ライフサイエンスコーパス: mitochondrial

1 Here, we reconstituted the maturation of mitochondrial [4Fe-4S] aconitase without artificial redu

2 oci, 62 interaction loci, and three loci for mitochondrial abundance at genome-wide significance.

3 th breast cancer, inversely correlating with mitochondrial abundance, type I IFN signaling and effect

4 This study highlights the importance of mitochondrial aconitase activity in the development of a

5 Thus, the precise cell types whose loss of mitochondrial activity and altered mtDNA copy number tha

6 Arginine therapy increases mitochondrial activity and reduces oxidative stress in c

7 characterizing the interaction between tumor mitochondrial activity and the tumor immune microenviron

8 ntify the regulation of GABA availability by mitochondrial activity as a biologically relevant mechan

9 Mitochondrial activity is a critical component of tumor

10 ated receptor gamma) agonist that stimulates mitochondrial activity, ameliorated pre-IBD symptoms.

11 romiscuity of SPT therefore links serine and mitochondrial alanine metabolism to membrane lipid diver

12 olar disorder do not appear to share similar mitochondrial alterations in the DLPFC.

13 Mitochondrial and cytosolic proteostasis are of central

14 ology in T. gondii and is important for both mitochondrial and general parasite metabolism.

15 depression-like behaviors through actions on mitochondrial and MSN structure and function.

16 t sequencing libraries of rNMPs derived from mitochondrial and nuclear DNA of budding and fission yea

17 A mitochondrial antioxidant reduced AF burden, restored I(

18 SIS, such insulin secretion was blocked with mitochondrial antioxidant SkQ1.

19 c acid-inducible gene I (RIG-I) and initiate mitochondrial antiviral signaling (MAVS) protein-depende

20 igger retinoic acid-inducible gene I (RIG-I)/mitochondrial antiviral signaling (MAVS)-dependent remod

21 abetic kidneys, a cardinal sign of disrupted mitochondrial architecture and bioenergetics.

22 Despite the decreased mitochondrial area, complex III and V expression increas

23 c or glycosomal pathways, we noted increased mitochondrial ATP production, but a net decrease in cell

24 We find that mitochondrial ATP synthesis decreases by approximately 5

25 nce of tightly regulated Ca(2+) dynamics for mitochondrial axonal transport, and the therapeutic prom

26 ccumulation period temporally coincides with mitochondrial BAX clustering and cytochrome c release.

27 Restoring mitochondrial bioenergetics in the colonic epithelium wi

28 Mitochondrial bioenergetics is dynamically coupled with

29 sured cell viability, mtDNA copy number, and mitochondrial bioenergetics utilizing trypan blue, South

30 quently, we found that labile heme regulates mitochondrial biogenesis and cell growth.

31 nown transcriptional regulators of postnatal mitochondrial biogenesis and function, serve a role in t

32 ereby alleviating telomere damage, defective mitochondrial biosynthesis and clearance, cell growth re

33 es, but upregulation in the genes related to mitochondrial Ca(2+) efflux pathways, suggesting a count

34 (2+)-gated ion channel complex that controls mitochondrial Ca(2+) entry and regulates cell metabolism

35 stimulation of BAT activates a PKA-dependent mitochondrial Ca(2+) extrusion via the mitochondrial Na(

36 otective cardiac inducible gene that reduces mitochondrial Ca(2+) influx and permeability transition

37 protects cells from bioenergetic crisis and mitochondrial Ca(2+) overload during periods of nutrient

38 so, they rely on activity-driven presynaptic mitochondrial Ca(2+) uptake to accelerate ATP production

39 We investigate the hypothesis that mitochondrial Ca(2+) uptake via MCU influences phototran

40 wn of Spata18 suppresses mitophagy, disturbs mitochondrial Ca2+ homeostasis, affects ATP production,

41 mitochondria-lysosome contacts in regulating mitochondrial calcium dynamics through the lysosomal cal

42 Our work raises the hypothesis that impaired mitochondrial calcium transport contributes to the patho

43 ial fatty acid oxidation as a consequence of mitochondrial calcium uniporter complex (MCUC) inhibitor

44 EMRE form the minimal functional unit of the mitochondrial calcium uniporter complex in metazoans, a

45 The mitochondrial calcium uniporter is a Ca(2+)-gated ion ch

46 Here, we report increased mitochondrial calmodulin kinase II (CaMKII) activation a

47 e oxygen species, are also key regulators of mitochondrial cell death pathways.

48 Currently, studying mitochondrial changes in multiple sclerosis is hampered

49 complex tissue environment and the synaptic mitochondrial changes that accompany its loss.

50 Here, we combined analyses of the mitochondrial COI gene and 11 microsatellite markers to

51 We analysed the mitochondrial COI gene of 84 butterfly species out of 90

52 te that serves as a direct electron donor to mitochondrial complex II.

53 The mitochondrial contact site and cristae organizing system

54 hagy, ultimately resulting in reduced axonal mitochondrial content that is restored by genetic inhibi

55 e nor sodium nitrite supplementation altered mitochondrial coupling efficiency in murine skeletal mus

56 c atrophy (ADOA), caused by mutations in the mitochondrial cristae biogenesis and fusion protein opti

57 oxidative stress to sensitize the network to mitochondrial criticality.

58 ion (PCR) protocol that targets the parasite mitochondrial cytochrome b gene.

59 ially for some pathological states, in which mitochondrial deficits are prominent and difficult to fi

60 ase 1 (PINK1) and parkin (PRKN) in mediating mitochondrial degradation (mitophagy) reaffirmed the imp

61 ession was suppressed, together with reduced mitochondrial density, and the brown progenitor cells so

62 he G2/M arrest was accompanied by apoptosis, mitochondrial depolarization, generation of reactive oxy

63 biological processes such as speciation and mitochondrial disease has been questioned.

64 s chromosomal, monogenic, multifactorial and mitochondrial diseases.

65 inant-negative mechanism to cause this fatal mitochondrial disorder.

66 Mitochondrial disorders are the result of nuclear and mi

67 ct, common findings in neurodegenerative and mitochondrial disorders.

68 zed sarcomeres, elevated cTnI expression and mitochondrial distribution and function like adult cardi

69 ER tubules formed by Drp1 promote mitochondrial division by facilitating ER-mitochondria i

70 entified to secrete greater concentration of mitochondrial DNA (mtDNA) compared to noncancer epitheli

71 ity ratio, distant pedigree computation, and mitochondrial DNA (mtDNA) copy number inference.

72 can cause mitochondrial toxicity, including mitochondrial DNA (mtDNA) depletion in several cases.

73 Mitochondrial DNA (mtDNA) resides in a high ROS environm

74 iation with low bronchoalveolar lavage fluid mitochondrial DNA and more severe disease.

75 es may reveal if the patterns here shown for mitochondrial DNA are also reflected in the nuclear geno

76 This was accompanied by lower mitochondrial DNA copy numbers (p < 0.001), mtND1 expres

77 could be limited by CGAS or STING knockdown, mitochondrial DNA depletion or mitochondrial outer membr

78 er premature aging caused by accumulation of mitochondrial DNA mutations in Polg(D275A) mice predispo

79 rial disorders are the result of nuclear and mitochondrial DNA mutations that affect multiple organs,

80 Pif1 helicase functions in both nuclear and mitochondrial DNA replication and repair processes, pref

81 e genetic information in their small genome (mitochondrial DNA) and the nucleus.

82 scular remodeling, mediates the link between mitochondrial dynamics and vascular smooth muscle cell (

83 mechanical roles in skeletal muscle and that mitochondrial dynamics can be manipulated to alter muscl

84 Although dysregulation of mitochondrial dynamics has been linked to cellular senes

85 These interactions alter mitochondrial dynamics in neurons, thereby facilitating

86 extracellular vesicles (sEVs) that activate mitochondrial dynamics, stimulate mitochondrial movement

87 n the absence of Fzo1, which is required for mitochondrial dynamics/respiration.

88 ial impairment is frequently associated with mitochondrial dysfunction and altered neurotransmission.

89 Age-related mitochondrial dysfunction and associated oxidative stres

90 Mitochondrial dysfunction has long been implicated in th

91 nt neurological deficits is not fully known, mitochondrial dysfunction is a key component in methamph

92 Mitochondrial dysfunction underlies many heritable disea

93 d consistent enrichment in oxidative stress, mitochondrial dysfunction, and transcription initiation

94 ed to elevated IL (interleukin)-6 levels and mitochondrial dysfunction, associated with increased mit

95 Under conditions of inherent or induced mitochondrial dysfunction, cancer cells manifest overlap

96 stered to patients with primary or secondary mitochondrial dysfunction, might be due to its function

97 Reactive oxygen species (ROS), mitochondrial dysfunction, telomere shortening, genomic

98 ed as novel pathomechanisms in diseases with mitochondrial dysfunction.

99 nd levels of another downstream product, the mitochondrial electron carrier coenzyme Q, both in cultu

100 Here we define the relative contribution of mitochondrial electron transport chain (ETC) derived H(2

101 the loss of dAKAP1-RNA interactions reduces mitochondrial electron transport chain activity.

102 in CLPP2 knockouts, without accumulation of mitochondrial-encoded counterparts in the same complex.

103 multifocal abnormal neuron or glial density, mitochondrial energetics, or neuroinflammation in ASD, a

104 x switched, representing central pathways of mitochondrial energy metabolism, including the respirato

105 ostnatal developmental maturation, including mitochondrial energy transduction, contractile function,

106 titatively evaluates sample-specific percent mitochondrial enrichment.

107 Consistently, mitochondrial ETC enzyme activities and membrane potenti

108 rase 1A (CPT1A), the rate-limiting enzyme of mitochondrial fatty acid (FA) transport, is repressed by

109 In summary, mtACP, as a key component of mitochondrial fatty acid biosynthesis, is important in g

110 flexible and almost exclusively dependent on mitochondrial fatty acid oxidation as a consequence of m

111 roscopy verified that PIM inhibitors promote mitochondrial fission and apoptosis in vivo.

112 Mitochondrial fission and fusion are highly regulated by

113 While both mitochondrial fission and mitochondrial fusion mutants s

114 his pattern is disrupted by mutations in the mitochondrial fission component dynamin DRP-1.

115 Mechanistically, PGAM5 is required for mitochondrial fission through dephosphorylating DRP1.

116 ultiple mechanisms contribute to communicate mitochondrial fitness to the rest of the cell.

117 (COX17) and ATP Synthase, H(+) transporting, Mitochondrial Fo Complex (ATP5H) in primary RGCs and in

118 In contrast, the mitochondrial form of NOC possesses high-amplitude circa

119 our work supports a mechanistic link between mitochondrial function and common neurodegenerative prot

120 Mitochondrial function and fatty acid and glucose metabo

121 cle mass, whereby it acts to maintain muscle mitochondrial function and limit autophagy.

122 r environment through coordinated changes in mitochondrial function and metabolism.

123 [4HNE] a byproduct of lipid peroxidation) on mitochondrial function and structure was assessed in HL1

124 ole, distinct from lipogenesis, of SREBP1 on mitochondrial function in mutant KRAS NSCLC.

125 Surprisingly, their mitochondrial function is diminished.

126 al and physiological analyses, we found that mitochondrial function is maintained in the presence of

127 ty of non-invasive techniques to investigate mitochondrial function of the CNS in vivo.

128 RR1 (CHCHD2) is a bi-organellar regulator of mitochondrial function that directly activates cytochrom

129 ential role for hnRNP H in basal and dynamic mitochondrial function that informs methamphetamine-indu

130 dinucleotide (NAD(+)) levels that compromise mitochondrial function trigger release of DNA damaging r

131 Identifying approaches to preserve mitochondrial function, adipose tissue integrity, and be

132 nd HepG2 cells induces glucose independence, mitochondrial function, and the acquisition of a transcr

133 gs reveal that human METTL15 is required for mitochondrial function, delineate the evolution of methy

134 xpressed genes (DEGs) had known or predicted mitochondrial function, of which oxidative phosphorylati

135 .6x10(8)+/-4.5x10(7), P<0.001) and augmented mitochondrial function.

136 leads to downregulation of genes that impact mitochondrial function.

137 and IDH2 that encode proteins necessary for mitochondrial function.

138 ypoxia resistance, a response that relies on mitochondrial function.

139 the most powerful intervention for promoting mitochondrial function; however, its impact on FRDA has

140 g plays a key role in spine loss when severe mitochondrial functional defects are present.

141 in liver cells, low-level PA (LPA) increases mitochondrial functions and alleviates the injuries indu

142 cantly enriched in osteoblast, neuronal, and mitochondrial functions.

143 s and anoxia, surprisingly we found that the mitochondrial fusion mutants eat-3 and fzo-1 are more re

144 While both mitochondrial fission and mitochondrial fusion mutants showed increased sensitivit

145 zed a mouse model carrying a knockout of the mitochondrial fusion-fission-related gene solute carrier

146 ficantly decreased protein expression of key mitochondrial genes including cytochrome C oxidase coppe

147 chondrial number and deregulation of several mitochondrial genes, suggesting towards a specific role

148 l benefits via transcriptional activation of mitochondrial genes.

149 shrimp Synalpheus microneptunus, a complete mitochondrial genome (22X coverage) assembled from short

150 , the myxozoan Henneguya salminicola, has no mitochondrial genome, and thus has lost the ability to p

151 on of oxidative damage, in particular in the mitochondrial genome.

152 n acts as a stress test for the integrity of mitochondrial genomes and sets the stage for replication

153 e genome, our de novo assembled O. nubilalis mitochondrial genomes contained 82 intraspecific substit

154 Prior to this study, complete mitochondrial genomes from Order Thysanoptera were restr

155 ledge of the structure and expression of the mitochondrial genomes of these human and animal pathogen

156 aviors, as well as reduced expression of the mitochondrial GTPase MFN2 in the NAc.

157 ent with previous reports from other models, mitochondrial H(2)O(2) emission and oxidative damage wer

158 These findings show that mitochondrial homeostasis as controlled by the PGC famil

159 identify a new paradigm that FOXM1 regulates mitochondrial homeostasis in a process independent of nu

160 s a specific role of AtPam16L in maintaining mitochondrial homeostasis, especially under stress condi

161 OPA1 is an important factor in mitochondrial homeostasis, including cristae remodeling;

162 HSP10, suggesting that Akt3 is required for mitochondrial homeostasis.

163 This is associated with a paradoxical mitochondrial hyper-function and increased oxidative str

164 linked to autism and schizophrenia, exhibit mitochondrial hyperactivity and altered group behavior.

165 n's disease (PD); however, it is unclear how mitochondrial impairment and alpha-synuclein pathology a

166 ns shows downregulation in the expression of mitochondrial influx Ca(2+) transporter genes, but upreg

167 e find neurons of the Fmr1(-/y) mouse have a mitochondrial inner membrane leak contributing to a "lea

168 Aifm2 associates with the outer side of the mitochondrial inner membrane.

169 essential for the proper architecture of the mitochondrial inner membrane.

170 tion system, we describe a mechanism for how mitochondrial inner-membrane fusion is regulated by the

171 mHTT crossing the MOM and entering into the mitochondrial intermembrane space, making it highly unli

172 dation generates a corresponding increase in mitochondrial JH(2)O(2) production, that the majority (~

173 ions showed a strong enrichment with typical mitochondrial lipids like cardiolipins and demonstrated

174 ormatic and cellular studies that HPDL has a mitochondrial localization signal and consequently local

175 ne potential; a subset had increased resting mitochondrial mass.

176 ice variants (MOCS1A) either localize to the mitochondrial matrix (exon 1a) or remain cytosolic (exon

177 First, the major redox couples in the mitochondrial matrix (NAD, NADP, thioredoxin, glutathion

178 follow different translocation routes before mitochondrial matrix import for cPMP biosynthesis involv

179 independently of the rest of the complex by mitochondrial matrix protease ClpXP, which selectively r

180 on products, ADP, is transported back to the mitochondrial matrix via the antiporter, again through a

181 cells is organized into nucleoids within the mitochondrial matrix, but how mtDNA nucleoids are formed

182 or the efficient import of proteins into the mitochondrial matrix, particularly if the function of th

183 and have shown activation of the intrinsic (mitochondrial mediated) apoptosis pathway in these cells

184 ate a large conductance channel in the inner mitochondrial membrane known as the PTP (permeability tr

185 hed cardiomyopathy, restored cardiac myocyte mitochondrial membrane potential and flavoprotein oxidat

186 Activation of PPAR-gamma partially restored mitochondrial membrane potential and IFN-gamma productio

187 andard chemotherapeutics sensitized cells to mitochondrial membrane potential loss and apoptosis.

188 ion identified chemical probes that regulate mitochondrial membrane potential, adenosine 5'-triphosph

189 metabolic remodeling deficits and decreased mitochondrial membrane potential; a subset had increased

190 ghtly controlled Ca(2+) channel of the inner mitochondrial membrane that regulates cellular metabolis

191 diolipin on the concave surface of the inner mitochondrial membrane, before oxidizing the lipid and i

192 hat the Mcl-1 TMD forms homooligomers in the mitochondrial membrane, competes with full-length Mcl-1

193 l-1 and Bok predominantly takes place at the mitochondrial membrane.

194 s a historic record of past drug treatments (mitochondrial memory) and renders the cancer patient sus

195 Mitochondrial metabolism and gene expression are highly

196 In this review, we highlight how mitochondrial metabolism determines HSC fate, and especi

197 ation has a conserved effect of upregulating mitochondrial metabolism in both fly and mammalian adipo

198 o mitochondria suggesting a putative role in mitochondrial metabolism.

199 The ER-mitochondrial Mg(2+) dynamics is selectively stimulated

200 We thus named this gene mitochondrial micropeptide-47 (Mm47).

201 Moreover, despite the disruption of the mitochondrial mitofilin protein complex at cristae junct

202 Mitochondrial morphology and activity regulation is esse

203 Mitochondrial morphology shifts rapidly to manage cellul

204 sing long-term, in vivo imaging, we examined mitochondrial motility in zebrafish sensory and motor ax

205 t activate mitochondrial dynamics, stimulate mitochondrial movements, and promote organelle accumulat

206 arization, an apparently critical element of mitochondrial mRNA stability and quality control.

207 ndent mitochondrial Ca(2+) extrusion via the mitochondrial Na(+)/Ca(2+) exchanger, NCLX.

208 tly, this defective CI-dependent decrease in mitochondrial NADPH production pathway or genetic ablati

209 olemmal mitochondria preferentially host the mitochondrial NCLX (Na(+)/Ca(2+) exchanger).

210 Target genes are the porcine mitochondrial ND2 and equine ATP 6-8 genes.

211 Deregulation of mitochondrial network in terminally differentiated cells

212 ruption of the mitochondrial network, as the mitochondrial network morphology was substantially resto

213 e directly involved in the disruption of the mitochondrial network, as the mitochondrial network morp

214 Knockdown of AtPAM16L caused reduction in mitochondrial number and deregulation of several mitocho

215 e that this was likely due to a reduction in mitochondrial one-carbon metabolism, resulting in reduce

216 -apoptotic BCL-2 proteins oligomerize at the mitochondrial outer membrane during MOMP, inducing pore

217 ell lymphoma (BCL-2) protein family regulate mitochondrial outer membrane permeabilization (MOMP), a

218 NG knockdown, mitochondrial DNA depletion or mitochondrial outer membrane permeabilization blockage v

219 en respiration and oxidative stress, whereby mitochondrial oxidant levels do not rise with increased

220 glucose was required for insulin to increase mitochondrial oxidants.

221 anslation at least in part by increasing the mitochondrial oxidation of glucose and glutamine carbons

222 rtum maturation and neonatal upregulation of mitochondrial oxidative capacity may protect against oxi

223 Metabolic shifting between glycolysis and mitochondrial oxidative phosphorylation has been implica

224 spiration unless glucose is present; and (c) mitochondrial oxidative stress must precede the insulin

225 in insulin secretion, partly due to reduced mitochondrial oxygen consumption rate, glucose-stimulate

226 Dominant mutations in the mitochondrial paralogs coiled-helix-coiled-helix (CHCHD)

227 hile both TDP-43 and CHCHD10 mutations drive mitochondrial pathogenesis, mechanisms underlying such p

228 opfii GT-II driven apoptosis corresponded to mitochondrial pathways; mitochondrial transmembrane resi

229 c enzyme with a cytosolic (Pck1/PEPCK-C) and mitochondrial (Pck2/PEPCK-M) isoform.

230 We show that the mitochondrial permeability transition pore regulator cyc

231 mine the effect of PIM loss or inhibition on mitochondrial phenotype and ROS.

232 ontrol enzymes will help unravel the role of mitochondrial plasticity in aging and disease.

233 s datasets showed significant enrichment for mitochondrial processes, as well as innate immunity, chr

234 The import machinery coordinates with mitochondrial proteases and chaperones to maintain the m

235 The mitochondrial protein Atg32 is the yeast SAR that mediat

236 patients, supporting the lack of deficit in mitochondrial protein import.

237 ins including consistent increases in NNT, a mitochondrial protein with essential roles in influencin

238 ession of nuclear-encoded, TIM23-transported mitochondrial proteins ACO2, TUFM, IDH3A, CLPP and mitoc

239 We highlight organism-wide differences in mitochondrial proteins including consistent increases in

240 ial proteases and chaperones to maintain the mitochondrial proteome.

241 Increasing evidence suggests that enhancing mitochondrial proteostasis may hold therapeutic potentia

242 study identified the cyclophilin D-dependent mitochondrial proton leak and uncoupling as a potentiall

243 -stimulated insulin secretion, by increasing mitochondrial proton leak.

244 cysteine-54 (C54) of the MPC2 subunit of the mitochondrial pyruvate carrier (MPC) is presented.

245 Mitochondrial pyruvate carrier 1 (MPC-1) appears to be a

246 Because PRKN is important in mitochondrial quality control and protection against str

247 y, this interaction is independent of Parkin mitochondrial recruitment and ligase activity but requir

248 Metabolic manipulations that increased mitochondrial redox generation promoted proline biosynth

249 romoted proline biosynthesis, while reducing mitochondrial redox potential and/or ATP synthesis impai

250 can be indirectly caused by oxidation of the mitochondrial replicase.

251 The dual mechanisms of increased mitochondrial respiration and enterohepatic bile acid re

252 ta/Delta mutants are profoundly deficient in mitochondrial respiration and Fe accumulation, both Cu-d

253 re no significant differences in measures of mitochondrial respiration between legs, but peroxisome p

254 that elevated non-vacuolar cysteine impairs mitochondrial respiration by limiting intracellular iron

255 Female newborns showed higher mitochondrial respiration compared to male newborns.

256 en electrode, we measured isolated rat liver mitochondrial respiration in the presence and absence of

257 Mitochondrial respiration increased in aSAT and correlat

258 ed glucose uptake and lower nutrient-induced mitochondrial respiration than wild-type (WT) cells.

259 type 2 diabetes medication metformin reduces mitochondrial respiration to control levels and signific

260 y controlling insulin action, lipolysis, and mitochondrial respiration to control the usage of substr

261 M induces Acod1 and itaconate, which reduced mitochondrial respiration via complex II inhibition.

262 e the glycolytic utilization of glucose from mitochondrial respiration, allowing for the maintenance

263 e-aged, obese, insulin-resistant men affects mitochondrial respiration, content and morphology in ske

264 ons of protein synthesis, energy metabolism, mitochondrial respiration, lipid and carbon metabolism a

265 e of ATP levels under conditions of impaired mitochondrial respiration.

266 naling that can regulate fuel metabolism and mitochondrial respiration.

267 hat venetoclax-sensitive myeloma has reduced mitochondrial respiration.

268 er, Mdm30 does not have a dramatic effect on mitochondrial respiration/function, and mRNA export occu

269 The in-vivo metabolic data were validated by mitochondrial respirometry, enzyme activity assays and g

270 saturated fatty acids (PUFAs) form cellular, mitochondrial, retinal, and other membranes highly impor

271 Mitochondrial ribosome and mitochondria-associated genes

272 tion on prokaryotic ribosomes and eukaryotic mitochondrial ribosomes.

273 f LRPPRC and PNPT1, two proteins involved in mitochondrial RNA catabolic processes and both negativel

274 cerbates DNA toxicity and host death without mitochondrial RNA or DNA depletion; moreover, autophagy

275 serve as transcription initiation factors of mitochondrial RNA polymerases in Saccharomyces cerevisia

276 A global profile of mitochondrial salvage and cell survival was observed in

277 e" mitochondrial stress in the intermembrane mitochondrial space and convey these signals through the

278 type of Split-GFP that we termed Bi-Genomic Mitochondrial-Split-GFP (BiG Mito-Split-GFP).

279 hin cell protrusions, a finding validated by mitochondrial staining.

280 ed PDH activity, and an impaired response to mitochondrial stress in affected cells.

281 nique topology of MUL1 enables it to "sense" mitochondrial stress in the intermembrane mitochondrial

282 Mitochondrial stress likely contributes to the late-onse

283 e of the endosomal adaptor Tollip during the mitochondrial stress response and identify its interacti

284 y mitochondrial stress, and the induction of mitochondrial stress results in at least some of the hir

285 t defects, given that hira-1 mutants display mitochondrial stress, and the induction of mitochondrial

286 e forms of cell stress, such as ER stress or mitochondrial stress, can also promote inflammatory resp

287 ocardial energy substrate use, and preserves mitochondrial structure and function after reperfusion.

288 ary techniques, we provide new insights into mitochondrial structure and function in alphaICs.

289 al an elaborate set of daily changes to cone mitochondrial structure and function.

290 many small vesicles (30 nm diameter) at the mitochondrial surface.

291 to variations in threonine (Thr) levels via mitochondrial threonyl-tRNA synthetase TARS2.

292 ncy virus infection, and their use can cause mitochondrial toxicity, including mitochondrial DNA (mtD

293 iac cells are disproportionately targeted by mitochondrial toxins resulting in a loss of cardiac func

294 l migration that is regulated by subcellular mitochondrial trafficking.

295 he mitochondria, including genes involved in mitochondrial translation.

296 osome 6, and had the highest upregulation in mitochondrial translation.

297 osis corresponded to mitochondrial pathways; mitochondrial transmembrane resistance (DeltaPsim) was a

298 or circuits.SIGNIFICANCE STATEMENT Disrupted mitochondrial transport has been linked to neurodegenera

299 previously unappreciated role for retrograde mitochondrial transport in the maintenance of a homeosta

300 oduction and NADH recycling, associated with mitochondrial uncoupling, were not compensated by increa