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1 aedalus (Daed), that is located on the outer mitochondrial membrane.
2 ondria and binds to cardiolipin in the inner mitochondrial membrane.
3 ase that regulates mPTP opening in the inner mitochondrial membrane.
4 elease of a proton gradient across the inner mitochondrial membrane.
5 enables colocalization with HK1 on the outer mitochondrial membrane.
6 d the correct distribution of cristae on the mitochondrial membrane.
7 C) is a major transport protein of the inner mitochondrial membrane.
8 tion of subunits of the translocase of outer mitochondrial membrane.
9 nd is consistently associated with the inner mitochondrial membrane.
10 bind either to the plasma membrane or to the mitochondrial membrane.
11 otenoid cleavage enzyme located in the inner mitochondrial membrane.
12 ize precursor translocation across the inner mitochondrial membrane.
13 n of mislocalized TA proteins from the outer mitochondrial membrane.
14 synthesis during erythropoiesis at the outer mitochondrial membrane.
15 energize precursor passage across the inner mitochondrial membrane.
16 in 1) and its receptor proteins on the outer mitochondrial membrane.
17 As, and other signaling enzymes to the outer mitochondrial membrane.
18 that we found was associated with the inner mitochondrial membrane.
19 th the phospholipid cardiolipin in the inner mitochondrial membrane.
20 cies by modulating the fluidity of the inner mitochondrial membrane.
21 latory mechanisms on both sides of the inner mitochondrial membrane.
22 a Ca(2+)-selective ion channel in the inner mitochondrial membrane.
23 dria by ubiquitinating proteins on the outer mitochondrial membrane.
24 f the elongating mitoribosome onto the inner-mitochondrial membrane.
25 ssociated with protein crowding in the inner mitochondrial membrane.
26 duced further hyperpolarization of the inner mitochondrial membrane.
27 l-1 and Bok predominantly takes place at the mitochondrial membrane.
28 ce quinone, while pumping protons across the mitochondrial membrane.
29 reduction of O(2) by complex IV in the inner mitochondrial membrane.
30 tion modulates the biophysical properties of mitochondrial membranes.
31 olipin (CL) is the signature phospholipid of mitochondrial membranes.
32 r systems that mimic the major components of mitochondrial membranes.
33 an altered lipid composition of both MAM and mitochondrial membranes.
34 erize and heterooligomerize in bacterial and mitochondrial membranes.
35 rate of ADP or ATP translocation across the mitochondrial membranes.
36 s of dynamic interactions between the ER and mitochondrial membranes.
37 inases I and II and creatine kinase bound to mitochondrial membranes.
38 compound SS-31 (elamipretide) with model and mitochondrial membranes.
39 the surface electrostatics of both model and mitochondrial membranes.
40 SPO), an activated glial marker expressed on mitochondrial membranes.
41 correcting for variable permeabilization of mitochondrial membranes.
43 stem 60-kD subunit, the translocase of outer mitochondrial membrane 40-kD subunit (TOM40), the TOM20s
44 ctional receptors in MAMs vs. the rest of ER/mitochondrial membranes, a parameter called the channel
45 t an atomic model of a substrate-bound inner mitochondrial membrane AAA+ quality control protease in
47 ial Rho (Miro) GTPases localize to the outer mitochondrial membrane and are essential machinery for t
48 icantly prevents maspin binding to the inner mitochondrial membrane and decreases cytochrome c releas
50 annelrhodopsin-2 fusion protein to the inner mitochondrial membrane and formation of functional catio
51 pin (CL), binds to transporters of the inner mitochondrial membrane and plays a central role in forma
52 is dependent upon MAO anchoring to the outer mitochondrial membrane and shuttling electrons through t
53 KA) and other signaling enzymes at the outer mitochondrial membrane and thereby controls mitochondria
54 the mitochondria by clustering on the outer mitochondrial membrane and thereby permeabilizing it.
55 may be responsible for release of cyt c from mitochondrial membranes and ensuing inactivation of its
57 to ensure the concerted transport of the two mitochondrial membranes and the correct distribution of
58 TcAPx-CcP was found closely associated with mitochondrial membranes and, most interestingly, with th
59 ependent on the proton gradient of the inner mitochondrial membrane, and it inhibits the activity of
60 we show that MDR-1 is present in the oocyte mitochondrial membrane, and it protects the female gamet
61 zed tail-anchored (TA) proteins of the outer mitochondrial membrane are cleared by a newly identified
63 ences in cardiolipin content between the two mitochondrial membranes, as well as dynamic fluctuations
65 and proteomic analysis, we showed that human mitochondrial membrane ATP synthase subunit O is an intr
66 AKAP1-PKA "signaling islands" from the outer mitochondrial membrane augments progression toward metas
67 ondrial disorders and are believed to target mitochondrial membranes because they are enriched in the
69 diolipin on the concave surface of the inner mitochondrial membrane, before oxidizing the lipid and i
72 subunits of succinate dehydrogenase (SDH), a mitochondrial membrane-bound enzyme complex that is invo
73 of the Golgi complex, peroxisomes, and outer mitochondrial membrane, but only detect very low steady-
74 trafficked normally to plasma, nuclear, and mitochondrial membranes, but caused reduced neurite outg
75 these proteins via its BH3 domain and to the mitochondrial membrane by a carboxyl-terminal sequence (
77 chain, translocates protons across the inner mitochondrial membrane by harnessing the free energy gen
79 t sites was modulated by the outer and inner mitochondrial membrane channels, voltage-dependent anion
80 hat the Mcl-1 TMD forms homooligomers in the mitochondrial membrane, competes with full-length Mcl-1
83 ysosomes precedes membrane permeabilisation, mitochondrial membrane depolarisation and caspase indepe
84 o safeguard mechanisms, induced by transient mitochondrial membrane depolarization and activation of
85 ibited mitochondrial respiration and induced mitochondrial membrane depolarization and apoptosis in a
86 LL-rearranged leukemia cells did not undergo mitochondrial membrane depolarization or apoptosis despi
87 affected mitochondrial respiration, elicited mitochondrial membrane depolarization, and disrupted mit
88 n tumor cell killing, caspase activation, or mitochondrial membrane dissipation by DOX, in human canc
90 PINK1 that fails to accumulate at the outer mitochondrial membrane, either by mutagenesis of this ne
91 Cardiolipin is a phospholipid of the inner mitochondrial membrane essential for the function of num
92 interacts with phospholipids, reducing inner mitochondrial membrane fluidity and the mobility of free
93 e we record AAC currents directly from inner mitochondrial membranes from various mouse tissues and i
94 es mitofusin 2, a membrane-bound mediator of mitochondrial membrane fusion and inter-organelle commun
95 tochondrial functions, including metabolism, mitochondrial membrane fusion and/or fission dynamics, a
97 In this study we report that MxB is an inner mitochondrial membrane GTPase that plays an important ro
99 xylic acid (TCA) cycle enzymes, which led to mitochondrial membrane hyperpolarization and increased r
103 equires division of both the inner and outer mitochondrial membranes (IMM and OMM, respectively).
104 Phospholipids are vital constituents of mitochondrial membranes, impacting the plethora of funct
105 Put6 and Put7 are tethered to the inner mitochondrial membrane in a large hetero-oligomeric comp
106 the disorganization of the cristae and inner mitochondrial membrane in several cancer cells and tumor
107 al claim that proteins ejected directly from mitochondrial membranes in our study are degraded, are i
110 -protein complex whose assembly in the inner mitochondrial membrane is facilitated by the scaffold fa
111 embrane protein primarily found in the outer mitochondrial membrane, is evolutionarily conserved and
112 diolipin (CL), the signature phospholipid of mitochondrial membranes, is important for cardiovascular
113 nsition pore, a nonspecific channel in inner mitochondrial membranes, is triggered by an elevated tot
114 ate a large conductance channel in the inner mitochondrial membrane known as the PTP (permeability tr
116 rusion by cation exchangers across the inner mitochondrial membrane may define the threshold; however
117 ine to phosphatidylethanolamine in the inner mitochondrial membrane, must undergo an autocatalytic se
118 Cardiolipin is an anionic lipid found in the mitochondrial membranes of eukaryotes ranging from unice
120 we report that mitoNEET regulates the outer-mitochondrial membrane (OMM) protein voltage-dependent a
122 ansmembrane beta-barrels of eukaryotic outer mitochondrial membranes (OMMs) are major channels of com
123 m in yeast by re-directing Psd1 to the outer mitochondrial membrane or the endomembrane system and sh
125 brogation of necrotic cell death mediated by mitochondrial membrane permeability transition, and open
126 eased production of reactive oxygen species, mitochondrial membrane permeability, and mitochondrial m
128 s of phosphatidylcholine (PC), a predominant mitochondrial membrane phospholipid, suggesting that the
129 acrophages overexpressing ACE have increased mitochondrial membrane potential (24% higher), ATP produ
130 mitochondria relies on maintaining the inner mitochondrial membrane potential (also known as DeltaPsi
131 in cytosolic calcium, prevented the loss of mitochondrial membrane potential (by 70%-80%), and resul
132 or of succinate dehydrogenase, Rhes disrupts mitochondrial membrane potential (DeltaPsi (m) ) and pro
135 ndrial mass, and live microscopic imaging of mitochondrial membrane potential (DeltaPsi(m)) and optic
136 owed a reduction in intact cell respiration, mitochondrial membrane potential (DeltaPsi(m)), ROS prod
137 gulate mitochondrial ETC flux and adjust the mitochondrial membrane potential (DeltaPsi(m)), to minim
141 egy enables a light-dependent control of the mitochondrial membrane potential (Deltapsim) and coupled
142 chondrial assessment indicated reduced inner mitochondrial membrane potential (DeltaPsim) and metabol
144 , sorafenib induces rapid dissipation of the mitochondrial membrane potential (DeltaPsim) that is acc
149 -cell RNA sequencing (RNA-seq), we show that mitochondrial membrane potential (MMP) distinguishes qui
150 ll MFGMs treatment significantly reduced the mitochondrial membrane potential (with an order of goat
152 he MB-gCs, in like manner to MB, can restore mitochondrial membrane potential after depolarization wi
153 -induced mild uncoupling is shown to protect mitochondrial membrane potential against FA-induced unco
154 hanistically, AMD1 depletion induced loss of mitochondrial membrane potential and accumulation of rea
155 chondrial structural rearrangements, loss of mitochondrial membrane potential and activation of mitop
157 ive oxygen species production, and decreased mitochondrial membrane potential and depolarization thre
158 TCA cycle metabolites, as well as decreased mitochondrial membrane potential and deranged mitochondr
159 energy deficiency, together with compromised mitochondrial membrane potential and elevated oxidative
160 hed cardiomyopathy, restored cardiac myocyte mitochondrial membrane potential and flavoprotein oxidat
161 olic activity was assessed as alterations in mitochondrial membrane potential and flavoprotein oxidat
162 etime becomes progressively shorter, and the mitochondrial membrane potential and glucose uptake beco
165 Activation of PPAR-gamma partially restored mitochondrial membrane potential and IFN-gamma productio
166 impaired mitochondrial respiration, loss of mitochondrial membrane potential and increased productio
167 tive or oxidative stress, yet exhibited high mitochondrial membrane potential and increased superoxid
169 itochondrial DNA, and a similar reduction in mitochondrial membrane potential and NDUFA9 protein abun
170 se invertebrate worms significantly improved mitochondrial membrane potential and oxidative stress, w
172 ochthonous lung cancer mouse model had lower mitochondrial membrane potential and reduced mitochondri
173 chondrial unfolded protein response, loss of mitochondrial membrane potential and sensitivity to mito
174 show that, while loss of Ucp2 does increase mitochondrial membrane potential and the production of r
176 of intracellular reactive oxygen species and mitochondrial membrane potential as well as microscopy (
177 ithdrawal, miR-450a overexpression decreased mitochondrial membrane potential but increased glucose u
178 cal in this quality-control process: loss of mitochondrial membrane potential causes PINK1 to accumul
179 e found that ME/CFS CD8+ T cells had reduced mitochondrial membrane potential compared with those fro
181 , we demonstrate that the distance-dependent mitochondrial membrane potential gradient exists in vivo
182 chanistically, cysteine deprivation leads to mitochondrial membrane potential hyperpolarization and l
183 e or electron transfer chain (ETC) mitigated mitochondrial membrane potential hyperpolarization, lipi
184 using PET imaging of (18)F-BnTP, we profile mitochondrial membrane potential in autochthonous mouse
185 omena were accompanied by increased synaptic mitochondrial membrane potential in both wt and Tg2576 m
186 ent of mitochondrial transport and protected mitochondrial membrane potential in cultured sensory neu
187 cal regions, (2) identifying regions of high mitochondrial membrane potential in live animals, (3) mo
189 alyzed the mitochondrial redox state and the mitochondrial membrane potential in mice of both sexes w
190 itochondrial function revealed a decrease in mitochondrial membrane potential in mutant Hsp27 express
192 eased mitochondrial NADH levels and restored mitochondrial membrane potential in p62-deficient cells.
193 also found that PA stimulation decreased the mitochondrial membrane potential in podocytes and induce
194 While the pharmaceutical agents decreased mitochondrial membrane potential in porcine fetal fibrob
195 able to record neuronal Ca(2+) responses and mitochondrial membrane potential in these nerve tissues.
199 on of COX6B2 attenuates OXPHOS and collapses mitochondrial membrane potential leading to cell death o
201 The model reveals that reduction in the mitochondrial membrane potential leads to significant de
202 andard chemotherapeutics sensitized cells to mitochondrial membrane potential loss and apoptosis.
203 asmic volume control, absence of significant mitochondrial membrane potential loss, and lack of activ
205 ds: Cardiac uptake and response to decreased mitochondrial membrane potential of (18)F-MitoPhos and (
208 ROS scavenging assays, wound healing assays, mitochondrial membrane potential readings, corneal fluor
210 change in NAD(+)/NADH is caused by increased mitochondrial membrane potential that impairs mitochondr
211 Treated lymphoma cells exhibited a reduced mitochondrial membrane potential that resulted in an irr
214 min treated animals maintained a more normal mitochondrial membrane potential while those isolated fr
215 n, accumulation of complex IV, and increased mitochondrial membrane potential with no change in mitoc
216 ablish a quantitative model to associate the mitochondrial membrane potential with the key pharmacoki
217 s with high concentrations of drug decreased mitochondrial membrane potential, a phenotype that was s
218 in mitochondrial respiration, impairment in mitochondrial membrane potential, aberrant mitochondrial
219 ion identified chemical probes that regulate mitochondrial membrane potential, adenosine 5'-triphosph
220 nt mitochondrial fragmentation, reduction in mitochondrial membrane potential, and a significant loss
221 ion, altered mitochondrial motility, reduced mitochondrial membrane potential, and diminished mitocho
222 essed mitochondrial gene expression, reduced mitochondrial membrane potential, and diminished oxygen
223 vities, respiratory responses, redox charge, mitochondrial membrane potential, and electron leak, we
225 ng dysregulates iron metabolism, depolarizes mitochondrial membrane potential, and induces cell death
226 is, decreasing PI3K and Akt phosphorylation, mitochondrial membrane potential, and modulating G1-S tr
227 the increase in ROS production, decrease of mitochondrial membrane potential, and proteasome activit
228 mitochondrial variables such as respiration, mitochondrial membrane potential, buffer calcium, and su
229 ed mitochondrial defects including collapsed mitochondrial membrane potential, dissipated ATP product
230 the cell cycle at S phase, depolarization of mitochondrial membrane potential, down-regulation of Bcl
232 ic overexpression of UQCRH in KMRC2 restored mitochondrial membrane potential, increased oxygen consu
233 hibited a lower rate of O(2) uptake, loss of mitochondrial membrane potential, increased reactive oxy
234 that is, they damage nuclear DNA, reduce the mitochondrial membrane potential, induce the epigenetic
235 take was TRPV1-dependent, dissipation of the mitochondrial membrane potential, inhibition of the mito
237 e oxygen species (ROS) activities, increased mitochondrial membrane potential, reduced calcium levels
238 ranslational modifications: respiration, the mitochondrial membrane potential, ROS, and apoptosis.
239 ssed produces a stable protein which impacts mitochondrial membrane potential, suggesting a potential
240 derived VCP mutant fibroblasts exhibit lower mitochondrial membrane potential, uncoupled respiration,
241 estingly, Abeta-CEL16&28 had depolarized the mitochondrial membrane potential, whereas Abeta-CEL16 ha
242 mitochondrial oxidative stress and decreased mitochondrial membrane potential, with higher mtDNA rele
243 tive imaging, bioenergetics measurements and mitochondrial membrane potential- and redox-sensitive dy
244 +) is reduced back to NADPH by activation of mitochondrial membrane potential-dependent nicotinamide
257 metabolic remodeling deficits and decreased mitochondrial membrane potential; a subset had increased
258 ase, which we propose maintains intermediate mitochondrial membrane potentials under physiologic cond
259 2-fold ROS generation, and a 50% decrease in mitochondrial membrane potentials with respect to equiva
262 ific targeting of Arf6 to plasma membrane or mitochondrial membranes promotes recruitment and colocal
263 ndrial Ca(2+) uptake is mediated by an inner mitochondrial membrane protein called the mitochondrial
264 Succinate dehydrogenase (SDH) is an inner mitochondrial membrane protein complex that links the Kr
269 ) myoblasts, and a significant enrichment of mitochondrial membrane proteins among proteins showing a
270 ctional and structural requirement of CL for mitochondrial membrane proteins has been studied in vitr
271 Mitochondrial density and the abundance of mitochondrial membrane proteins in skeletal muscle incre
273 teins into soluble, peripheral, and integral mitochondrial membrane proteins, and the assignment of 8
275 ked to Fragile-X syndrome elevates the inner mitochondrial membrane proton leak, leading to increased
276 we show that GSDME-N also permeabilizes the mitochondrial membrane, releasing cytochrome c and activ
278 D multisubunit channel residing in the inner mitochondrial membrane required for mitochondrial Ca(2+)
282 ciated X apoptosis regulator (BAX), an outer mitochondrial membrane-targeting pro-apoptotic protein,
283 ndently of one another to sites on the inner mitochondrial membrane that are in proximity to contact
284 ghtly controlled Ca(2+) channel of the inner mitochondrial membrane that regulates cellular metabolis
285 ctivation of signaling pathways in the inner mitochondrial membrane, thereby modulating its function
286 DP prevented astrocyte loss by targeting the mitochondrial membrane to prevent the hyperoxia-induced
287 tes a hetero-oligomeric complex on the inner mitochondrial membranes to maintain crista structure.
288 how they associate with protein complexes in mitochondrial membranes to support bioenergetics and mai
290 n particular, we identify a network of inner mitochondrial membrane transporters as a hub required fo
292 s targeted to protein complexes on the inner mitochondrial membrane via affinity for cardiolipin to p
293 drial morphology, and Ca(2+) permeability of mitochondrial membrane was investigated in the presence
294 l-CoA synthetase ACSL1, and localizes to the mitochondrial membrane where it likely activates long ch
295 ukaryotic AAA+ ATPase localized to the outer mitochondrial membrane, where it is thought to extract m
296 olipin (CL) is the signature phospholipid of mitochondrial membranes, where it is synthesized locally
297 ut this form also plays a structural role on mitochondrial membranes, which is independent of phospha
298 ide a 30- to 90-nm invagination of the outer mitochondrial membrane, whose necked aperture to the cyt
299 al E3 ubiquitin ligase anchored in the outer mitochondrial membrane with its RING finger domain facin
300 Mst1/2 from the cytosol to the phagosomal or mitochondrial membrane, with ROS subsequently activating