ライフサイエンスコーパス: mitochondria

1 s are those in the chloroplast, cytosol, and mitochondria.

2 Red Blood Cells of some RTT patients retain mitochondria.

3 ly generated ROS co-localized with polarized mitochondria.

4 t is ubiquitously expressed and localized in mitochondria.

5 ity of PINK1 in the recruitment of Parkin to mitochondria.

6 and functionally different from normal cell mitochondria.

7 way by which these signals are integrated in mitochondria.

8 the role of NT-PGC-1alpha in brown adipocyte mitochondria.

9 oxygen species (ROS) generation in isolated mitochondria.

10 enting protein aggregate accumulation within mitochondria.

11 the ER often forming a network that embraced mitochondria.

12 to a corresponding egg or zygote with normal mitochondria.

13 fects of H2S relate to its interactions with mitochondria.

14 ovides an elevated (1) O2 environment in the mitochondria.

15 primarily produced by NADPH oxidases and not mitochondria.

16 accumulation and lipotoxic dysregulation of mitochondria.

17 abolished the transfer of both alpha-SYN and mitochondria.

18 xenal, which changes the redox status of the mitochondria.

19 ochondria pathways to traffic from the ER to mitochondria.

20 rnae are separated and "land-locked" between mitochondria.

21 utamine, pyruvate, glucose, or palmitate, in mitochondria.

22 of clathrin-coated vesicles, phagosomes, and mitochondria.

23 sessed because their levels are regulated by mitochondria.

24 ls provide evidence that mensacarcin targets mitochondria.

25 hondrial proteins in whole, respiring murine mitochondria.

26 lysosomal transporter partially localized to mitochondria.

27 protein fusion protein was found targeted to mitochondria.

28 quence affected the amount of Polbeta in the mitochondria.

29 th isoforms are found in the nucleus and the mitochondria.

30 ulate translation in yeast but not mammalian mitochondria.

31 ch is essential for elimination of unhealthy mitochondria.

32 ancreatic tissue, acinar cells, and isolated mitochondria.

33 proteins localized to structures surrounding mitochondria.

34 domains are maintained by Ca(2+) uptake into mitochondria.

35 r and colocalizes in spherical bodies around mitochondria.

36 lly regulate autophagic clearance of damaged mitochondria.

37 ng the chloroplast, peroxisome, cytosol, and mitochondria.

38 ere not previously annotated as localized to mitochondria.

39 IGF-1 robustly induced BNIP3 accumulation in mitochondria.

40 contents are essential to the maintenance of mitochondria.

41 ear receptor, induces apoptosis by targeting mitochondria.

42 Alkylation is predominantly observed within mitochondria, a source, yet not a sink, of AcroB adducts

43 ive ROS production by complex II in isolated mitochondria: (a) complex II inhibition by atpenin A5 or

44 ndurance, strongly suggesting myricetin as a mitochondria-activating agent.

45 Such an achievement, in concert with a mitochondria-adapted CRISPR/Cas9 platform, could prompt

46 lian cells and for the clearance of paternal mitochondria after embryonic fertilization in C. elegans

47 Impaired mitochondria and accumulated H2O2 production resulted in

48 The ablation of BCO2 causes dysfunctional mitochondria and altered energy metabolism, which furthe

49 is necessary and sufficient to target it to mitochondria and another that is necessary and sufficien

50 clustered LDs that are in close proximity to mitochondria and are lipolytically degraded.

51 We update theoretical maximum ATP yields by mitochondria and cells catabolizing different substrates

52 ram-negative bacteria and organelles such as mitochondria and chloroplasts is the presence of an oute

53 s and maintenance of cell organelles such as mitochondria and chloroplasts require the import of many

54 addition to well-known bacterial origins for mitochondria and chloroplasts, multiple origins of bacte

55 thways by which vMIA traffics from the ER to mitochondria and clusters at the OMM.

56 of apoptosis (vMIA) traffics from the ER to mitochondria and clusters at the outer mitochondrial mem

57 in comparison to sham revealed a relation to mitochondria and cytoskeleton in both species.

58 DDX3 localized to the mitochondria and DDX3 inhibition with RK-33 reduced mito

59 of cardiolipin were associated with tubular mitochondria and enhanced oxidative phosphorylation.

60 on-dependent superoxide dismutases (SODs) in mitochondria and glycosomes.

61 e analyzed outer membrane fractions of yeast mitochondria and identified four new channel activities:

62 Localization of MITF to the mitochondria and its interaction with mitochondrial prot

63 e (CcO) terminates the respiratory chains of mitochondria and many bacteria.

64 t chain, mtDNA-depleted cells still maintain mitochondria and many mitochondrial functions.

65 se hiPSCs contained morphologically abnormal mitochondria and melanosomes, and exhibited marked funct

66 Axonal transport of mitochondria and mitochondrial fission and fusion contri

67 ROS originate from mitochondria and NADPH oxidases.

68 It was found to be very well suited to image mitochondria and nuclear chromatin in two color, 2C-SIM,

69 st that CENP-F might act as a transporter of mitochondria and other cellular cargoes by attaching the

70 od for investigating the innate structure of mitochondria and other important life supporting organel

71 Mitochondria and other organelles were displaced to the

72 nd the increased release of ROS from cardiac mitochondria and other sources likely contributes to the

73 two ways: by direct contact with neighboring mitochondria and over longer distances.

74 Unlike their descendants, mitochondria and plastids, bacteria do not have dedicate

75 state, blocking the translocation of Bax to mitochondria and preventing apoptosis.

76 Sulfide inhibits mitochondria and reduces ROS production.

77 ein is located in the intermembrane space of mitochondria and released into bloodstream during pathol

78 ndrial DNA (mtDNA) with functional exogenous mitochondria and selection in a restrictive medium.

79 xicity, due to reduced striatal synaptosomal mitochondria and synaptic vesicular proton pump protein

80 We find that Psd1 is localized to both mitochondria and the ER.

81 The mitochondria and the nucleus communicate to coordinate e

82 exemplary misfolded proteins associate with mitochondria and their consequences on OXPHOS.

83 ly proteins bind inactive full-length BAK at mitochondria and then dissociate following exposure of t

84 INK1, a kinase associated with mitophagy, on mitochondria and translocated into the nucleus, where it

85 inhibits ATP synthase activity from isolated mitochondria and triggers caspase-dependent apoptosis in

86 ated by CREB consists of 'Gene expression', 'Mitochondria', and 'Signalling', while in neurons it is

87 phosphorylation and ubiquitination, perturb mitochondria, and initiate degenerative inflammatory res

88 -induced local energy deficit and preserving mitochondria, and peripheral Wallerian degeneration in v

89 ed protein (Drp1) and its translocation into mitochondria, and prevented mitochondrial fragmentation.

90 Dysfunctional mitochondria appear to be involved in many diseases thro

91 This research reveals that mitochondria are a bona fide target of Coxiella effector

92 tochondria-associated membranes (MAM), where mitochondria are closely apposed with the endoplasmic re

93 Mitochondria are crucial compartments of eukaryotic cell

94 esponses specific for damaged or superfluous mitochondria are crucial for the maintenance of cellular

95 Mitochondria are essential cytoplasmic organelles that g

96 Mitochondria are essential organelles that host crucial

97 Mitochondria are known for their role in ATP production

98 Mitochondria are multifaceted and indispensable organell

99 Mitochondria are organelles indispensable for maintenanc

100 Mitochondria are particularly susceptible to oxidative s

101 Cancer cell mitochondria are promising anticancer drug targets becau

102 we find that peritoneal-resident macrophage mitochondria are recruited to phagosomes and produce mit

103 We show that stressed mitochondria are removed from axons triggered by the bul

104 Mitochondria are responsible for bioenergetics, metaboli

105 Mitochondria are thought to have originated as free-livi

106 Mitochondria are vulnerable to oxidative stress, which c

107 tinct interactions between tumor drivers and mitochondria as critical modifiers of tumorigenicity and

108 serine-glycine cycle and produce ethanol in mitochondria as opposed to slow growing cells.

109 taposition of endoplasmic reticulum (ER) and mitochondria as well as endosomes.

110 active oxygen species, the damage on DNA and mitochondria, as well as the activation of apoptotic eve

111 The mitochondria-associated ER membrane (MAM) plays a critic

112 Some of these proteins localize at mitochondria-associated membranes (MAM), where mitochond

113 ions, called nanotunnels, that contact other mitochondria at relatively long distances.

114 urth band corresponds to the accumulation of mitochondria at the basal portion of the RPE, as identif

115 dition, IL-6, via STAT3-mediated feedback to mitochondria, autonomously adjusts mitochondrial superox

116 ave demonstrated for the first time that the mitochondria-based piezosensors are able to detect ion f

117 re found to be due to calcium entry into the mitochondria, because the swelling induced by metformin

118 , by increasing both mitophagic activity and mitochondria biogenesis.

119 ver, LDs are not required for FA delivery to mitochondria but instead function to prevent acylcarniti

120 tivation of mNEET did not affect the size of mitochondria but that the frequency of intermitochondria

121 the removal of the damaged and dysfunctional mitochondria by a double-membrane autophagic process via

122 expression promotes the clearance of damaged mitochondria by augmenting autophagy signalling via acti

123 ort that mitophagy, the selective removal of mitochondria by autophagy, positively regulates hepatic

124 ALS mutant SOD1 inhibits axonal transport of mitochondria by inducing PINK1/Parkin-dependent Miro1 de

125 oglitazone may regulate energy metabolism in mitochondria by inhibiting the electron transfer activit

126 se model, we show that H. pylori deregulates mitochondria by two novel mechanisms, both rather associ

127 ract to regulate the turnover and quality of mitochondria, by increasing both mitophagic activity and

128 signaling, including the role of Ca buffers, mitochondria, Ca leak, and regulation of diastolic [Ca(2

129 Mitochondria can be both an H2S source and sink, and man

130 Mammalian mitochondria can be transferred between cells both in cu

131 Together, our findings indicate that mitochondria can modulate subcellular functional special

132 ormal lifespan in diverse longevity pathways.Mitochondria can undergo shape changes as a result of fu

133 d prevent potential loss and swelling of the mitochondria caused by mutant Htt.

134 otes mitophagy that eliminates dysfunctional mitochondria characterized by low membrane potential and

135 of zebrafish cones revealed that nearly 100 mitochondria cluster at the apical side of the inner seg

136 Thus, L. pneumophila can shut down ER-mitochondria communication through cleavage of syntaxin

137 cytosol while their levels were decreased in mitochondria compared to Nx.

138 myeloid leukemia (AML) cells have increased mitochondria compared with nonmalignant CD34(+) hematopo

139 Mitochondria comprise the primary reactive oxygen specie

140 stingly, we discovered that tightening of ER-mitochondria contacts by overexpression of VAPB or PTPIP

141 urther, vMIA hydrophobic interactions and ER-mitochondria contacts facilitate proper organization of

142 PDZD8 was necessary for the formation of ER-mitochondria contacts in mammalian cells.

143 ntified PDZD8 as an ER protein present at ER-mitochondria contacts.

144 Human mitochondria contain a genome (mtDNA) that encodes essen

145 ts not only help in the understanding of how mitochondria cope with replicative stress but can also e

146 that targeting a redox cycling nitroxide to mitochondria could prevent reactive oxygen species accum

147 pIX-SDT caused cell membrane damage prior to mitochondria damage and upregulated the expression of Fa

148 paternal mitochondrial genomes or destroying mitochondria delivered to the zygote by the sperm [4-13]

149 sized that this variation in respiration per mitochondria depends on plasticity in cristae density, a

150 ed mutagenesis and use of STAT3 knockout and mitochondria-depleted cells.

151 oring protein syntaphilin via a new class of mitochondria-derived cargos independent of Parkin, Drp1,

152 is produced by ATP-citrate lyase (ACLY) from mitochondria-derived citrate or by acetyl-CoA synthetase

153 al modeling revealed that Pex15 molecules at mitochondria display age-independent Msp1 sensitivity.

154 Previously, we showed that mitochondria-driven pre-senescent phenotype diminishes t

155 o Salmonella during xenophagy, as well as to mitochondria during mitophagy.

156 one-dependent cAMP response locally, affects mitochondria dynamics and protects from apoptotic cell d

157 Impaired mitochondria dynamics and quality control are involved i

158 e, isoleucine (Ile), and valine (Val) in the mitochondria efficiently allows the formation of ATP by

159 as the Oxa1 is required for the insertion of mitochondria-encoded membrane proteins.

160 study, we examine the assembly of the MECA (mitochondria-endoplasmic reticulum [ER]-cortex anchor),

161 How mitochondria escape this irreversible defect accumulatio

162 Brown adipose tissue (BAT) mitochondria exhibit high oxidative capacity and abundan

163 ial mitophagy receptor involved in targeting mitochondria for autophagic degradation.

164 teins prone to aggregation are imported into mitochondria for degradation.

165 promotes Bak enrichment at the ER to tether mitochondria for efficient calcium transfer.

166 fter synthesis to transfer the enzyme to the mitochondria for subsequent activation.

167 Mitochondria form close physical associations with the e

168 Mitochondria form extensive networks constantly remodele

169 Here we show that PrP(C) is present in brain mitochondria from 6-12 week old wild-type and transgenic

170 ic immunocapture to rapidly purify HA-tagged mitochondria from homogenized mammalian cells in approxi

171 Oxygen consumption in freshly isolated mitochondria from mice treated with Honokiol showed enha

172 , yet the bioenergetic respiratory status of mitochondria from prion-infected animals is unknown.

173 ast, oxidized CLs were readily hydrolyzed in mitochondria from wild-type mice during oxidative stress

174 Subpopulations of mitochondria from young and old mouse kidney resemble th

175 Using vesicles prepared from mammalian mitochondria (from Bos taurus) and from the bacterium Pa

176 eneous redistribution of nucleoids among the mitochondria, generating a population of mitochondria ta

177 sferase (ChAT) enzyme expression, fragmented mitochondria, glial cell activation, muscle atrophy, wei

178 The accumulation of dysfunctional mitochondria has been implicated in aging, but a deeper

179 lasma membrane potential of excitable cells, mitochondria have thus far eluded optogenetic control.

180 rary to the prevailing concept of intronless mitochondria, here we present evidence that mitochondria

181 processes required for clearance of damaged mitochondria: (i) general autophagy initiation and (ii)

182 e useful for investigating the importance of mitochondria in a variety of biological processes.

183 get; however, the pathophysiological role of mitochondria in ADPKD remains uncharacterized.

184 Until recently, the dual roles of mitochondria in ATP production (bioenergetics) and apopt

185 ensity and increased the presence of damaged mitochondria in BAT.

186 Remarkable new roles for mitochondria in calcium handling, apoptosis, heme turnov

187 n D1-MSNs, consistent with increased smaller mitochondria in D1-MSN dendrites after repeated cocaine.

188 r the vectorial transfer of imported iron to mitochondria in developing red cells and of PCBP1 and NC

189 lation enhances autophagosome recruitment to mitochondria in HeLa cells.

190 activity and the physiological properties of mitochondria in hippocampal neurons.

191 intracellular fate of endocytosed exogenous mitochondria in human iPS-derived cardiomyocytes and pri

192 ptosis based on release of cytochrome c from mitochondria in lysates human embryonic kidney cells HEK

193 sm as part of their lethality and can damage mitochondria in mammalian cells.

194 diseases due in part to the central role of mitochondria in metabolism, ROS regulation, and proteost

195 Generating dysfunctional mitochondria in MSCs using rhodamine 6G pretreatment als

196 ucted analysis of bidirectional movements of mitochondria in primary motor neuron axons expressing wi

197 Mechanistically, we show that mitochondria in senescent cells lose the ability to meta

198 significantly slower retrograde transport of mitochondria in Ser135Phe, Pro39Leu and Arg140Gly mutant

199 y of sesamol and unveiling the importance of mitochondria in sesamol-induced effects using a human he

200 ress and decreased the membrane potential of mitochondria in SNc dopaminergic neurons.

201 a lipid raft-like domain closely apposed to mitochondria in such a way that the 2 organelles are abl

202 our data suggest that PrP(C) can be found in mitochondria in the absence of disease, old age, mutatio

203 We studied the role of mitochondria in this process using budding yeast as a mo

204 or the health and physiological functions of mitochondria, including complementation of damaged mitoc

205 es Actr10 as a factor necessary for dynactin-mitochondria interaction, enhancing our understanding of

206 teracts with LC3/GABARAP proteins, targeting mitochondria into autophagosomes for degradation.

207 (hereafter referred to as PMI), which drives mitochondria into autophagy without collapsing their mem

208 The entry of calcium into mitochondria is central to metabolism, inter-organelle c

209 demonstrate that the initiation mechanism in mitochondria is distinct from that in the well-studied n

210 ons revealed that the capacity to traffic to mitochondria is encoded within the first 84 amino acids

211 acid, via fusion of phospholipid vesicles to mitochondria isolated from DHA-fed mice, rescued the maj

212 -disease-associated proteins can be found in mitochondria, it remains unclear how mitochondrial dysfu

213 es and provides concrete evidence that yeast mitochondria lack mechanisms for removal of ribonucleoti

214 virus signal-anchored protein known as viral mitochondria-localized inhibitor of apoptosis (vMIA) tra

215 of ribosome quality control specifically on mitochondria-localized ribosomes, ultimately preventing

216 energic stimulation, while no evidence for a mitochondria-located NOS was obtained.

217 e corresponding probes selectively targeting mitochondria, lysosomes, and F-actin demonstrate low tox

218 vement of additional H. pylori activities in mitochondria-mediated effects.

219 Whereas apoptosis and mitochondria-mediated necrosis signaling is well establi

220 chemistry strategies to target compounds to mitochondria, mitochondrial probes, and sensors, and exa

221 athways suggest that uptake of EGFP-labelled mitochondria occurs via an actin-dependent endocytic pat

222 rases (RNAPs) are present in phage T7 and in mitochondria of all eukaryotes.

223 s essential for calcium (Ca(2+)) uptake into mitochondria of all mammalian tissues, where it regulate

224 SDH1 to SDH4 subunits in bacteria and in the mitochondria of animals and fungi.

225 To clarify this function, we examined the mitochondria of cyst-lining cells in ADPKD model mice (K

226 Mitochondria of eukaryotic cells contain a labile copper

227 Using BH3 profiling, we find that mitochondria of many adult somatic tissues, including br

228 ondrial movements in neurons, is directed to mitochondria of tumor cells.

229 ium channel Kv1.3 is highly expressed in the mitochondria of various cancerous cells.

230 ere largely corrected by targeting Stard7 to mitochondria or treating epithelial cells with a mitocho

231 Mitochondria organelles have small circular genomes with

232 mitted equally well into the nucleus and the mitochondria, our results support a view of the cytosoli

233 hos burden and inversely proportional to the mitochondria OxPhos capacity.

234 nteractions independently of conventional ER-mitochondria pathways to traffic from the ER to mitochon

235 Mitochondria-penetrating peptides (MPPs) are specific ta

236 namics of IRE1 deactivation by regulating ER-mitochondria physical contacts and the autophosphorylati

237 Our data reveal 2D dynamics of the mitochondria, plasma membrane and filopodia, and the 2D

238 Hepatic mitochondria play a central role in the regulation of in

239 Mitochondria play a primary role in the pathophysiology

240 Damaged mitochondria pose a lethal threat to cells that necessit

241 restricted to the perinuclear area, with few mitochondria present at the cell periphery.

242 el 1 (VDAC1) induced Parkin translocation to mitochondria, presumably by stimulating ROS generation.

243 eraction, enhancing our understanding of how mitochondria properly localize in axons.

244 New therapeutic strategies targeting mitochondria protection and cellular bioenergetics are p

245 iration levels toggled SOD1 in or out of the mitochondria, respectively.

246 gests that the regulation of autophagy by ER-mitochondria signaling is at least partly dependent upon

247 ndings indicate that alterations in neuronal mitochondria structure are very sensitive to the tissue

248 f Rab5 and endosomal-mediated degradation of mitochondria, suggesting cross-talk between these two pa

249 anterograde transporters of cargos, such as mitochondria, synaptic vesicle precursors, neurotransmit

250 the mitochondria, generating a population of mitochondria tailored to seedling growth.

251 ically encoded Ca(2+) sensors, we found that mitochondria take up Ca(2+) when it accumulates either i

252 well as misfolded endogenous proteins inside mitochondria takes place via their sequestration into a

253 nally, we review published attempts to apply mitochondria-targeted agents for the treatment of cancer

254 e investigated a size-controlled, dual tumor-mitochondria-targeted theranostic nanoplatform (Porphyri

255 MES complex is an endoplasmic reticulum (ER)-mitochondria tether composed of four proteins, three of

256 n on autophagy are a consequence of their ER-mitochondria tethering function.

257 (Mfn2), a membrane protein implicated in ER-mitochondria tethering, also shows reduced expression in

258 a coactivator 1alpha (PGC-1alpha), and fewer mitochondria than controls from untreated AML animals.

259 sfer protein Stard7 promotes uptake of PC by mitochondria, the importance of this pathway for mitocho

260 Mitochondria, the ubiquitous power packs in nearly every

261 ipids are main fuels for cellular energy and mitochondria their major oxidation site.

262 ssion during spermatogenesis and the sperm's mitochondria, thereby increasing migration velocity and

263 sary and sufficient for Vms1 localization to mitochondria, through binding the MTD in an interaction

264 er challenge in distributing and maintaining mitochondria throughout their arbors.

265 A from an egg or zygote containing defective mitochondria to a corresponding egg or zygote with norma

266 ism of Nur77-dependent clearance of inflamed mitochondria to alleviate inflammation.

267 re an LGP2-MDA5 oligomer shuttles NS3 to the mitochondria to block antiviral signaling.

268 This approach primed mitochondria to immediately increase their oxygen consum

269 ents showed that transplantation of isolated mitochondria to ischemic heart tissue leads to decreases

270 niporter activity compromises the ability of mitochondria to maintain distinct Ca(2+) domains.

271 mplex 1 activity, increased vulnerability of mitochondria to mitochondrial stressors, leading to elev

272 x (gamma-TuRC), and is sufficient to convert mitochondria to MTOCs independent of core pericentriolar

273 ence appear to be involved in the priming of mitochondria to perform uncoupled respiration downstream

274 'quasisynaptical' feeding of calcium to the mitochondria to promote oxidative phosphorylation.

275 K2-mediated selective targeting of uncoupled mitochondria to the autophagic machinery.

276 the pre-apoptotic proteins translocate from mitochondria to the cytosol during HI through the Src ki

277 reticulum [ER]-cortex anchor), which tethers mitochondria to the ER and plasma membrane.

278 heart by transplanting respiration-competent mitochondria to the injured region.

279 t loss of fusion capacity targets fragmented mitochondria to the pre-autophagic pool and upregulates

280 In mitochondria, TOM and TIM complexes transport nuclear-en

281 ial dynamics is a conserved process by which mitochondria undergo repeated cycles of fusion and fissi

282 Diverse protein import pathways into mitochondria use translocons on the outer membrane (TOM)

283 genesis and removal of damaged/dysfunctional mitochondria via mitophagy.

284 Mechano-stimulation of mitochondria - via encounter with motile intracellular p

285 , and thus endurance capacity, is set by the mitochondria volume.

286 sely, stimulating the export of calcium from mitochondria was also neuroprotective.

287 A disturbed distribution pattern of mitochondria was predominantly present in TCM.

288 To date, fragmentation of mitochondria was studied either in dissociated cultured

289 Using isolated cardiac mitochondria, we demonstrate a novel mechanism by which

290 ER contacts with mitochondria were abundant in all compartments, with the

291 consumption rate (OCR) and ATP production by mitochondria were ameliorated by NTZ in real time by vir

292 ulb epithelial cells had high viability, and mitochondria were polarized.

293 otes Nur77 translocation from the nucleus to mitochondria, where it interacts with tumor necrosis fac

294 MCU clearly enhanced the Ca(2+) uptake into mitochondria, which significantly promoted ROS productio

295 he mother cell, in part through tethering to mitochondria, while the disaggregase Hsp104 helps to dis

296 vacuoles containing degenerated and swollen mitochondria with cristolysis.

297 mitochondrial turnover, by targeting damaged mitochondria with low membrane potential to mitophagy.

298 The treatment of control mitochondria with the acetylating agent acetic anhydride

299 Collectively, these results show that intact mitochondria with their mtDNA payload are transferred in

300 he diverse complement of proteins present in mitochondria, yet the rules that govern this selection a