrane potential and firing activity evoked by NMDAR a
63 athy, restored cardiac myocyte mitochondrial membrane potential and flavoprotein oxidation, and preve
65 progressively shorter, and the mitochondrial membrane potential and glucose uptake become progressive
67 t1a KO hepatocytes had reduced mitochondrial membrane potential and higher mitochondrial reactive oxy
69 hNs, which likely led to depolarized resting membrane potential and increased spontaneous firing.
70 ive stress, yet exhibited high mitochondrial membrane potential and increased superoxide generation i
72 sed a transient depolarization of the plasma membrane potential and induced an imbalance of intracell
74 f this current and contribute to the resting membrane potential and intrinsic properties of developin
75 n, synaptic vesicle transport, regulation of membrane potential and lipid biosynthesis increased.
80 e worms significantly improved mitochondrial membrane potential and oxidative stress, with correspond
82 ransport chain from NADH to O(2) generates a membrane potential and pH gradient of protons that can e
84 g cancer mouse model had lower mitochondrial membrane potential and reduced mitochondrial functionali
85 y play a crucial role in setting the resting membrane potential and regulating cellular excitability.
86 lycolysis is required to maintain the plasma membrane potential and that plasma membrane depolarizati
87 channels controlling the myometrial resting membrane potential and the mechanism of transition to a
88 ky integrator, where the input signal is the membrane potential and the output is the occupancy of a
89 cient VSMCs exhibited more polarized resting membrane potentials and higher protein kinase B (Akt) ac
90 but are constitutively open at physiological membrane potentials and modulated by calmodulin (CaM) in
91 individual mitochondrion can have disparate membrane potentials and that interventions causing acute
92 ochondrial-encoded proteins, respiration and membrane potential, and an increase of reactive oxygen s
93 atory responses, redox charge, mitochondrial membrane potential, and electron leak, we found minimal
96 en consumption, increased fission, decreased membrane potential, and increased expression of the mito
97 s iron metabolism, depolarizes mitochondrial membrane potential, and induces cell death specifically
98 PP was sufficient to reduce OXPHOS capacity, membrane potential, and promoted mitochondrial fission.
99 in ROS production, decrease of mitochondrial membrane potential, and proteasome activity modulation,
100 between inorganic ion distribution, resting membrane potential, and the DeltaG' of ATP hydrolysis: a
101 which differ in their morphology, mobility, membrane potential, and vicinity to other organelles.
102 th interferes with local ionic environments, membrane potentials, and transepithelial potentials, res
104 bioenergetics measurements and mitochondrial membrane potential- and redox-sensitive dyes are used to
105 lity grows as a smooth nonlinear function of membrane potential; and (2) a "population" framework, wh
106 o address these limitations, we use the cell membrane potential as a bioenergetic indicator of EET by
107 ar reactive oxygen species and mitochondrial membrane potential as well as microscopy (confocal laser
108 ptical method for observing rapid changes in membrane potential at temporal resolutions of ~25 ns.
109 variables such as respiration, mitochondrial membrane potential, buffer calcium, and substrate effect
110 -450a overexpression decreased mitochondrial membrane potential but increased glucose uptake and viab
111 t, in male myocytes, Kv2.1 channels regulate membrane potential but not Ca(V)1.2 channel clustering.
112 s with sex: in males, Kv2.1 channels control membrane potential but, in female myocytes, Kv2.1 plays
114 onal significance of regulation of dendritic membrane potential by the sodium-leak channel complex, a
115 calcium, prevented the loss of mitochondrial membrane potential (by 70%-80%), and resulted in a 40%-5
116 otential and to subthreshold fluctuations in membrane potential can also modulate excitability in imp
117 -of-the-art VoltageFluor-type dye respond to membrane potential changes in a similar manner to the pa
120 d to kinetic data on cGMP activity and early membrane potential changes measured in bulk cell populat
121 The calcium deficit was related to resting membrane potential changes that led to abnormal inactiva
123 ibition, synaptically driven fluctuations in membrane potential, changes in cellular conductance and
124 E/CFS CD8+ T cells had reduced mitochondrial membrane potential compared with those from healthy cont
125 dly adapting currents that did not depend on membrane potential, confirming that fast adaptation does
126 reverse-mode H(+) transport depended on the membrane potential, cytosolic P(i) concentration, and ma
127 ce of SCI (chronic depolarization of resting membrane potential) decrease sensitivity to opioid-media
128 l blocker nimodipine could hyperpolarize the membrane potential, decrease the spontaneous activity, a
129 g Delta9-THC showed a hyperpolarized resting membrane potential, decreased spontaneous firing rate, i
130 e dehydrogenase, Rhes disrupts mitochondrial membrane potential (DeltaPsi (m) ) and promotes excessiv
132 Additionally, 1-6 disrupt mitochondrial membrane potential (DeltaPsi(m)) and induce oxidative st
134 ndrial ETC flux and adjust the mitochondrial membrane potential (DeltaPsi(m)), to minimize reactive o
136 r the generation and maintenance of a normal membrane potential (DeltaPsi) across the inner mitochond
137 nels in the thylakoid membrane dissipate the membrane potential (Deltapsi) component to allow for a h
138 (ITC) results, we propose that the bacterial membrane potential (Deltapsi) is possibly an underestima
140 H 5.0 to 9.0 in the absence or presence of a membrane potential (DeltaPsi, interior positive), and th
142 ssment indicated reduced inner mitochondrial membrane potential (DeltaPsim) and metabolic plasticity
147 a; either possessing a previously undetected membrane potential-dependent firing or regular firing ph
148 back to NADPH by activation of mitochondrial membrane potential-dependent nicotinamide nucleotide tra
149 al defects including collapsed mitochondrial membrane potential, dissipated ATP production, and eleva
150 at S phase, depolarization of mitochondrial membrane potential, down-regulation of Bcl-2 expression
152 ugh their preference for certain patterns of membrane potential due to their intrinsic properties.
153 ells, which can generate large transients in membrane potential during the propagation of action pote
155 will deepen our understanding of the role of membrane potential dynamics in the regulation of many bi
157 -electronics, including electronic assays of membrane potential dynamics, nano-electronic actuation o
162 drugs on epithelial TREK-1 currents, plasma membrane potential (Em), and intracellular Ca(2+) (iCa)
163 ross the membrane, contributing to the cross-membrane potential essential for a myriad of cellular ac
164 lysosomal membranes, where it establishes a membrane potential essential for lysosomal function and
165 uoles from Arabidopsis sense and control the membrane potential essentially via the K(+)-permeable TP
166 ounterbalanced by a high mitochondrial inner membrane potential, even under conditions of severe mito
167 ing the last three decades, the subthreshold membrane potential events that cause changes in dopamine
168 bining high-resolution optical recordings of membrane potential, exocytosis, and Ca(2+) in cultured h
169 in synaptic inputs activation, subthreshold membrane potential fluctuations, and output spike trains
170 rupture occurred after loss of mitochondrial membrane potential, followed by entry of bile, cell deat
171 , +100 mV depolarisation relative to resting membrane potential following 40 mV hyperpolarising prepu
172 A technology that simultaneously records membrane potential from multiple neurons in behaving ani
173 action causes a hyperpolarizing shift of the membrane potential from resting value, mediated by an in
174 ies subpopulations of neutrophils where cell-membrane potential functions as a rheostat to modulate t
175 Ca(2+) uptake is driven by the sizable inner-membrane potential generated by the electron-transport c
176 te that the distance-dependent mitochondrial membrane potential gradient exists in vivo in mice.
177 tain oxidative phosphorylation by creating a membrane potential gradient that is generated by the ele
179 ferent tissues with widely different resting membrane potentials has been shown to be equal to the Ne
181 l potassium conductance, a more negative DCT membrane potential, higher expression of phosphorylated
182 cysteine deprivation leads to mitochondrial membrane potential hyperpolarization and lipid peroxide
183 transfer chain (ETC) mitigated mitochondrial membrane potential hyperpolarization, lipid peroxide acc
184 ptic depolarisation and irreversible loss of membrane potential in CA1 neurons from diseased animals
185 ptic depolarisation and irreversible loss of membrane potential in CA1 neurons from diseased animals
186 ptic depolarisation and irreversible loss of membrane potential in CA1 neurons from diseased animals
191 ularity, as well as depolarizing the resting membrane potential in mHb ChNs in control-sleep mice.
193 ochondrial redox state and the mitochondrial membrane potential in mice of both sexes with geneticall
196 harmaceutical agents decreased mitochondrial membrane potential in porcine fetal fibroblasts, the num
197 These findings highlight the importance of membrane potential in regulating cell physiology and gro
201 ion of UQCRH in KMRC2 restored mitochondrial membrane potential, increased oxygen consumption, and at
202 r rate of O(2) uptake, loss of mitochondrial membrane potential, increased reactive oxygen species (R
205 rove that light driven perturbations of cell membrane potential induce homeostatic reactions and modu
206 m by which they transform an electrochemical membrane potential into biologically useful chemical ene
207 on channel activation in mammalian cells and membrane potential is an early indicator of control of t
208 ed this view, and we now know that bacterial membrane potential is dynamic and plays signaling roles
210 e capacity of this H(+) pump to recharge the membrane potential is rooted in its voltage- and pH-depe
211 xpand our understanding of how modulation of membrane potential is used as a mechanism of development
214 ttenuates OXPHOS and collapses mitochondrial membrane potential leading to cell death or senescence.
215 reveals that reduction in the mitochondrial membrane potential leads to significant decreases in bot
217 anges in mitochondrial activity with reduced membrane potential, low ATP production, and high lactate
221 Mathematical formulations of mitochondrial membrane potential, mitochondrial Ca(2+) cycling, mitoch
223 encing (RNA-seq), we show that mitochondrial membrane potential (MMP) distinguishes quiescent from cy
225 Numerical simulation suggests a change in membrane potential of - 15-20 mV mimics altering tempera
226 found that NPY signaling hyperpolarized the membrane potential of a subset of excitatory IC neurons
228 a(2+) transient firing regulated the resting membrane potential of colonic tissues as a specific Ano1
229 segments of mitochondria and can rescue the membrane potential of damaged mitochondria by ER-associa
231 cellular potassium concentration affects the membrane potential of neurons, and, thus, neuronal activ
233 n voltage-dependent K(+) currents or resting membrane potential of UBSM cells, suggesting that these
234 r in obesity and suggest that hyperpolarized membrane potential of, and potentiated inhibitory inputs
237 d with intercellular heterogeneity of plasma membrane potential or the phases of the cell cycle.
238 t on orchestrated fluctuations in the plasma membrane potential or voltage, which are mediated via th
240 for maintaining highly stereotyped infraslow membrane potential oscillations of dopamine ARC neurons.
241 e of lactation, TIDA neurons shift to faster membrane potential oscillations, a reconfiguration that
242 entation of neuron and field to estimate the membrane potential perturbation in pyramidal cells.
243 an important role in regulating cell volume, membrane potential, pH, secretion, and the reversal pote
244 uitinates proteins on mitochondria that lost membrane potential, promoting the elimination of damaged
246 radiol reduced both potassium current in the membrane potential range typically achieved during respo
247 ride and thereby neuronal parameters such as membrane potential rather than acting as a presynaptic g
248 erturbations in mitochondrial morphology and membrane potential, reduced ATP production, and increase
249 es (ROS) activities, increased mitochondrial membrane potential, reduced calcium levels, and also hig
251 e mitochondria decreased mitochondrial mass, membrane potential, respiration, and electron transport
252 increases synaptic activity that depolarizes membrane potential responses at the behaviorally relevan
254 tivity and chronic depolarization of resting membrane potential (RMP) that is maintained by cAMP sign
256 We identified a repertoire of subthreshold membrane potential signatures associated with distinct i
257 ical and non-canonical Wnt pathways regulate membrane potential signifying a very early event in the
258 iently alleviated when comparable changes in membrane potential simultaneously occur in each of the c
261 rmore, mutant pollen tubes had less negative membrane potentials, substantiating a mechanistic role f
262 a stable protein which impacts mitochondrial membrane potential, suggesting a potential third coding
263 reveal a primary functional role for resting membrane potential taking place within the first 3 h aft
264 +)/NADH is caused by increased mitochondrial membrane potential that impairs mitochondrial electron t
265 rods lacking CNG channels exhibit a resting membrane potential that was ~10 mV hyperpolarized compar
267 ibutes to setting the hair cell and afferent membrane potentials; the potassium efflux from type I ha
268 er conduction by hyperpolarizing the resting membrane potential, thereby increasing Na(+) channel ava
269 n potential threshold and a more depolarized membrane potential, thus reducing membrane excitability.
270 ow electrical currents underlying changes in membrane potential to leak to 'coupled' partners, dampen
271 espiratory complexes, these cells generate a membrane potential to support uptake of calcium into the
272 introduce basic biophysical theories of the membrane potential to the microbiology community and dis
273 and phospholipid membranes in the absence of membrane potential, toxins that bind VSD and modulate th
274 riguing connection between ribosomes and the membrane potential, two fundamental properties of cells.
275 s hyperpolarized with respect to the resting membrane potential, type-1 metabotropic glutamate recept
276 propose maintains intermediate mitochondrial membrane potentials under physiologic conditions, thus m
277 ll patch clamp experiments and assessment of membrane potential using the slow voltage-sensitive dye
279 ensitive dye (VSD) imaging, which visualizes membrane potential variations in the CN and its branches
283 tained locomotion periods, cortical neuronal membrane potential was at its most depolarized and least
284 e TSPAN-7 KD also enhanced Ca(2+) entry when membrane potential was clamped with depolarization, the
286 Surprisingly, a high mitochondrial inner membrane potential was maintained in MitoPark SNc DaNs.
287 try, Western blotting, and patch clamping of membrane potentials was performed to evaluate the molecu
289 chain (ETC) complex I, IV, V activities, and membrane potential were performed in the ventrolateral m
291 a-CEL16&28 had depolarized the mitochondrial membrane potential, whereas Abeta-CEL16 had increased mi
292 ry electron transfer and establishing strong membrane potential, which is key to biofilm matrix produ
293 ells, the NKA generates the negative resting membrane potential, which is the basis for almost all as
294 properties, including depolarization of the membrane potential while simultaneously decreasing actio
295 imals maintained a more normal mitochondrial membrane potential while those isolated from untreated a
296 vo Furthermore, we show that dissipating the membrane potential with an ionophore decreases the preva
297 itative model to associate the mitochondrial membrane potential with the key pharmacokinetic paramete
298 is unaffected by collapsing the mitochondria membrane potential with the uncoupler carbonyl cyanide m
299 eration, and a 50% decrease in mitochondrial membrane potentials with respect to equivalent concentra
300 oxidative stress and decreased mitochondrial membrane potential, with higher mtDNA release in brain a