ライフサイエンスコーパス: autophagosome

1 closes to form a double-membrane vesicle (an autophagosome).

2 ng the autophagy machinery, and building the autophagosome.

3 -far-unidentified proteins and lipids to the autophagosome.

4 f-eating by a double-membrane organelle, the autophagosome.

5 ates RILP expression and its localization to autophagosomes.

6 delivery to lysosomes within double membrane autophagosomes.

7 hagosomes without impeding the completion of autophagosomes.

8 proteins localise to the plasma membrane and autophagosomes.

9 ry, but failed to develop into LC3B-positive autophagosomes.

10 lethanolamine (PE) on the surface of nascent autophagosomes.

11 fically bridge the ubiquitinated cargos into autophagosomes.

12 ER), mitochondria, endosomes, lysosomes, and autophagosomes.

13 ulated both autophagic flux and clearance of autophagosomes.

14 ice and rats (but not controls) had multiple autophagosomes.

15 tion kinase complex subunit ATG13 to nascent autophagosomes.

16 facilitates incorporation of aggregates into autophagosomes.

17 nits, clathrin, actin and ARP2/3 proteins to autophagosomes.

18 cells by increasing the percentage of filled autophagosomes.

19 ysosomes via double-membrane vesicles called autophagosomes.

20 s not alter VacA trafficking to lysosomes or autophagosomes.

21 chanisms necessary for clearance of synaptic autophagosomes.

22 alization and co-localized with LC3-positive autophagosomes.

23 40 at distinct ER domains to package ER into autophagosomes.

24 ons lysosomes and prevents their fusion with autophagosomes.

25 autophagic flux, and marked accumulation of autophagosomes.

26 ntation, disorganised cristae, and increased autophagosomes.

27 mitochondria followed by sequestration into autophagosomes.

28 rafficking route delivers it directly to the autophagosomes.

29 in autophagic flux, possibly due to unsealed autophagosomes.

30 ociates with azurophilic granules and LC3(+) autophagosomes.

31 ATG9 vesicles, thereby enabling growth into autophagosomes.

32 ei formation and cytokinesis where they form autophagosomes.

33 d by double-membrane-bound organelles called autophagosomes.

34 ct from LC3B lipidation onto double-membrane autophagosomes.

35 Microscopy confirmed autophagosome accumulation after genetic or small interf

36 s AMPK activation triggers localized hillock autophagosome accumulation and mitophagy, ultimately res

37 v1g1 in UBQLN2 knockout HeLa cells increased autophagosome acidification, suggesting a therapeutic ap

38 on in HeLa cells reduced autophagic flux and autophagosome acidification.

39 in the location and density of lysosomes and autophagosomes along the axon shaft.

40 ses, including endosome formation, fusion of autophagosomes/amphisomes with lysosomes, and apoptosis.

41 protein expression correlated with increased autophagosome and autolysosome formation in renal tubula

42 is completed by SNARE-mediated fusion of the autophagosome and endolysosome membranes.

43 nked to disruption of autophagy and impaired autophagosome and lysosome function.

44 eliminates damaged mitochondria through the autophagosome and lysosome pathways.

45 Time-lapse imaging of autophagosomes and ATP/ADP levels in migrating cells in

46 Dox-induced autophagosomes and autolysosome accumulation were confir

47 I is relatively specifically associated with autophagosomes and autolysosomes (in the absence of cond

48 a multifocal disease process resulting from autophagosomes and autolysosomes accumulation, altered e

49 s have increases in lipid droplet-containing autophagosomes and autolysosomes and defective lysosomal

50 crophages and increases its association with autophagosomes and autolysosomes.

51 ated using electron microscopic detection of autophagosomes and by measuring LC3B protein lipidation

52 iculum (ER) serves as an initiation site for autophagosomes and is also remodeled in response to nutr

53 While biogenesis of autophagosomes and late endosomes occurs continuously at

54 tion of atherosclerosis and abnormalities of autophagosomes and lysosomes in macrophages with reducti

55 Autophagosomes and lysosomes isolated from HCV-infected

56 ay that degrades cellular components through autophagosomes and lysosomes, mediates the downregulatio

57 educed BECN1 levels and blocks the fusion of autophagosomes and lysosomes.

58 e of autolysosomes, a fusion intermediate of autophagosomes and lysosomes.

59 demonstrate predominant localization within autophagosomes and lysosomes.

60 not return to vacuoles such as lysosomes or autophagosomes and macrophages did not die.

61 or nitrogen starvation, MoHMT1 localises to autophagosomes and MoHMT1 mutants display defects in aut

62 The accumulation of autophagosomes and p62 protein in cardiomyocytes was als

63 ecessary for the maturation and clearance of autophagosomes and that defects in transport and ATG-4.2

64 NUB1 moreover increased autophagosomes and the recruitment of lysosomes to aggre

65 uestosomes within double-membraned vesicles (autophagosomes), and sequestosomes within multivesicular

66 Complex I generates the autophagosome, and Complex II is crucial for endosomal t

67 nous organelles, including mitochondria, the autophagosome, and endolysosome.

68 phosphorylation, STING rapidly transits into autophagosomes, and IRF3 activation, interferon producti

69 sential for retrograde transport of neuronal autophagosomes, and surprisingly, their biogenesis as we

70 ns of pre-autophagosomes, tubular ER, mature autophagosomes, and the ubiquitin proteasome system duri

71 results indicate that SphK2 is required for autophagosome- and lysosome-mediated catabolism of intra

72 During this process, autophagosomes are formed de novo by membrane fusion eve

73 ease, and influences the way we consider how autophagosomes are formed.

74 dinate trafficking and clearance of synaptic autophagosomes are poorly understood.

75 s support a novel role for autophagy and the autophagosome as a previously unidentified compartment t

76 isassembly of autophagy proteins from mature autophagosomes as well as delaying fusion of autophagoso

77 e mutation on downstream pathways leading to autophagosome assembly.

78 n the daytime, endoplasmic reticula (ER) and autophagosomes associate more with mitochondria, and mit

79 Moreover, AtEHs/Pan1-regulated autophagosomes associate with ER-PM contact sites (EPCS)

80 ise overexposure triggers recruitment of the autophagosome-associated protein MAP1LC3B (LC3B; microtu

81 or Vps13 in the sequestration of the ER into autophagosomes at late endosomes.

82 within double-membrane delimited structures (autophagosomes) before lysosomal fusion.

83 ay, wherein RILP integrates the processes of autophagosome biogenesis and retrograde transport to con

84 ificant decrease in the rate of constitutive autophagosome biogenesis during aging and observed prono

85 understanding of the mechanisms involved in autophagosome biogenesis has increased substantially dur

86 cally expressing WIPI2B effectively restored autophagosome biogenesis in aged neurons.

87 ssary and fully sufficient to rescue blocked autophagosome biogenesis in ATG2A/ATG2B KO cells, implyi

88 Autophagosome biogenesis involves de novo formation of a

89 including neurons, Leu negatively regulates autophagosome biogenesis via its metabolite, acetyl-coen

90 centrosome occurs during starvation-induced autophagosome biogenesis, but how centrosomal proteins r

91 G16L1 (E3) complex are two critical steps in autophagosome biogenesis, connected by WIPI2.

92 nto the core molecular mechanisms underlying autophagosome biogenesis, with a specific emphasis on me

93 ated, albeit not fully overlapping, roles in autophagosome biogenesis.

94 lly analyze the molecular basis of selective autophagosome biogenesis.

95 rs and TBK1 as principal drivers of targeted autophagosome biogenesis.

96 with transient and incomplete inhibition of autophagosome biogenesis.

97 agy protein implicated at distinct phases of autophagosome biogenesis.

98 e for LC3 lipidation, which is a key step in autophagosome biogenesis.

99 n of Atg9 and COPII vesicles at the start of autophagosome biogenesis.

100 esicles to provide a source of lipids during autophagosome biogenesis.

101 umbers suggesting an unexpected RILP role in autophagosome biogenesis.

102 TF in melanoma cells increases the number of autophagosomes but is not sufficient to induce autophagi

103 ATG9A is not incorporated into autophagosomes but is proposed to supply so-far-unidenti

104 gaxonin-E3 ligase controls the production of autophagosomes by a reversible, ubiquitin-dependent proc

105 Autophagy receptors package the ER into autophagosomes by binding to the ubiquitin-like yeast pr

106 -related HD cellular phenotypes, we examined autophagosomes by electron microscopy.

107 lux and increases the steady-state levels of autophagosomes by increasing the expression of Arl8b, wh

108 During macroautophagic stress, autophagosomes can be produced continuously and in high

109 tion as evidenced by the accumulation of the autophagosome cargo protein p62/SQSTM1, and a poorly ind

110 e, leading to accumulation of non-functional autophagosome, cathepsin B release and pineoblastoma cel

111 In neurons, defects in autophagosome clearance have been associated with neurod

112 highlighting a functional role for VAMP7 in autophagosome clearance that has previously been sidelin

113 idues blocks filament formation in vitro and autophagosome closure and HIV-1 release in human cells.

114 es drive membrane scission in HIV-1 release, autophagosome closure, multivesicular body biogenesis, c

115 Here, we establish a FACS-based HaloTag-LC3 autophagosome completion assay to screen a genome-wide C

116 nt domain, which is found to be required for autophagosome completion but dispensable for ESCRT-I com

117 ion of autophagy-related genes particularly, autophagosome complex.

118 /2-dependent signalling and the formation of autophagosome complexes.

119 JIP3-mediated retrograde transport, and that autophagosomes containing synaptic material mature in th

120 tions in autophagy result from a blockage of autophagosome degradation rather than an increase in aut

121 osomes in many cellular functions, including autophagosome degradation, cholesterol homeostasis, anti

122 athway where double-membrane vesicles called autophagosomes deliver cytoplasmic content to the lysoso

123 e altered, and there are long delays between autophagosome delivery and FA disassembly.

124 processed, infectious virus progenies within autophagosome-derived vesicles.

125 Finally, mature autophagosomes detach from the ER membrane by an as yet

126 nd triggered by dysregulated accumulation of autophagosomes due to upregulation of Rubicon.

127 tochondria were sequestrated by LC3-positive autophagosomes during mitophagy.

128 d ultrastructural characteristics typical of autophagosomes during the late stage of infection.

129 d early by ZIKV infection, and impairment of autophagosome elongation by the class III phosphatidylin

130 s a significant increase in puncta of LC3(+) autophagosomes, endogenous levels of LC3-II, and ultrast

131 ring the past few decades has elucidated how autophagosomes engulf their substrates selectively.

132 P(2) -dependent regulatory loop that impacts autophagosome flux by affecting Rab7 cycling and PLEKHM1

133 c components by multilayered vesicles called autophagosomes, followed by lysosomal fusion and degrada

134 g of TET2, as well as its recruitment to the autophagosome for degradation.

135 C6, activation of AMPK mobilizes Kif19a into autophagosomes for degradation in airway epithelial cell

136 a, which in turn engulf alpha-synuclein into autophagosomes for degradation via selective autophagy (

137 ABARAP proteins, targeting mitochondria into autophagosomes for degradation.

138 d by triggering the formation of surrounding autophagosomes for delivery to lysosomes.

139 ith ATG8, a ubiquitin-like protein directing autophagosome formation and cargo recruitment.

140 PCM1 enhances GABARAP/WIPI2/p62-positive autophagosome formation and flux but has no significant

141 nism, we identified H1N1-induced blocking of autophagosome formation and inhibition of autophagic flu

142 ompound C markedly abrogated lithium-induced autophagosome formation and mitigated the protective eff

143 in ubiquitin binding, was also defective in autophagosome formation and recruitment to the Atg12-5-1

144 Mammalian ATG8 proteins drive autophagosome formation and selective removal of protein

145 s associated with impaired rapamycin-induced autophagosome formation and trafficking to lysosomes in

146 Autophagosome formation and Unc-51-like autophagy activa

147 ial cells, with a constitutive deficiency in autophagosome formation as detected with the mCherry-eGF

148 phosphorylation at Ser-177 was required for autophagosome formation but not for Optn recruitment to

149 athway directly and indirectly contribute to autophagosome formation during starvation.

150 er FIP200 around NBR1 cargo and induce local autophagosome formation enforces cargo specificity and r

151 Four functional protein groups involved in autophagosome formation had conserved and non-conserved

152 nserved components, suggesting plasticity in autophagosome formation in fungi.

153 Transmission EM revealed abundant autophagosome formation in response to both stimuli.

154 positive puncta become larger in cells where autophagosome formation is abrogated, and are prominent

155 of HCMV-infected monocytes, as repression of autophagosome formation led to cellular death of infecte

156 atform on which the critical early events of autophagosome formation occurred, including LC3-membrane

157 es encoding the key enzymes or regulators in autophagosome formation or autophagic process, including

158 pharmacologic treatments that either inhibit autophagosome formation or block the fusion of autophago

159 ave been described and involve inhibition of autophagosome formation or indirect mechanisms.

160 the direct roles of the various PRMTs during autophagosome formation remain unclear.

161 Autophagosome formation requires multiple autophagy-rela

162 as it depletes normal-functioning DNM2 from autophagosome formation sites on recycling endosomes by

163 ATG4B stimulates autophagy by promoting autophagosome formation through reversible modification

164 restraining UNC-51 activity, RPM-1 inhibits autophagosome formation to affect axon termination, syna

165 autophagy-related protein (ATG)7, ATG2b, and autophagosome formation Unc-51 like kinase 1, and the ge

166 While early stages of autophagosome formation were unaffected, we detected the

167 e review current knowledge of the process of autophagosome formation with special emphasis on the ver

168 iquitin ligase activity restricts UNC-51 and autophagosome formation within specific axonal compartme

169 translation shutoff, cell cycle arrest, and autophagosome formation, all of which enhance virus repl

170 d conversion of LC3B-I to LC3B-II, decreased autophagosome formation, and increased p62 level compare

171 the fundamental mechanisms of the control of autophagosome formation, and provide a molecular switch

172 in regulators, WHAMM and JMY, participate in autophagosome formation, but the signals linking autopha

173 In contrast, activation of autophagosome formation, either by starvation or by inhi

174 of proteins, which either directly regulate autophagosome formation, for example, components of the

175 in 7 (Atg7), proteins involved in phagophore-autophagosome formation, in ALD.

176 This "scission" step is, thus, critical for autophagosome formation, is defective in a human disease

177 ntrolled transcription and was essential for autophagosome formation, PERK acted in a transcription-i

178 LC3-lipidation, the signature of autophagosome formation, results from a complex ubiquiti

179 of the cellular sites believed to engage in autophagosome formation, review basic mechanisms used to

180 ased expression of AtEH/Pan1 proteins boosts autophagosome formation, suggesting independent and redu

181 A/1B-light chain 3 (LC3)BII/I expression and autophagosome formation.

182 contact sites is a principal contributor to autophagosome formation.

183 phagy adaptors if it has mechanisms to block autophagosome formation.

184 upstream autophagy factors drives continued autophagosome formation.

185 s role in selective autophagy initiation and autophagosome formation.

186 ites of cytosolic bacterial cells to promote autophagosome formation.

187 acid starvation, ATG9A traffics to sites of autophagosome formation.

188 eir role in early stages of autophagy during autophagosome formation.

189 r a crosstalk between cargo condensation and autophagosome formation.

190 urons after SE, together with an increase in autophagosome formation.

191 domain, and ATG9A vesicles together initiate autophagosome formation.

192 t has no significant effect on LC3B-positive autophagosome formation.

193 th kinetics similar to that seen in cellular autophagosome formation.

194 omplex is recruited by WIPI2b to the site of autophagosome formation.

195 ransport hub supplying various components of autophagosome formation.

196 n Atg8 (LC3 in mammals), which is needed for autophagosome formation.

197 thway, and their lipidation is essential for autophagosome formation.

198 range of developmental processes, including autophagosome formation.

199 recycling, thereby preventing endosomes and autophagosomes from reaching lysosomes.

200 ng which prevacuolar compartments (PVCs) and autophagosomes fuse with the vacuole membrane (tonoplast

201 nalling molecule NF-kappaB and impairment of autophagosome fusion to lysosomes, a key process in auto

202 osome degradation rather than an increase in autophagosome generation.

203 potential donor membranes for this sustained autophagosome growth, but specific machinery to support

204 The purified autophagosomes had double- or multiple-membrane structur

205 -standard assay for assessing the numbers of autophagosomes in cells.

206 Recent studies established that nascent autophagosomes in distal axons move predominantly in the

207 nistic analysis showed a reduction of mature autophagosomes in LRRK2 G2019S fibroblasts, which was re

208 s with the cochaperone BAG3 and localizes to autophagosomes in mitosis, and STIM1 protein levels are

209 observed pronounced morphological defects in autophagosomes in neurons from aged mice.

210 interact to enhance abnormal accumulation of autophagosomes in neurons.

211 mes are distinct from endocytic vesicles and autophagosomes in that they are single-membrane bound va

212 EphrinB2-deficient osteocytes displayed more autophagosomes in vivo and in vitro, and EphrinB2-Fc tre

213 rambling activity and yield markedly smaller autophagosomes, indicating that lipid scrambling by ATG9

214 endosomes, multivesicular bodies, and early autophagosomes induced by Etf-1, and they provide host-c

215 beled host-cell membranes were trafficked to autophagosomes induced by the E. chaffeensis type IV sec

216 tophagy and that acute Mn exposure increases autophagosome induction/formation.

217 and II (PI3KC3-C1 and -C2) are essential for autophagosome initiation and maturation, respectively, f

218 deliver the PI4-kinase, PI4KIIIbeta, to the autophagosome initiation site.

219 -transfer protein likely operating at the ER-autophagosome interface.

220 tion of a double-membrane vesicle called the autophagosome is a key event in the transport of multipl

221 formation of the double-membrane compartment autophagosome is seeded by small vesicles carrying membr

222 LC3-II, a standard marker for autophagosomes, is generated by the conjugation of cytos

223 d kinase 1/Parkin (Pink1/Parkin) pathway and autophagosomes labeled with the autophagy proteins autop

224 s in the first intron of genes that regulate autophagosome/lysosomal degradation, mitochondrial traff

225 gy substrate and is subjected to cytoplasmic autophagosome-lysosome degradation, via the autophagy pr

226 as recently emerged as a master regulator of autophagosome-lysosome function, controlling the express

227 down of Arl8b in HCV-infected cells restored autophagosome-lysosome fusion and autophagic flux to lev

228 e LAMP-2 isoform B (LAMP-2B) as required for autophagosome-lysosome fusion in human cardiomyocytes (C

229 17 (STX17), a protein that is essential for autophagosome-lysosome fusion in non-CMs.

230 creased LC3 turnover after treatment with an autophagosome-lysosome fusion inhibitor, chloroquine, in

231 g routes including late endosome maturation, autophagosome-lysosome fusion, crinophagy and lysosome-r

232 m late endosomes and releases a regulator of autophagosome-lysosome fusion, PLEKHM1, from the membran

233 ng (HOPS) complex, which plays a key role in autophagosome-lysosome fusion.

234 CC that inhibits autophagic flux by blocking autophagosome-lysosome fusion.

235 er of LC3-positive structures with defective autophagosome-lysosome fusion.

236 Syntaxin 17 (Stx17) has been implicated in autophagosome-lysosome fusion.

237 bited lamin degradation, likely by hampering autophagosome-lysosome fusion.

238 HOS-defective cells because of inhibition of autophagosome-lysosome fusion.

239 activity and deplete RAS proteins through an autophagosome-lysosome-mediated degradation pathway.

240 , whereas LRRK2-R1441C induced a decrease in autophagosome/lysosome fusion and increased lysosomal pH

241 ard genetic screens, we then determined that autophagosome maturation in the cell body depends on the

242 an essential role during LC3 lipidation and autophagosome maturation.

243 protein drastically reduces the formation of autophagosomes mediated by TRIM23 or TBK1.

244 n enigmatic step in de novo formation of the autophagosome membrane compartment is the expansion of t

245 support the delivery of lipid to the growing autophagosome membrane has remained unknown.

246 pids such as phosphatidylethanolamine in the autophagosome membrane.

247 t is the origin and lipid composition of the autophagosome membrane?

248 ever, including, What determines the site of autophagosome nucleation?

249 its LC3-binding LIR motifs strongly decrease autophagosome numbers suggesting an unexpected RILP role

250 echanism by which HCV increases steady-state autophagosome numbers while simultaneously inhibiting fl

251 nfirmed that the Dox-induced accumulation of autophagosomes occurs due to blockage of the lysosomal d

252 croscopy showed that lysosomes interact with autophagosomes on detyrosinated microtubules.

253 Here, we report that the release of autophagosome precursors from recycling endosomes is med

254 ssion of LRRK2-G2019S or hWT-LRRK2 inhibited autophagosome production, whereas LRRK2-R1441C induced a

255 the first regulator of ATG16L1 turn-over and autophagosome production.

256 We discovered that a pre-autophagosome protein ATG9A was enriched in DNs when a p

257 d that compounds that interact with both the autophagosome protein microtubule-associated protein 1A/

258 2 transgenic animals revealed alterations in autophagosome puncta number reflecting those phenotypes

259 nally, serine 34/35 phosphorylation enhances autophagosome recruitment to mitochondria in HeLa cells.

260 Some of these compounds targeted mHTT to autophagosomes, reduced mHTT levels in an allele-selecti

261 n of SNAP23 inhibited the association of the autophagosome regulators ATG16L1 and ATG9 compartments b

262 gy-related SNARE protein syntaxin17 with the autophagosome remained unaffected.

263 anistic underpinning for the formation of an autophagosome selectively around the cytosolic cargo, th

264 roteins, in which double-membraned vesicles (autophagosomes) sequester cytoplasmic cargos, which are

265 es for hours to days, illustrating efficient autophagosome sequestration but delayed lysosomal fusion

266 Autophagy comprises the processes of autophagosome synthesis and lysosomal degradation.

267 Among these are the Barkor/ATG14L autophagosome targeting sequence (BATS), which makes aut

268 ing levels of disease-causing proteins using autophagosome-tethering compounds.

269 scade that culminates in the formation of an autophagosome that degrades cellular cargo.

270 volving de novo formation of double membrane autophagosomes that capture cytosolic constituents (carg

271 move and remodel cellular membranes to form autophagosomes that enclose and metabolize cytoplasmic c

272 s involves the formation of double-membraned autophagosomes that engulf the cargoes destined for degr

273 the cargo to the UBLs present on the forming autophagosome, the latter proteins were proposed to effe

274 iciency did not impair autophagy initiation, autophagosome to lysosome fusion, or protease activities

275 tophagosome formation or block the fusion of autophagosomes to endolysosomal compartments caused an i

276 facilitate their interaction and fusion with autophagosomes to initiate autophagy.

277 al infection and incorporates it into mature autophagosomes to mediate an efficient lysosomal clearan

278 Autophagosomes transfer cytosolic material to acidified

279 precluding premature dynein recruitment and autophagosome transport.

280 tubule capture event leads to delivery of an autophagosome, triggering FA disassembly.

281 nce that DNs evolve from dysfunctions of pre-autophagosomes, tubular ER, mature autophagosomes, and t

282 scovered K(+)channels that are important for autophagosome turnover and lysosomal pH regulation and a

283 expression of Armus, a RAB7-GAP required for autophagosome turnover and whose add-back rescues autoph

284 intenance of axonal growth-cone dynamics and autophagosome turnover.

285 , suggesting a neuron-specific alteration in autophagosome turnover.

286 TT patients display a defective formation of autophagosomes under conditions of nutrient starvation a

287 vivo by the state of neuronal activity, that autophagosomes undergo UNC-16/JIP3-mediated retrograde t

288 tion-dependent manner, and recruited them to autophagosomes via interaction of the EXO70D AIM with th

289 association of lipid rafts with HCV-induced autophagosomes was confirmed by Western blotting, immuno

290 of Pg or localization inside double-membrane autophagosomes was evident, with dividing Pg suggesting

291 and a dramatic decrease in ER packaging into autophagosomes was observed.

292 Bacterium-containing autophagosomes were absent within the cytoplasm.

293 the formation of the double-membrane vesicle autophagosome, which is the functional unit of autophagy

294 Internalized MOG colocalized with autophagosomes, which can protect from destructive proce

295 oplasmic components in specialized vesicles, autophagosomes, which transport the cargo to the degrada

296 of cytoplasmic contents by double-membraned autophagosomes, which ultimately fuse with lysosomes to

297 phagy pathway that result from the fusion of autophagosomes with late endosomes.

298 autophagosomes as well as delaying fusion of autophagosomes with the vacuole.

299 ation enhanced the localization of ASOs into autophagosomes without altering intracellular concentrat

300 translocation of SNAREs Stx17 and SNAP29 on autophagosomes without impeding the completion of autoph