ライフサイエンスコーパス: mitochondrial

1 We previously discovered that the mitochondrial AAA+ unfoldase ClpX promotes heme biosynth

2 tigates cold IRI-associated renal injury via mitochondrial actions and could represent a novel therap

3 Regulation of mitochondrial activity allows cells to adapt to changing

4 onstrate that Nat1 deletion promotes reduced mitochondrial activity and is associated with ectopic li

5 Several markers of decreased mitochondrial activity during prion infection have been

6 The mitochondrial adaptor molecule MAVS plays critical roles

7 investigate this disconnect, we analyzed 41 mitochondrial and 4 nuclear genomes from passenger pigeo

8 Both mitochondrial and barrier defects were largely corrected

9 Mitochondrial and enzyme defects predominate as disease-

10 vation plays a pivotal role in Abeta-induced mitochondrial and synaptic dysfunction.

11 ated pathology, oxidative stress, as well as mitochondrial and synaptic dysfunction.

12 t SS31 may confer protective effects against mitochondrial and synaptic toxicities in APP transgenic

13 1 cell-cycle arrest and subsequent intrinsic mitochondrial apoptosis and is shared by all preimmune m

14 effects culminated in the activation of the mitochondrial apoptosis pathway.

15 sfunction observed in type 1 diabetes alters mitochondrial ATP and IFNgamma production; the latter is

16 oup D2 protein (FANCD2) functionally impacts mitochondrial ATP production through its interaction wit

17 ansduction and stress responses, whereas the mitochondrial ATP synthase F0 subunit component is a vas

18 oss leads to a cell-autonomous defect in the mitochondrial B12 metabolism and that itaconyl-CoA is a

19 ctivating, substrate-analog inhibitor of the mitochondrial B12-dependent methylmalonyl-CoA mutase (MU

20 to up-regulation of lipase 3 and enzymes for mitochondrial beta-oxidation.

21 In pancreatic beta-cells, mitochondrial bioenergetics control glucose-stimulated i

22 hat it is essential for functions apart from mitochondrial bioenergetics.

23 Aged CPCs fail to activate mitochondrial biogenesis and increase proteins involved

24 nd, most notably, age-related impairments in mitochondrial biogenesis and mitochondrial function.

25 aintains mitochondrial dynamics and enhances mitochondrial biogenesis and synaptic activity in APP mi

26 Thus, DMF induces mitochondrial biogenesis primarily through its action on

27 on of toxic glucose metabolites and inducing mitochondrial biogenesis to restore mitochondrial functi

28 d is the first drug demonstrated to increase mitochondrial biogenesis with in vivo human dosing.

29 The observation that DMF stimulates mitochondrial biogenesis, gene expression and function s

30 th an increased pool of free NADH, increased mitochondrial biogenesis, triggering of the mitochondria

31 tify a novel molecular mechanism that limits mitochondrial Ca(2+) overload to prevent cell death.

32 Blocking mitochondrial Ca(2+) uniporter activity compromises the

33 )-activated Ca(2+) channel complex mediating mitochondrial Ca(2+) uptake, a process crucial for Ca(2+

34 the endoplasmic reticulum, a key mediator of mitochondrial Ca(2+) uptake.

35 In addition, treatment with the mitochondrial Ca(2+)-buffering protein parvalbumin signi

36 Long-sought transporters involved in mitochondrial calcium influx and efflux have recently be

37 in understanding the forms and quantities of mitochondrial calcium stores is needed.

38 The mitochondrial calcium uniporter (MCU) is a highly select

39 se defects can be corrected by silencing the mitochondrial calcium uniporter (MCU).

40 The mitochondrial calcium uniporter is a Ca(2+)-activated Ca

41 To obtain a unified picture of mitochondrial calcium utilization, a parallel advance in

42 erflow metabolism observed may indicate that mitochondrial catabolic capacity is a key constraint set

43 tion and morphology in NSCs, these data link mitochondrial complex function to efficient lineage prog

44 sociated with specific reduction in striatal mitochondrial Complex-I (NDUFS4) in rotenone-treated mut

45 Mitochondrial components are recognized as danger-associ

46 as compared to ZL controls, while UCP-1 and mitochondrial concentrations were significantly decrease

47 tro, acute high glucose treatment reduces ER-mitochondrial contact in retinal endothelial cells.

48 Our findings establish an elevating mitochondrial cristae density as a regulatory mechanism

49 elucidates the unexplained processing of the mitochondrial cysteine desulfurase Nfs1 in yeast.

50 o provide structure-function properties of a mitochondrial cysteine desulfurase.

51 to control excessive fission and associated mitochondrial deficits.

52 , we describe culture conditions to maintain mitochondrial-depleted cells for up to 30 d with minimal

53 nide m-chlorophenyl hydrazone (CCCP)-induced mitochondrial depolarization decreased mitochondrial mas

54 cell death in a process that was preceded by mitochondrial depolarization.

55 Mitochondrial-derived peptides (MDPs) and their analogs

56 (22%), SCA6 (14%), EA2 (13%), SPG7 (10%) and mitochondrial disease (10%).

57 The most common pediatric mitochondrial disease is Leigh syndrome, an episodic, su

58 ion suggests that it could be considered for mitochondrial disease therapy and/or therapy in muscle d

59 iagnostic work-up of patients with suspected mitochondrial disease.

60 Mitochondrial disorders affecting oxidative phosphorylat

61 ochondrial fragmentation by the treatment of mitochondrial division inhibitor 1 (mdivi-1), a mitochon

62 s key to the retromer-dependent recycling of mitochondrial DLP1 complex during mitochondrial fission

63 iasis, HAT), contains a kinetoplast with the mitochondrial DNA (kDNA), comprising of >70% AT base pai

64 To fill this gap, we analyzed ancient mitochondrial DNA (mtDNA) from Scythians of the North Po

65 In recent years mitochondrial DNA (mtDNA) has transitioned to greater pr

66 ctive oxygen species (ROS), membrane damage, mitochondrial DNA (mtDNA) integrity, morphology, phenoty

67 pyrimidine salvage pathway, is essential for mitochondrial DNA (mtDNA) maintenance.

68 This was tested using a major mitochondrial DNA (mtDNA) survey and sequencing of two n

69 ed following incubation of HOS cells lacking mitochondrial DNA (mtDNA) with functional exogenous mito

70 ation promoted excess cytosolic extrusion of mitochondrial DNA along with increased reactive oxygen s

71 ta, dated on the assumption of a "universal" mitochondrial DNA clock are not valid.

72 diation analysis estimated that decreases in mitochondrial DNA copy number, a measure of mitochondria

73 males and females; however Y chromosome and mitochondrial DNA haplogroups were not associated with a

74 hondrial respiratory capacity and release of mitochondrial DNA into the cytosol.

75 Human mitochondrial DNA is transcribed by POLRMT with the help

76 Diabetic D2 mice manifested increased mitochondrial DNA lesions (8-oxoguanine) exclusively loc

77 ad geographic range using microsatellite and mitochondrial DNA loci.

78 The m.3243A > G mitochondrial DNA mutation was originally described in p

79 NA accumulation triggers cytosolic escape of mitochondrial DNA, which engages cGAS.

80 reduces mitochondrial dysfunction, maintains mitochondrial dynamics and enhances mitochondrial biogen

81 ated in aging, but a deeper understanding of mitochondrial dynamics and mitophagy during aging is mis

82 that SLC25A46 may play an important role in mitochondrial dynamics by mediating mitochondrial fissio

83 how that a subset of SLC25A46 interacts with mitochondrial dynamics components and the MICOS complex.

84 However, reactivation of mitochondrial dynamics only occurs after transfer to ger

85 is known to participate in the regulation of mitochondrial dynamics through interaction with the mito

86 Alveolar epithelial cell (AEC) mitochondrial dysfunction and apoptosis are important in

87 higher levels of toxic glucose metabolites, mitochondrial dysfunction and apoptosis.

88 bone marrow was associated with progressive mitochondrial dysfunction and consequent exacerbation of

89 treatment reversed metabolic abnormalities, mitochondrial dysfunction and kidney pathology.

90 Fatty liver, oxidative stress, and mitochondrial dysfunction are key pathophysiological fea

91 links extracellular inflammatory signals to mitochondrial dysfunction during AKI partly via PPARGC1A

92 These findings provide a novel mechanism for mitochondrial dysfunction in lipotoxic cardiomyopathy.

93 In conclusion, intrinsic mitochondrial dysfunction observed in type 1 diabetes al

94 During sepsis and shock states, mitochondrial dysfunction occurs.

95 Among these, lipid metabolism and mitochondrial dysfunction proteins were overrepresented.

96 Glomerular endothelial mitochondrial dysfunction was associated with increased

97 microvascular dysfunction and cardiomyocyte/mitochondrial dysfunction).

98 ns and stressors, impaired immune responses, mitochondrial dysfunction, and neuroinflammation.

99 mineralization, cytoskeletal rearrangement, mitochondrial dysfunction, and reduced type 1 collagen s

100 eviates, respectively, high-fat diet-induced mitochondrial dysfunction, hepatosteatosis, and insulin

101 Interestingly, these cells exhibited mitochondrial dysfunction, indicated by reactive oxygen

102 treatment reduces Abeta production, reduces mitochondrial dysfunction, maintains mitochondrial dynam

103 3 kinase-mTOR signaling, impaired autophagy, mitochondrial dysfunction, stem cell exhaustion, epigene

104 nes, and subsequent epithelial disorders and mitochondrial dysfunction.

105 y the accumulation of protein aggregates and mitochondrial dysfunction.

106 ndling and increased oxidative stress due to mitochondrial dysfunction.

107 (mef8) line exhibited reduced editing at 38 mitochondrial editing sites and increased editing at 24

108 Thus, MEF8 has two antagonistic effects on mitochondrial editing: stimulatory, which requires a cat

109 efore the absence of MEF8 affects 11% of the mitochondrial editome.

110 These data unveil two novel mitochondrial effectors in H. pylori-host interaction wi

111 extensive glutamine utilization and impaired mitochondrial electron flow.

112 on was originally described in patients with mitochondrial encephalomyopathy, lactic acidosis, and st

113 plasma citrulline were highly suggestive of mitochondrial encephalopathy, lactic acidosis and stroke

114 The brain has the highest mitochondrial energy demand of any organ.

115 that selectively targets the altered form of mitochondrial energy metabolism in tumour cells, causing

116 athways altered in subjects with SZ involved mitochondrial energy production and the regulation of pr

117 tabolism in tumour cells, causing changes in mitochondrial enzyme activities and redox status that le

118 ed, C1qbp restored OXPHOS protein levels and mitochondrial enzyme activities in C1qbp(-/-) MEFs.

119 erturbation revealed physiological roles for mitochondrial enzyme COX10-mediated oxidative phosphoryl

120 w show that a number of enzymatically active mitochondrial enzymes associated with the TCA cycle are

121 Mitochondrial extracts derived from heterozygous Polbeta

122 ion of the 5'-adenylated BER intermediate in mitochondrial extracts.

123 llular defects that mimicked deficiencies in mitochondrial Fe-S cluster synthesis including an increa

124 cluster assembly machinery resides to mature mitochondrial Fe/S cluster-containing proteins.

125 elated proteins are dramatically affected by mitochondrial ferritin overexpression.

126 Axonal transport of mitochondria and mitochondrial fission and fusion contribute to this reju

127 cycling of mitochondrial DLP1 complex during mitochondrial fission and provide a novel therapeutic ta

128 We observed mitochondrial fission during osmotic stress, but blockin

129 ndrial dynamics through interaction with the mitochondrial fission factor Drp1 in fed cells and in au

130 ochondrial division inhibitor 1 (mdivi-1), a mitochondrial fission inhibitor.

131 Here, we show that mitochondrial fission is triggered by mechanical forces.

132 Overall, succinate promotes DRP1-mediated mitochondrial fission via GPR91, consequently stimulatin

133 ial for physiological and pathophysiological mitochondrial fission.

134 cium ([Ca(2+)]cyto), aerobic glycolysis, and mitochondrial fission.

135 role in mitochondrial dynamics by mediating mitochondrial fission.

136 Mitochondrial flux from ASMCs to T cells was partially F

137 We find that the mitochondrial form of arginase (ARG2), which hydrolyzes

138 ficance of these abnormalities, we inhibited mitochondrial fragmentation by the treatment of mitochon

139 Drp1-induced mitochondrial fragmentation prevented replication of C.

140 sildenafil that, through adverse effects on mitochondrial function and endoplasmic reticulum stress,

141 the finding of age-associated alterations in mitochondrial function and morphology in NSCs, these dat

142 neage progression of adult NSCs and identify mitochondrial function as a potential target to ameliora

143 Mechanistically, inhibition of mitochondrial function increased autophagy and decreased

144 py and/or therapy in muscle disease in which mitochondrial function is important.

145 muscarinic receptor-dependent regulation of mitochondrial function via AMPK.

146 Parameters of pancreatitis, mitochondrial function, autophagy, ER stress, and lipid

147 Although the role of CL in mitochondrial function, biogenesis, and genome stability

148 Concordantly, PDK3 knockdown improved mitochondrial function, emphasizing the role of PDK3 ina

149 impairments in mitochondrial biogenesis and mitochondrial function.

150 inducing mitochondrial biogenesis to restore mitochondrial function.

151 are mediated through alterations in hepatic mitochondrial function.

152 vitro and in vivo and effectively protected mitochondrial function.

153 g downstream oxidative damage and preserving mitochondrial function.

154 Key mitochondrial functions such as ATP production, Ca(2+) u

155 that the Mdm30-Ubp2-Rsp5 crosstalk regulates mitochondrial fusion by coordinating an intricate balanc

156 to the relevance of RNA pseudouridylation in mitochondrial gene expression.

157 ed as key post-transcriptional regulators of mitochondrial gene expression.

158 mitochondrial DNA copy number, a measure of mitochondrial genome abundance, mediated 12% of the asso

159 This is because the mitochondrial genome is placed in a novel nuclear enviro

160 lagellate Diplonema papillatum (Euglenozoa), mitochondrial genome rearrangements have resulted in nea

161 Additionally, a finished mitochondrial genome sequence of 135,790 bp was obtained

162 hilst highlighting the necessity of complete mitochondrial genome sequencing in the diagnostic work-u

163 Currently, complete mitochondrial genomes (mitogenomes) are available from a

164 In this study, we sequenced complete mitochondrial genomes from three congeneric Decemunciger

165 The number of mitochondrial genomes varies depending on the cell's ene

166 caused by mutations in both the nuclear and mitochondrial genomes.

167 al consideration has been given to targeting mitochondrial glutamate metabolism to control neurotrans

168 plant stress signaling by increased rates of mitochondrial H2O2 production, leading to part of the SA

169 ility, formation of reactive oxygen species, mitochondrial health, as well as cell morphology and det

170 ta directly interacted functionally with the mitochondrial helicase TWINKLE.

171 canonical autophagy, resulting in changes of mitochondrial homeostasis and alterations in GC and anti

172 at MIC60 performs dual functions to maintain mitochondrial homeostasis.

173 A crystal structure of the mitochondrial Hsp90, TRAP1, revealed that the catalytica

174 ronic pulmonary oxygen sensing by triggering mitochondrial hyperpolarization and release of mitochond

175 Mitochondrial hyperpolarization, which can promote mitoc

176 ate the regulatory mechanism of mIDH2 (mouse mitochondrial IDH2), we used lysine-to-glutamine (KQ) mu

177 The mitochondrial import component Mim1 forms a channel that

178 Inhibition was prevented by an antioxidant, mitochondrial inhibitors, or inhibition of NO formation.

179 port the need for additional research on the mitochondrial inhibitory and antiestrogenic effects of Q

180 SLC25A24 encodes a mitochondrial inner membrane ATP-Mg/Pi carrier.

181 The permeability of the mitochondrial inner membrane to HNO2, but not to NO2(-),

182 We evaluated mitochondrial integrity using MitoTracker Green and cyto

183 protein phosphatase that is targeted to the mitochondrial intermembrane space (IMS) where it interac

184 S cluster synthesis including an increase in mitochondrial iron levels, a decrease in the activities

185 pool localized in the matrix where also the mitochondrial iron-sulfur (Fe/S) cluster assembly machin

186 To date, the role of the mitochondrial isoform of OGT (mOGT) remains largely unkn

187 In summary, we have uncovered a novel human mitochondrial KMT that introduces a methyl modification

188 used by mutations in OPA1, a gene encoding a mitochondrial large GTPase involved in cristae structure

189 osome markers (E-M81, E-M78, and J-M267) and mitochondrial lineages such as U6b, in addition to commo

190 c distribution and phylogenetic structure of mitochondrial lineages that have survived in contemporar

191 cted cells and relies on regulation of MCL-1 mitochondrial localization and BFL-1 transcription by th

192 Fancd2 mitochondrial localization requires Atad3.

193 om the C. elegans VAPB homolog VPR-1 promote mitochondrial localization to actin-rich I-bands in body

194 -induced obese mice decreased acetylation of mitochondrial long-chain acyl-CoA dehydrogenase, a known

195 igate whether IGF signaling is essential for mitochondrial maintenance in cancer cells and whether th

196 duced mitochondrial depolarization decreased mitochondrial mass and Mfn2 levels, which were rescued w

197 calcium and phosphorus were pervasive in the mitochondrial matrices of a variety of mammalian cell ty

198 unctional protein localized primarily in the mitochondrial matrix and has roles in inflammation and i

199 ion channel that transports Ca(2+) into the mitochondrial matrix to modulate metabolism.

200 wild-type MDH2 cDNA restored MDH2 levels and mitochondrial MDH activity.

201 ER to mitochondria and clusters at the outer mitochondrial membrane (OMM).

202 t an atomic model of a substrate-bound inner mitochondrial membrane AAA+ quality control protease in

203 es mitofusin 2, a membrane-bound mediator of mitochondrial membrane fusion and inter-organelle commun

204 lates Mitofusin, which is required for outer mitochondrial membrane fusion.

205 Blue/green reduced mitochondrial membrane potential (MMP) and lowered intra

206 TCA cycle metabolites, as well as decreased mitochondrial membrane potential and deranged mitochondr

207 Complex I inhibition resulted in lower mitochondrial membrane potential and higher cytosolic RO

208 chondrial unfolded protein response, loss of mitochondrial membrane potential and sensitivity to mito

209 also found that PA stimulation decreased the mitochondrial membrane potential in podocytes and induce

210 mPTP opening decreases the mitochondrial membrane potential leading to the activati

211 derived VCP mutant fibroblasts exhibit lower mitochondrial membrane potential, uncoupled respiration,

212 an altered lipid composition of both MAM and mitochondrial membranes.

213 y with decreased NAA/Cr levels suggests that mitochondrial metabolic dysfunction persists after surge

214 (e.g., PDK3), ameliorating PDH activity and mitochondrial metabolism and further affecting motor beh

215 r label-free quantification of intracellular mitochondrial modifications that alter cytoplasmic condu

216 nd significant ultrastructural impairment of mitochondrial morphology with a loss of internal cristae

217 nscriptional process that creates functional mitochondrial mRNAs in Kinetoplastids.

218 tion yielded in higher levels of circulating mitochondrial (mt)DNA, soluble thrombomodulin (sCD141) a

219 ing levels of long-chain triacylglycerols in mitochondrial myopathy correlate with the severity of OX

220 Imaging in whole rat hearts indicated mitochondrial network formation and fusion activity in v

221 d, UCP1-negative unilocular adipocytes, with mitochondrial network fragmentation, disorganised crista

222 rge GTPase involved in cristae structure and mitochondrial network fusion.

223 wed decreased complex I activity and altered mitochondrial network morphology.

224 in particular loss of dopaminergic neurons, mitochondrial network structure, reduced ATP production,

225 damaged or stressed compartments within the mitochondrial network.

226 ed against label-based image analysis of the mitochondrial network.

227 BACKGROUND & AIMS: The mitochondrial nicotinamide adenine dinucleotide (NAD) ki

228 inhibits DNA replication in the kinetoplast (mitochondrial nucleoid) and nucleus.

229 METHOD: Mitochondrial O2 consumption and adenosine triphosphate

230 pletion increased SOD2 acetylation, elevated mitochondrial O2(. -), and diminished endothelial nitric

231 All mitochondrial outer membrane channels known to date are

232 We conclude that the mitochondrial outer membrane contains a considerably lar

233 nd MceA is a complex-forming effector at the mitochondrial outer membrane during Coxiella infection.

234 biogenesis and increase proteins involved in mitochondrial oxidative phosphorylation in response to D

235 transduction through apparent reductions in mitochondrial oxidative phosphorylation, increases in su

236 gene, pMitoTimer, that allows assessment of mitochondrial oxidative stress and mitophagy in vivo, an

237 Age-dependent elevation in mitochondrial oxidative stress is widely posited to be a

238 rane space (IMS) where it interacts with the mitochondrial oxidoreductase import and assembly protein

239 strain 263K suffer from a severe deficit in mitochondrial oxygen consumption in response to the resp

240 tongue squamous carcinoma SAS cells through mitochondrial pathway.

241 HIF-1 to sequester FAs in LDs away from the mitochondrial pathways for oxidation and ROS generation,

242 HA-fed mice, rescued the major losses in the mitochondrial phospholipidome and complexes I, IV, and V

243 he suggestions by earlier in vivo studies of mitochondrial processing, we found that these enzymes ar

244 usion injury is largely attributed to excess mitochondrial production of reactive oxygen species (ROS

245 ely 1 h) and is specifically degraded by the mitochondrial protease Lon.

246 SCO1 is a ubiquitously expressed, mitochondrial protein with essential roles in cytochrome

247 ficient cells exhibited decreased GFP-tagged mitochondrial proteins inside the vacuole and decreased

248 in (Dox)-cardiotoxicity via deacetylation of mitochondrial proteins.

249 ine kinase 2 (TK2), a critical enzyme in the mitochondrial pyrimidine salvage pathway, is essential f

250 Recent studies have shown that mitochondrial pyruvate carrier 1 (MPC1), a crucial playe

251 lates macrophage activation by reprogramming mitochondrial pyruvate metabolism.

252 Inheritance of a less than critical mitochondrial quantity causes a severe decline of replic

253 d cellular models have now demonstrated that mitochondrial reactive oxygen species (ROS) signal to su

254 Analyses included assessment of viability, mitochondrial reactive oxygen species (ROS), membrane da

255 +) increases may stimulate the production of mitochondrial reactive oxygen species and contribute to

256 s coupled to pro-fission phosphorylation and mitochondrial recruitment of the fission GTPase dynamin-

257 Still, the mitochondrial redox status did not change with Z-3-hexen

258 em in order to optimize linker stability for mitochondrial release.

259 ndrial membrane potential and sensitivity to mitochondrial removal and apoptosis.

260 urce of oocytes for infertility treatment or mitochondrial replacement therapy for mtDNA disease.

261 red insulin signaling and insulin-stimulated mitochondrial respiration and glycolysis.

262 iency is associated with inhibited complex I mitochondrial respiration due to lack of NADH for the el

263 osis in patients' lymphocytes, a decrease in mitochondrial respiration in patient fibroblasts with a

264 NAL displayed a higher baseline mitochondrial respiration rate than SAL.

265 ess so for a subset of genes associated with mitochondrial respiration.

266 perate to enhance ANT transport capacity and mitochondrial respiration.

267 m mice treated with Honokiol showed enhanced mitochondrial respiration.

268 ncy results in cholesterol-dependent reduced mitochondrial respiratory capacity and release of mitoch

269 k between an imbalanced stoichiometry of the mitochondrial respiratory chain complexes and skin infla

270 e terminal electron-accepting complex of the mitochondrial respiratory chain.

271 ein that plays a role in the assembly of the mitochondrial respiratory chain.

272 b NF-kappaB, and p53 signaling, and diminish mitochondrial respiratory gene expression, spare respira

273 The abnormal axon morphology and mitochondrial retrograde transport defects observed in a

274 les in inflammation and infection processes, mitochondrial ribosome biogenesis, and regulation of apo

275 discuss the individual role that each has in mitochondrial RNA biology.

276 h factor adaptor protein that contributes to mitochondrial ROS production.

277 icular, at tyrosine 48-is a key modulator of mitochondrial signaling, its action and molecular basis

278 series discusses the relative importance of mitochondrial sites for ROS production, ROS signaling-me

279 These data support the idea that CaMKI links mitochondrial stress with the PINK1/Parkin and DJ-1 mech

280 Ts and displayed indicators of oxidative and mitochondrial stress, supportive of their NETotic tenden

281 ondrial hyperpolarization, which can promote mitochondrial superoxide release, was detected during ac

282 tochondrial hyperpolarization and release of mitochondrial superoxide which, after conversion to hydr

283 In cell culture, CnnT targets to the mitochondrial surface, recruits the MT nucleator gamma-t

284 to control cells, the probands' cells showed mitochondrial swelling, which was exacerbated upon treat

285 SWIB5 interacts with other mitochondrial SWIB proteins.

286 The presence and dynamics of mitochondrial synthasomes were investigated by native el

287 chondria or treating epithelial cells with a mitochondrial-targeted antioxidant.

288 t kidney epithelial cells (NRK-52E) with the mitochondrial-targeted H2 S donor, AP39, during in vitro

289 rgeting of Vms1 is mediated by its conserved mitochondrial targeting domain (MTD), which, in unstress

290 Mitochondrial targeting of Vms1 is mediated by its conse

291 in the glycosylation of a restricted set of mitochondrial targets.

292 Studies of mitochondrial transcription have used a reductionist app

293 Mitochondrial transport in axons is critical for neural

294 g., the nuclear tRNA(Gly) and tRNA(Leu), the mitochondrial tRNA(Val) and tRNA(Pro)) were strongly ass

295 osttranslational signals governing beta-cell mitochondrial turnover are unknown.

296 The results indicate that mitochondrial UCP3 activity affects metabolism well beyo

297 itochondrial membrane potential and deranged mitochondrial ultra-structure in these model systems.

298 it decreased uncoupling protein 3 (UCP3) and mitochondrial uncoupling.

299 mitochondrial biogenesis, triggering of the mitochondrial unfolded protein response, loss of mitocho

300 Furthermore, the efficient tumor and mitochondrial uptake of (177) Lu-PPNs greatly enhanced t