ライフサイエンスコーパス: mitochondria

1 maximal level (i.e., mild depolarization of mitochondria).

2 st CAE, even though it was not imported into mitochondria.

3 ferin and proteins, apparently associated to mitochondria.

4 egulates mitophagy to control the quality of mitochondria.

5 and intracellular labeling on the surface of mitochondria.

6 he mitochondrial fission regulator Drp1 onto mitochondria.

7 cient to confer import and processing in the mitochondria.

8 a novel role for this family of receptors in mitochondria.

9 duced alignment to neighboring inner-segment mitochondria.

10 e/S proteins, explaining the essentiality of mitochondria.

11 on cytoplasmic ribosomes, and imported into mitochondria.

12 o in regions of ER in close association with mitochondria.

13 s, where peripheral ER tubules interact with mitochondria.

14 ase from the ER and subsequent uptake by the mitochondria.

15 production when compared with interfibrillar mitochondria.

16 oper physical and functional organization of mitochondria.

17 used an inducible method to reroute TPD54 to mitochondria.

18 n reflect iron transport into the cytosol or mitochondria.

19 transporter capable of importing NAD(+) into mitochondria.

20 t be possible without the supportive role of mitochondria.

21 pathway for Ca(2+) uptake into photoreceptor mitochondria.

22 length due to increased volume of individual mitochondria.

23 sary for robust oxidative phosphorylation in mitochondria.

24 nd blocks the uptake of NAD(+) into isolated mitochondria.

25 species (ROS) which subsequently damages the mitochondria.

26 e compartments in the cancer cell, including mitochondria.

27 study, we found the FOXM1 protein inside the mitochondria.

28 esence of several ubiquinones in Arabidopsis mitochondria.

29 ein that distributes between the cytosol and mitochondria.

30 ke structures near envelope glycoproteins or mitochondria.

31 sulted in accumulation of P-STAT3(Ser727) in mitochondria.

32 78 resolubilizes and reactivates proteins in mitochondria.

33 ones produce energy using a large cluster of mitochondria.

34 tophagy, the selective autophagic capture of mitochondria.

35 biogenesis in Gram-negative bacteria and in mitochondria.

36 TIM23 and inhibits protein import in intact mitochondria.

37 n bacteria and eukaryotic organelles such as mitochondria.

38 er temperature (26 degrees C) compared to RM mitochondria (30 degrees C).

39 movement of MTs, endoplasmic reticulum (ER), mitochondria, acidic organelles, F-actin, keratin, and s

40 tochondria to the stromal ME, thus improving mitochondria activity in recipient MSC.

41 Mechanistically, mitochondria aggregate and depolarize after stress becau

42 Furthermore, targeting viperin to mitochondria also increased the rate at which HADHB is r

43 p.Glu140* affected FKBP8 localization to the mitochondria and created a truncated form of the FKBP8 p

44 cause increased perinuclear localization of mitochondria and decreased cell proliferation, altered e

45 e at which HADHB is retrotranslocated out of mitochondria and degraded, providing an additional mecha

46 While the effect of ROS on mitochondria and endoplasmic reticulum (ER) has been wel

47 reduced expression of genes associated with mitochondria and fatty acid oxidation in RYR1 mutants wh

48 5C, or USP15 interferes with EL targeting of mitochondria and functionally uncouples BAX clustering f

49 rectly activates cytochrome c oxidase in the mitochondria and functions in the nucleus as a transcrip

50 morphological and functional changes in host mitochondria and how this manipulation can influence mic

51 l molecule elesclomol escorted copper to the mitochondria and increased cytochrome c oxidase levels i

52 n increase in the number of smaller, simpler mitochondria and increased metabolic activity in cones.

53 metric Ca(2+) indicator targeted to neuronal mitochondria and intravital multiphoton microscopy, we f

54 M) in human locates at the inner membrane of mitochondria and is best known for its role in regulatin

55 ein (AKAP) 1, modulating its localization to mitochondria and its interaction with protein kinase A (

56 timing of parkin recruitment to depolarized mitochondria and its modulation by kenpaullone in real t

57 lic diseases, but structural organization of mitochondria and low sample availability pose distinctiv

58 SH/GRX systems of the cytosol, chloroplasts, mitochondria and nucleus, we have only scratched the sur

59 cribe a novel pathway that originates in the mitochondria and operates upstream of the CRL2(VHL) liga

60 the exception of the specialized genomes of mitochondria and plastids, all genetic information is se

61 he lipid composition of E. gracilis strain Z mitochondria and plastids, and of plastid subfractions (

62 sts, dual mRNAs encoded proteins localize in mitochondria and produce higher PCC enzyme activity vs.

63 concert with increased number and fusion of mitochondria and production of reactive oxygen species.

64 fatty acid oxidation from ATP generation in mitochondria and promotes energy dissipation as heat.

65 ids, we find that cysteine is most toxic for mitochondria and show that elevated non-vacuolar cystein

66 reticulum and strikingly increased number of mitochondria and small vesicles.

67 voltage-dependent anion channel-1 (VDAC1) in mitochondria and that INSR knockdown triggers robust mit

68 e complex interaction and cross talk between mitochondria and the associated miRNAs.

69 at the TGN, were individually relocalised to mitochondria and the content of the subsequently re-rout

70 Gram-negative bacteria, mitochondria, and chloroplasts all possess an outer memb

71 ular compartments (i.e., nucleus, lysosomes, mitochondria, and cytoplasm) is extremely advantageous i

72 ensity in presynaptic terminals, presynaptic mitochondria, and in dendritic spines of xCT(-/-) mice.

73 riptional mechanisms of nuclear control over mitochondria, and may help to understand the aetiology o

74 ocases, stabilize protein homeostasis within mitochondria, and, in particular, increase the levels an

75 Mitochondria are an essential organelle in most eukaryot

76 Mitochondria are arrayed in a periodic pattern in Caenor

77 In skeletal muscle fibers, mitochondria are densely packed adjacent to myofibrils b

78 Mitochondria are dynamic organelles that can change shap

79 Mitochondria are essential cellular organelles that play

80 Mitochondria are essential in most eukaryotes and are in

81 Mitochondria are essential metabolic hubs that dynamical

82 Mitochondria are essential organelles in eukaryotes.

83 Mitochondria are highly dynamic organelles that can exhi

84 Mitochondria are important sources of energy, but they a

85 Mitochondria are key sources of intracellular oxidative

86 et which differs after nuclear lysis in that mitochondria are not degraded but are modified by the vi

87 hagy and accelerating the removal of damaged mitochondria are of interest for developing a disease-mo

88 While existing evidence indicates that some mitochondria are retrogradely transported for degradatio

89 Mitochondria are signaling hubs in eukaryotic cells.

90 We find that mitochondria are small and fragmented and translocate ap

91 underlying IRGM-mediated quality control of mitochondria are still not fully understood.

92 Mitochondria are susceptible to oxidative damage, and he

93 These findings identify mitochondria as a major target of glucotoxicity.

94 We found that TILs accumulated depolarized mitochondria as a result of decreased mitophagy activity

95 Mammalian mitochondria assemble four complexes of the respiratory

96 t and reveal increases in local viscosity on mitochondria associated with mitochondria-lysosome conta

97 that forms regulatory DRMs in the ER, called mitochondria-associated ER membranes (MAM).

98 However, the specific SSBP1 mitochondria-associated function in retinal ganglion cel

99 Mitochondrial ribosome and mitochondria-associated genes were identified as top gen

100 way in Drosophila melanogaster involving the mitochondria-associated protein Dosmit.

101 TPase) dynamin-related protein (Drp1) severs mitochondria at endoplasmic reticulum (ER)-mitochondria

102 ly, although P466L mutant was present in the mitochondria at greater levels, unlike del(A420-A463) mu

103 ial-encoded subunits for complex assembly in mitochondria await discovery.

104 pathologically low or high variability moved mitochondria away from percolation which reduced the eff

105 ver, hyperfusion does not completely connect mitochondria because Opa1 and mitofusin 1, two other dyn

106 nto cells, BAXT182I resided predominantly on mitochondria, because of its slow retrotranslocation and

107 rmeabilization (MOMP), a phenomenon in which mitochondria become porous and release death-propagating

108 betaOHB oxidation in mitochondria boosts the synthesis of cytosolic aspartate

109 tion capacities were 40-60% lower in Taz(KD) mitochondria, but an up-regulation of glutamate oxidatio

110 onstrated that DNMT1 is not localized within mitochondria, but it is associated with the mitochondria

111 ciated with structure-related dysfunction in mitochondria, but three-dimensional characterizations of

112 family BH3 protein Bim promotes apoptosis at mitochondria by activating the pore-forming proteins Bax

113 CUb subunit of the MCU-complex in regulating mitochondria Ca(2+) influx dynamics, acute cardiac injur

114 Inhibition of ER-to-mitochondria Ca(2+) transfer may represent a general the

115 due to improvement of endoplasmic reticulum-mitochondria calcium homeostasis with hepatic HAX-1 inac

116 erefore, self-DNA leaked from the nucleus or mitochondria can also serve as a cGAS ligand to activate

117 me, myofibrils, sarcomeric organization, and mitochondria can be visualized and quantified within a s

118 In tumor tissues, mitochondria can switch metabolic phenotypes to meet the

119 Abnormal mitochondria can trigger a series of human diseases, suc

120 Normal mitochondria can trigger intrinsic apoptosis by releasin

121 e we show that the dramatically disorganized mitochondria caused by a mitochondrial fission-defective

122 iration due to futile proton leak in Fmr1 KO mitochondria caused by coenzyme Q (CoQ) deficiency and a

123 ent on mitochondrial functions, thus placing mitochondria centrally in maintaining homeostasis upon i

124 Mitochondria, chloroplasts and Gram-negative bacteria ar

125 nker-NifK translational polyprotein in plant mitochondria, confirmed by identification of the polypro

126 of the ROS-generating protein Nox4 at the ER-mitochondria contact sites (MAMs) is a pro-survival mech

127 s mitochondria at endoplasmic reticulum (ER)-mitochondria contact sites, where peripheral ER tubules

128 lipid exchange and membrane tethering at ER-mitochondria contacts.

129 rt chains and propagate more vigorously than mitochondria containing deleterious mutations in hetreop

130 oth plasticity and evolved changes in muscle mitochondria contribute to thermogenesis at high altitud

131 Mitochondria contribute to tumor growth through multiple

132 also between these organelles and the ER and mitochondria, controls their metabolic flux and their dy

133 Excessive Ca(2+) taken up by mitochondria could lead to cell death.

134 lability of selective fluorescent probes for mitochondria could play an important role in the future

135 ee radical scavenger synthesized by neuronal mitochondria, decreases with aging and neurodegeneration

136 oxygen species on mitochondrial calcium and mitochondria-dependent apoptosis in cardiac myocytes.

137 at they actively took up material, including mitochondria, derived from cardiomyocytes.

138 nger signals from injured cell mitochondria (mitochondria-derived damage-associated molecular pattern

139 of oxidative phosphorylation (OXPHOS) within mitochondria did not appear until the 1930s.

140 g super-resolution microscopy to investigate mitochondria, discuss the strengths and opportunities of

141 roapoptotic peroxidase that is released from mitochondria during sustained oxidative stress.

142 als that TPP can maintain stable affinity to mitochondria during the restructuring of mitochondrial n

143 Multiple pathogens affect mitochondria dynamics and functions to influence their i

144 a likely mechanistic linker between neuronal mitochondria dysfunction and neuroinflammation in neurod

145 ac dysfunction, pathological remodeling, and mitochondria dysfunction, as well.

146 Bilaterian mitochondria-encoded tRNA genes, key players in mitochon

147 MDC biogenesis requires the ER-mitochondria encounter structure (ERMES) and the conserv

148 e, and especially focus on the links between mitochondria, endoplasmic reticulum (ER), and lysosomes

149 hanistically, we show that the disruption of mitochondria-endoplasmic reticulum (ER) contact sites (M

150 lum (ER) and to the cell surface, but not to mitochondria, endosomes, or lipid droplets.

151 erein, nLC-MS/MS was used to interrogate the mitochondria-enriched proteome of heart and skeletal mus

152 Brown adipose tissue (BAT) contains mitochondria-enriched thermogenic fat cells (brown adipo

153 In turn, mitochondria facilitate cytosolic proteostasis.

154 s were sequentially recruited to depolarized mitochondria followed by sequestration into autophagosom

155 systems to supply oxygen to skeletal muscle mitochondria for energy production needed during physica

156 ol gamma is the only DNA polymerase found in mitochondria for most animal cells.

157 l cells, increasing delivery of substrate to mitochondria for progesterone production.

158 ion of Cx43 in HSPC or culture with isolated mitochondria from Cx43 deficient HSPCs.

159 pression and was accompanied by transport of mitochondria from mesothelial cells to OvCa cells.

160 nd their wild-type littermates as well as in mitochondria from postmortem brain tissues of unaffected

161 of the iron-sulfur biogenesis machinery, in mitochondria from TAZ-KO mouse cells and in CL-deleted y

162 identification and removal of dysfunctional mitochondria from the cell, a process of mitochondrial q

163 nd synthesized protein mtCO1 were similar in mitochondria from YAC128 mice and their wild-type litter

164 Mitochondria fulfill essential roles in ATP production,

165 ring ATP7 and COG, are necessary to maintain mitochondria functional integrity and localization to sy

166 Mitochondria harboring wild-type genomes have functional

167 Persistent accumulation of damaged mitochondria has been implicated in many neurodegenerati

168 Mitochondria have a central role in regulating a range o

169 These data reinforce that mitochondria have both biochemical and biomechanical rol

170 ated a significant increase of dysfunctional mitochondria in Angpt2-silenced tumor cells, thereby res

171 Despite the established role of mitochondria in cancer, the mechanisms by which mitochon

172 be the primary pathway for Ca(2+) entry into mitochondria in eukaryotes.

173 Thus, we explored the integrity of forebrain mitochondria in Fmr1 knockout mice during the peak of sy

174 maintenance of a homeostatic distribution of mitochondria in neurons and illustrates the downstream e

175 merging evidence points to a central role of mitochondria in psychiatric disorders.

176 ETC activities in both populations of heart mitochondria in T2DM rats were unchanged.

177 e report structural features of postsynaptic mitochondria in the pre-Botzinger complex (pre-BotC) of

178 al an unrecognized possible role of neuronal mitochondria in the regulation of microglial activation,

179 was an enrichment in genes localizing to the mitochondria, including genes involved in mitochondrial

180 Mdm2 translocates to damaged mitochondria independently of parkin, enhances parkin-de

181 ta-cell hyperplasia, reflecting a beneficial mitochondria-induced fat-to-pancreas interorgan signalin

182 unctions to mating-type, such as uniparental mitochondria inheritance, (3) accumulation in the margin

183 Additionally, our study positions mitochondria-initiated signaling as key element of the V

184 ising their adequate function: (1) a loss of mitochondria inside their lobular appendages, which may

185 uction in CCN6 expression decreases the RER- mitochondria inter-membrane distance.

186 te mitochondrial division by facilitating ER-mitochondria interactions.

187 Mitochondria internalised not only the bioenergetic memb

188 MitoPunch', a device that transfers isolated mitochondria into mouse and human cells.

189 chondrial proteins that export iron from the mitochondria into the cytosol.

190 highly conserved mechanism to clear damaged mitochondria involves the E3 ubiquitin ligase Parkin and

191 Modern day aerobic respiration in mitochondria involving complex I converts redox energy i

192 demonstrated that the major phospholipase in mitochondria, iPLA(2)gamma (patatin-like phospholipase d

193 Mitochondria is a double membrane-bound cellular organel

194 enosine triphosphate (ATP) synthase in human mitochondria is a membrane bound assembly of 29 proteins

195 h the most effective way to deliver drugs to mitochondria is by covalently linking them to a lipophil

196 The connectivity of mitochondria is regulated by a balance between fusion an

197 dy indicate that metabolic function of heart mitochondria is unchanged in the face of oxidative stres

198 y (i.e., selective autophagic degradation of mitochondria) is also active after myotube formation.

199 We also used mitochondria isolated from postmortem brain tissues of u

200 ts the stage for the development of advanced mitochondria isolation protocols for distinct cell types

201 levels and restores NAD(+) uptake into yeast mitochondria lacking endogenous NAD(+) transporters.

202 pa allowed us to precisely localize sites of mitochondria-lysosome contact and reveal increases in lo

203 Moreover, mitochondrial calcium uptake at mitochondria-lysosome contact sites was modulated by the

204 al viscosity on mitochondria associated with mitochondria-lysosome contact.

205 ve-cell microscopy, we identified a role for mitochondria-lysosome contacts in regulating mitochondri

206 However, whether mitochondria-lysosome contacts serve additional function

207 Mitochondria-lysosome interactions are essential for mai

208 alization and dynamic tracking of functional mitochondria-lysosome interactions in living cells.

209 rescence intensity indicates the progress of mitochondria-lysosome interplay during mitophagy.

210 has been linked to its critical role in the mitochondria maintenance.

211 Our studies suggest the host cell mitochondria may be a therapeutic target.IMPORTANCE Huma

212 Targeting H(2)S to the mitochondria may be of therapeutic benefit in the preven

213 parkin-dependent ubiquitination of the outer mitochondria membrane protein mitofusin1.

214 f molecular danger signals from injured cell mitochondria (mitochondria-derived damage-associated mol

215 R1 (neighbour of BRCA1) and the recycling of mitochondria (mitophagy), and peroxisomes (pexophagy).

216 his study increases our understanding of how mitochondria modulate neuronal homeostasis and social be

217 In kinetoplastid mitochondria, most of the molecular machineries and gene

218 ate homeostasis is the release of functional mitochondria (Mt) that are taken up by other cells to im

219 by fatty acid synthase, FASN) and one in the mitochondria (mtFAS).

220 Upon TTX (tetrodotoxin) exposure, mitochondria near Na(V)1.5 channels accumulated more Ca(

221 cal pH values at defined sublocations within mitochondria of respiring yeast cells by fusing a pH-sen

222 The mitochondria of various tissues from mice, naked mole ra

223 on of calcium that has aggregated within the mitochondria of vascular smooth muscle cells can drive a

224 We applied our construct-mitochondria-OFF (mtOFF)-to understand how metabolic sta

225 combining 13 polypeptides synthesized within mitochondria on mitochondrial ribosomes (mitoribosomes)

226 is uL18-Like proteins are targeted to either mitochondria or chloroplasts.

227 l Ca(2+) uniporter (MCU), which implicates a mitochondria-originated death mechanism.

228 ys, such as the ubiquitin-proteasome system, mitochondria per se can influence protein homeostasis of

229 Mitochondria play a key role in oncogenesis and constitu

230 Mitochondria play an essential role in cellular metaboli

231 e aims of this study were to define the role mitochondria play in this process and examine the potent

232 h their many and varied metabolic functions, mitochondria power life.

233 further found that subjacent subsarcolemmal mitochondria preferentially host the mitochondrial NCLX

234 In addition, the proportion of mitochondria presented with enlarged compartments and fi

235 ciated with an accumulation of dysfunctional mitochondria, producing excessive reactive oxygen specie

236 ysical and functional uncoupling of LDs from mitochondria, reducing fatty acid metabolism while incre

237 Mitochondria regulate ATP production, metabolism, and ce

238 Ca(2+) uptake by mitochondria regulates bioenergetics, apoptosis, and Ca(

239 To accomplish these roles, mitochondria rely on the genetic information in their sm

240 Retinal mitochondria remain damaged and vicious cycle of free ra

241 We show how targeting MOFs toward mitochondria represents a valuable strategy for the deve

242 The biogenesis of mitochondria requires the import of hundreds of precurso

243 Here, we aimed to investigate how mitochondria respond to acute DNA damage with respect to

244 Mitochondria respond to DNA damage and preserve their ow

245 respiratory chain activity is related to the mitochondria's ability to release cytochrome c into the

246 Intriguingly, also axonal mitochondria show signs of damage, such as fusion/fissio

247 Mitochondria, so much more than just being energy factor

248 e potential, and increased expression of the mitochondria-specific protein chaperones, HSP60 and HSP1

249 t through a dedicated platform formed by the mitochondria-specific protein mS39.

250 further demonstrated that rapid screening of mitochondria-specific therapeutic drugs to evaluate thei

251 The internal mitochondria structure was successfully identified by re

252 ization signal and consequently localizes to mitochondria suggesting a putative role in mitochondrial

253 ts, were unchanged or upregulated in mutator mitochondria, suggesting a robustness to mtDNA mutation.

254 ) concentrations in isolated brain and heart mitochondria, synaptosomes, fibroblasts, and thymocytes

255 e phosphorylation inhibition, we developed a mitochondria-targeted triphenylphosphonium-conjugated AT

256 at can be therapeutically exploited with the mitochondria-targeting compound alexidine dihydrochlorid

257 hosts, thereby promoting the development of mitochondria-targeting imaging probes and therapies in t

258 arization of cristae and crista junctions in mitochondria tethered to the SSC in OHCs.

259 ive deterioration of functional integrity of mitochondria that establishes a historic record of past

260 t (FWGE), increases the carbon flux into the mitochondria, the expression of key elements of the Kreb

261 HSCs keep and accumulate dysfunctional mitochondria through asymmetric segregation during activ

262 rial localization by modulating transport of mitochondria through interaction with PGAM5.

263 phagy that identifies and eliminates damaged mitochondria through the autophagosome and lysosome path

264 ore, we delineate the mechanism by which the mitochondria, through MUL1 ligase, can inhibit the CRL2(

265 polymerizing actin filaments pushing against mitochondria, thus generating a counter force on the spi

266 ed for optimal usage of energy stores by the mitochondria to drive efficient germination.

267 onger timeframe, driving calcium overload of mitochondria to induce inflammation and dendritic atroph

268 ed to develop new therapeutics targeting the mitochondria to prevent or reverse disease-specific path

269 rmining the ratio of a protein translated in mitochondria to that of a protein translated in the cyto

270 A selective inheritance by supplying healthy mitochondria to the pole plasm.

271 Donor healthy HSPC transfer functional mitochondria to the stromal ME, thus improving mitochond

272 Overall, our findings outline an extended mitochondria-to-nucleus retrograde signaling pathway tha

273 This inhibitor was mitochondria toxic and cytotoxic to colorectal cancer ce

274 nase (AMPK) in HSPC, dramatically increasing mitochondria transfer to BM MSC.

275 ic Cx43-deficient chimeric mice show reduced mitochondria transfer, which was rescued upon re-express

276 Mitochondria undergo dynamic fusion/fission, biogenesis

277 can uniquely redistribute adjacent to forced mitochondria-vacuole contact sites.

278 e Parkin promotes the degradation of damaged mitochondria via mitophagy and mutations in Parkin are a

279 tions of stress the import of MNRR1 into the mitochondria was blocked, allowing the protein to accumu

280 ctly examine Ca(2+) uptake in zebrafish cone mitochondria, we found that loss of MCU reduces but does

281 By using an electrical circuit model of mitochondria, we quantify mitochondrial ATP synthesis ra

282 isualize the process of translation in human mitochondria, we report ~3.0 angstrom resolution structu

283 close proximity to subjacent subsarcolemmal mitochondria; we further found that subjacent subsarcole

284 subsequent diffusive oxygen delivery to the mitochondria were diminished in patients with COPD compa

285 oreceptors was not greatly affected, but the mitochondria were enlarged and had reduced alignment to

286 Mitochondria were evaluated using electron microscopy.

287 the isolated cell protrusions suggested that mitochondria were found in high numbers within cell prot

288 , 26, and 30 degrees C), revealed that heart mitochondria were less coupled at a lower temperature (2

289 rom this study indicate that mahi-mahi heart mitochondria were more temperature sensitive compared to

290 The purified mitochondria were suitable for enzyme activity analyses

291 a green fluorescent reporter protein to the mitochondria when expressed in ARPE-19 cells.

292 however, other possible roles of CypD in the mitochondria which may or may not be linked with the MPT

293 cerolipids are the main structural lipids in mitochondria, while glycosyldiacylglycerols are the majo

294 owed that MTCH2 and MTCH2x were localized to mitochondria with a long t (1/2) (>36 h).

295 e conversion, Coupa can simultaneously label mitochondria with blue fluorescence and lysosomes with r

296 Incubation of Taz(KD) mitochondria with exogenous CoA partially rescued pyruva

297 nto the mitochondrial matrix was possible in mitochondria with MCI >= 7.

298 Here, we examined the arrangement of the mitochondria within the inner segment in detail using th

299 t IRGM is crucial for the normal function of mitochondria, yet, the molecular mechanisms underlying I

300 n compete with the oxidation of mediators by mitochondria, yielding an overall respiratory activity c