ライフサイエンスコーパス: late endosome

1 veloped viruses that enter cells through the late endosome.

2 CLIC4 is co-localized with MMP14 in the late endosome.

3 me causes the 5-HT(2C)R to be stalled in the late endosome.

4 verse cell types that accumulated as dilated late endosomes.

5 alization in early endosomes and transfer to late endosomes.

6 liver them by membrane fusion and fission to late endosomes.

7 suggest a rationale for phlebovirus entry in late endosomes.

8 elles, including the trans-Golgi network and late endosomes.

9 ceptor DMA-1 on dendrites by targeting it to late endosomes.

10 osis and low pH-dependent membrane fusion in late endosomes.

11 ized at the plasma membrane and in early and late endosomes.

12 ation of intraluminal vesicles (ILVs) within late endosomes.

13 hanisms, including physical sequestration in late endosomes.

14 n of ZIP14 from plasma membrane to early and late endosomes.

15 amplitudes, particularly at the acidic pH of late endosomes.

16 ir ability to restrict entry and fusion from late endosomes.

17 mportant regulator for AMSH3 function at the late endosomes.

18 bnormally associated with PAI-1 in early and late endosomes.

19 protein that captures vesicles inbound from late endosomes.

20 ndependent Mannose 6-Phosphate Receptor from late endosomes.

21 vation required for MMP14/TIMP2 targeting to late endosomes.

22 ty greatly reduced cortactin localization to late endosomes.

23 s revealed that ALIX and AMSH3 colocalize on late endosomes.

24 5 were trafficked sequentially from early to late endosomes.

25 Internalized BCR localized normally to late endosomes.

26 ion by enzymes such as DNase II localized in late endosomes.

27 (EGA), that prevents transport from early to late endosomes.

28 ation of a complex between NRP-1 and RAB7 in late endosomes.

29 ost, influenza A virus transits via early to late endosomes.

30 to early endosomes, recycling endosomes and late endosomes.

31 mimicked gradual acidification from early to late endosomes.

32 arly/recycling endosomes and subsequently to late endosomes.

33 ys via distinct intracellular trafficking to late endosomes.

34 ansport of the ubiquitinated form of CAV1 to late endosomes.

35 t endogenous GMFG localized within early and late endosomes.

36 n of early endosomes to Rab9/CD63-containing late endosomes.

37 regulates transport from early endosomes to late endosomes.

38 h the endocytosed BCRs through the early and late endosomes.

39 fered with trafficking of CAV1 from early to late endosomes.

40 w-density-lipoprotein (LDL)-cholesterol from late endosomes.

41 requires multiple fusion events at early and late endosomes.

42 s, which prevents the maturation of early to late endosomes.

43 questration of the ER into autophagosomes at late endosomes.

44 examined Rab GTPase expression in early and late endosomes.

45 egrin beta(1), and traffic through early and late endosomes.

46 (V)1.2 channels from dyads to Rab-7-positive late endosomes.

47 for viruses that enter cells by fusing with late endosomes.

48 ane in i mp mutants, accumulating instead in late endosomes.

49 urs mainly in lysosomes and is negligible in late endosomes.

50 b5-positive early endosomes to Rab7-positive late endosomes.

51 een the ER and several organelles, including late endosomes.

52 l receptors, and low pH to trigger fusion in late endosomes.

53 esult from the fusion of autophagosomes with late endosomes.

54 gionella-containing vacuole and to early and late endosomes.

55 fection, whereas Ad35 and Ad26 accumulate in late endosomes 2 to 8 h postinfection.

56 e two lipid receptors, which interact in the late endosome(9), are necessary for the membrane fusion

57 increased numbers of significantly enlarged late endosomes, a phenotype that was mimicked by the fus

58 8/LAMTOR1-mediated peripheral positioning of late endosomes allows delivery of SRC proto-oncogene, no

59 RNA-bearing Rab7a late endosomes also associate with ribosomes, and real-t

60 roper sorting of MMP14 into the lumen of the late endosome and its proteolytic activation in lipid ra

61 t with the HOPS complex, a component for the late endosome and lysosome fusion machinery, and enhance

62 phagosome acidified rapidly and acquired the late endosome and lysosome protein LAMP1.

63 ate that the ESCRTs can function at both the late endosome and the vacuole membrane to mediate cargo

64 irectly engages the retromer at the early or late endosome and traffics to the TGN/Golgi via the retr

65 nd L2/DNA complexes segregate from L1 in the late endosome and travel to the nucleus, IFN-gamma treat

66 oncomitant impairment of reovirus transit to late endosomes and a delay in reovirus disassembly.

67 or NPC2 leads to cholesterol accumulation in late endosomes and causes neuronal dysfunction and neuro

68 ntly, the rates of ligand-induced sorting to late endosomes and degradation of EGFR-AMSH were dramati

69 fficking of epidermal growth factor (EGF) to late endosomes and degradation of its receptor were impa

70 ith ALIX and is required for PAR1 sorting at late endosomes and degradation.

71 growth factor receptors (EGFR) from early to late endosomes and enhanced activation of EGFR signallin

72 d for optimal influenza virus trafficking to late endosomes and for consequent fusion, entry, and inf

73 with impaired influenza virus trafficking to late endosomes and hence with fusion and entry.

74 ases targeting of the MMP14/TIMP2 complex to late endosomes and increases trafficking of MMP14 from e

75 rafficking of internalized beta1 integrin to late endosomes and its ultimate degradation.

76 Met (MET), and shunts their trafficking into late endosomes and lysosomal degradation.

77 s are the major Ca(2+)-permeable channels on late endosomes and lysosomes (LEL).

78 predominantly localized to the membranes of late endosomes and lysosomes (LELs).

79 cterized by impaired cholesterol efflux from late endosomes and lysosomes and secondary accumulation

80 delayed trafficking of EGF to LAMP1-positive late endosomes and lysosomes and slowed EGF receptor (EG

81 Overall, our results identify Lamp1(+) late endosomes and lysosomes as portals for passing prot

82 cross presentation of antigens delivered to late endosomes and lysosomes by uptake of anti-DEC205 an

83 at the surface of intralysosomal vesicles of late endosomes and lysosomes catalyzed in a stepwise fas

84 py, we found that TRPML1 channels present in late endosomes and lysosomes formed stable complexes wit

85 Activation of mTORC1 on late endosomes and lysosomes is facilitated by amino-aci

86 tively within the acidic microenvironment of late endosomes and lysosomes of cancer cells (pH 5.4) an

87 We confirm that Sph accumulates in late endosomes and lysosomes of cells derived from Niema

88 Lgmn is a cysteine protease of late endosomes and lysosomes that can be secreted; it ex

89 w enhanced cellular retention of LNPs inside late endosomes and lysosomes, and increased gene silenci

90 P(Sc) aggregates primarily accumulate within late endosomes and lysosomes, organelles that participat

91 l8b, bringing about clustering and fusion of late endosomes and lysosomes.

92 ly affected the albumin distribution between late endosomes and lysosomes.

93 nsient (kissing) or complete fusions between late endosomes and lysosomes.

94 ng endosomes and an even smaller fraction in late endosomes and lysosomes.

95 t KIF1A and KIF1Bbeta bind preferentially to late endosomes and lysosomes.

96 ansported into cellular compartments such as late endosomes and lysosomes.

97 Rab7-expressing compartments, which includes late endosomes and lysosomes.

98 h, and likely caused by, delayed fusion with late endosomes and lysosomes.

99 ology and mislocalization of DAF-4/BMPRII to late endosomes and lysosomes.

100 their origins from intraluminal vesicles of late endosomes and of a lysosomal compartment, respectiv

101 to PI(4,5)P(2) causes Rab7 dissociation from late endosomes and releases a regulator of autophagosome

102 s traffic through the endocytic pathway into late endosomes and reside there for up to 24 h after inc

103 ates alpha1B-adrenergic receptor transfer to late endosomes and that Rab9 regulates this process and

104 expression enhances, EGFR trafficking to the late endosomes and that the effect of Rab31 silencing co

105 sized lysosomal proteins are targeted to the late endosomes and the ATP7A copper transporter is trans

106 and PtdIns(4,5)P2 that are colocalized with late endosomes and the endoplasmic reticulum.

107 olesterol accessible to a D4H probe, between late endosomes and the PM.

108 ARF6 compared with ApoE3, trapping ABCA1 in late-endosomes and impairing its recycling to the cell m

109 stic of the plasma membrane, early endosome, late endosome, and lysosome.

110 , the cortical ER marker Rtn1 accumulated at late endosomes, and a dramatic decrease in ER packaging

111 FgVps35-GFP co-localized with both early and late endosomes, and associated with the trans-Golgi netw

112 for SERINC5 down-regulation, trafficking to late endosomes, and exclusion from newly synthesized vir

113 ion bottleneck imposed by their residency in late endosomes, and it also suggests that such structure

114 s by sequential fusion with early endosomes, late endosomes, and lysosomes.

115 usion of the phagosome with early endosomes, late endosomes, and lysosomes.

116 that is independent of the retromer complex, late endosomes, and recycling endosomes.

117 Late endosomes are a major trafficking hub in the cell a

118 tol-3-phosphate-binding protein recruited to late endosomes, as an important regulator of IRT1-depend

119 in-mediated clustering of cholesterol-loaded late endosomes at the Golgi region, a process regulated

120 BACE1 is predominantly accumulated within late endosomes at the synapses of AD-related mutant huma

121 f Notch receptor trafficking to Rab7-labeled late endosomes but not early endosomes.

122 The EGFR colocalized with the late endosome, but no significant colocalization of the

123 vator inhibitor-1 (PAI-1) into the early and late endosomes by 4- to 5-fold prior to AIF nuclear tran

124 in VPS33B selectively disrupt recruitment to late endosomes by RILP or binding to its partner VIPAS39

125 tether with endocytic organelles (lysosomes/late endosomes) by forming membrane contact sites.

126 show that Rab27a controls the trafficking of late endosomes carrying phosphatidylinositol 4-kinase ty

127 Here, we show an essential function for late endosomes carrying the p14-MP1 (LAMTOR2/3) complex

128 3) Late endosomes, cisternae, and multivesicular bodies acc

129 ated GTP-binding protein 7 (Rab7)-associated late endosomes compared with their nonlipidated counterp

130 l 3-phosphate (PI3P) in vivo and acts in the late endosome compartment.

131 form 1a.H(+) provokes a specific staining of late endosome compartments (pH 5.0-5.5) after 5 h of inc

132 utophagic traffic by impairing the fusion of late endosome compartments with the tonoplast.

133 ntaining Sorting Nexin 16 and a reduction in late endosomes containing Rab11.

134 of causing the mis-trafficking of early and late endosomes containing uPAS cargo and leading to AIF-

135 Taken together, our results suggest that late endosomes contribute to the regulation of cell migr

136 TrkB and CaSR colocalize within late endosomes, cotraffic and coactivate GSK3, which ser

137 brane protein 8 (VAMP8), an R-SNARE found on late endosomes, could increase tau secretion.

138 Interference of early and late endosomes disrupts intercellular movement of SHR.

139 No large late endosomes filled with VZV particles were observed i

140 requires traffic through early endosomes to late endosomes followed by transient (kissing) or comple

141 TPase Rab7 to transition ERBB2 from early to late endosome for degradation.

142 e the intracellular sorting of AMPARs toward late endosomes for degradation.

143 In NMDAR-LTD, however, they are diverted to late endosomes for degradation.

144 d type Orai1 is trafficked to Rab 7-positive late endosomes for lysosomal degradation.

145 ld type Orai1 is trafficked to Rab7-positive late endosomes for lysosomal degradation.

146 ntaphilin cargos, which then share a ride on late endosomes for transport toward the soma.

147 UMB and NUMBL resulted in a partial block of late endosome formation, resulting in sustained ERBB2 si

148 Late endosomes from Munc13-4-KO neutrophils show decreas

149 eticulum-resident VAP proteins that regulate late endosome function under regulation of Rab7-GTP.

150 ed through actin-dependent exocytosis of the late endosome in a vasodilator-stimulated phosphoprotein

151 were used to show that Spdo is sorted toward late endosomes in a Numb-dependent manner.

152 Unesterified cholesterol accumulates in late endosomes in cells expressing the misfolded cystic

153 on in the soma and abnormal retention within late endosomes in distal axons of mutant hAPP neurons.

154 mparably relocate with a subset of early and late endosomes in four different human glioma cell lines

155 VAMP8 staining was preferentially found on late endosomes in N2a cells.

156 accumulates heavily inside cholesterol-rich late endosomes in Npc1(-/-) cells.

157 ation of SERINC5 and localization to Rab7(+) late endosomes in T cells.

158 Our findings thus reveal that late endosomes interact with RNA granules, translation m

159 suggesting that TLR4 transport from early to late endosomes is interrupted, which may contribute to e

160 demonstrate that secretion of exosomes from late endosomes is required for directionally persistent

161 te of constriction and fission for early and late endosomes is spatially and temporally linked to con

162 in human DCs, TLR triggering induces tubular late endosomes, labeled by fluorescent LDL.

163 PRPH2 is first targeted to the lumen of the late endosome (LE) en route to the cilia.

164 Here we show that the late endosome (LE) is the main waystation that criticall

165 entry, polyomavirus SV40 is sorted from the late endosome (LE) to the endoplasmic reticulum (ER) to

166 Loss of USP32 inhibits late endosome (LE) transport and recycling of LE cargos,

167 lysosomal compartment arising from fusion of late endosome (LE) with lysosome is required for recogni

168 usion defects, but accumulated regulators of late endosome (LE)/autophagosome maturation.

169 s trafficked through the exocytic pathway to late endosomes (LE) and lysosomes (Ly) (LE/Ly) to global

170 choriomeningitis virus, which enter through late endosomes (LE).

171 exin A2 (ANXA2) co-localizes with PS-ASOs in late endosomes (LEs) and enhances ASO activity.

172 or that mediates the retrograde transport of late endosomes (LEs) and interacts with dysbindin, a sub

173 is, we observed that the recruitment of host late endosomes (LEs) and lysosomes is reduced in uis4(-)

174 s that inhibition of cholesterol export from late endosomes (LEs) inhibits Stx6-dependent integrin re

175 te antisense oligonucleotides (PS-ASOs) from late endosomes (LEs) is a rate-limiting step and a poorl

176 but specific, dispersal of lysosomes (lyso)/late endosomes (LEs) that is mediated by inhibition of a

177 paired dynein-driven retrograde transport of late endosomes (LEs).

178 rane-enclosed endocytotic organelles, mainly late endosomes (LEs).

179 unit 1 (Blos1) leads to the repositioning of late endosomes (LEs)/lysosomes to the microtubule-organi

180 H (ELC) and is localized at ESCRT-I-positive late endosomes likely through its PI3P and actin binding

181 evels enhanced EGFR co-localization with the late endosome/lysosomal marker, lysosomal-associated mem

182 ) membrane-tethering complex is required for late endosome-lysosome and autophagosome-lysosome fusion

183 ity of its effector, HOPS, which facilitates late endosome-lysosome fusion and the consumption of AP-

184 ation to an association with the TfR1 at the late endosome-lysosome.

185 between human and mouse, is localized to the late endosome/lysosome and interacts with the lysosomal

186 e, we show that TMEM106B is localized in the late endosome/lysosome compartments and TMEM106B levels

187 ial content are selectively delivered to the late endosome/lysosome for degradation, providing eviden

188 Furthermore, ASO rapidly trafficked to the late endosome/lysosome in poor productive uptake cells c

189 d the number of vacuoles that accumulate the late endosome/lysosome marker LAMP-1 during macrophage i

190 The Rab7 marker for the late endosome/lysosome route was also capable of discrim

191 raction with Tom1 allow Tollip to facilitate late endosome/lysosome trafficking in response to mitoch

192 Cs displayed increased expression of Rab7, a late endosome/lysosome-associated small GTPase.

193 retention of L2 and the viral genome in the late endosome/lysosome.

194 s-induced PINK1/parkin-dependent MDVs to the late endosome/lysosome.

195 Late endosomes, lysosomes, and endoplasmic reticulum wer

196 l pathway, leading to a dramatic increase in late endosomes, lysosomes, and light-dependent PR degene

197 bcellular distribution of Hyal1 as early and late endosomes, lysosomes, and recycling vesicles.

198 tinct ClC-3 splice variants targets ClC-4 to late endosome/lysosomes (ClC-3a and ClC-3b) or recycling

199 led that *0401 molecules traffic through the late endosome/lysosomes while *0402 molecules traffic in

200 cholesterol at membrane contacts between the late endosomes/lysosomes (LEL) and the endoplasmic retic

201 of raft partitioning led to mistargeting to late endosomes/lysosomes because of a failure to recycle

202 mHtt was targeted preferentially to the late endosomes/lysosomes compared with wild-type Htt.

203 that accumulation of free cholesterol in the late endosomes/lysosomes of Arf6 KO MEFs results from mi

204 pids and other storage lipids in selectively late endosomes/lysosomes of NPC1-KO cells.

205 Moreover, we show that p97 helps clear late endosomes/lysosomes ruptured by endocytosed tau fib

206 n PSEN2 that directs this gamma-secretase to late endosomes/lysosomes via a phosphorylation-dependent

207 A fraction of Stx3 is localized to late endosomes/lysosomes, although how it traffics there

208 410S at acidic pH, a reduced LDL delivery to late endosomes/lysosomes, and an increased release in th

209 ACE1 accumulation in the early endosomes and late endosomes/lysosomes, and decreased levels of BACE1

210 Full-length E3/49K was not detected in late endosomes/lysosomes, but the C-terminal fragment ac

211 Whereas ClC-3a and ClC-3b are present in late endosomes/lysosomes, ClC-3c is targeted to recyclin

212 w-density lipoprotein-derived cholesterol in late endosomes/lysosomes, disruption of endocytic traffi

213 etion, and inhibited by chemical ablation of late endosomes/lysosomes, suggesting a lysosomal secreto

214 concentrates at contacts between the ER and late endosomes/lysosomes, where it interacts with GTP-Ra

215 as lysobisphosphatidic acid, is enriched in late endosomes/lysosomes, where it plays a key role in t

216 ked colocalization of internalized TfR1 with late endosomes/lysosomes, whereas attenuating the lysoso

217 ed SPIONs are internalized and accumulate in late endosomes/lysosomes, while aminolipid-SPIONs reside

218 tor (LDLR) that promotes LDLR degradation in late endosomes/lysosomes.

219 embrane, causing cholesterol accumulation in late endosomes/lysosomes.

220 ocopies PSEN2 and shifts its localization to late endosomes/lysosomes.

221 sitol (3,5)-bisphosphate, a key component of late endosomes/lysosomes.

222 iments revealed that ABHD6 co-localizes with late endosomes/lysosomes.

223 o with the plasma membrane and Rab7-positive late endosomes/lysosomes.

224 s required for MAPK and mTOR1 signaling from late endosomes/lysosomes.

225 total EGFR levels and its redistribution to late endosomes/lysosomes.

226 e by causing the accumulation of pMHC inside late endosomes/lysosomes.

227 r Rab11 and to a much lesser extent with the late endosome marker Rab7.

228 orted by colocalization with LysoTracker and late endosome markers.

229 Not surprisingly, this late endosome marking depends on the intra-organelle pH,

230 (RabGTPase 7 is known to be associated with late endosome maturation).

231 HOPS-dependent trafficking routes including late endosome maturation, autophagosome-lysosome fusion,

232 n homolog (PTEN), which facilitates early to late endosome maturation, decreased MIG6, and also incre

233 te endosomes, suggesting a delay in early-to-late endosome maturation.

234 thepsin-dependent inflammasome activation in late endosomes, may trigger innate immunity.

235 together these components localize to an ER-late endosome MCS.

236 At these ER-late endosome MCSs, mitochondria are also recruited to f

237 ollowed by clearance of the plasma membrane, late endosomes, mitochondria and the endoplasmic reticul

238 k Rab7 activation and show severe defects in late endosome morphology and endosomal LDL trafficking,

239 ns-Golgi network, plasma membrane, apoplast, late endosome/multivesicular bodies (MVB), transitory la

240 EEA1-positive early endosomes, Rab7-positive late endosomes/multivesicular bodies, and LAMP1-positive

241 nge of Ypt7p on multivesicular bodies (MVBs)/late endosomes must take place before HOPS can mediate t

242 While biogenesis of autophagosomes and late endosomes occurs continuously at axon terminals, no

243 We show that RNA-bearing late endosomes often pause on mitochondria and that mRNA

244 vidence suggests that cleavage occurs in the late endosome or lysosome during endocytic recycling.

245 Anterograde transport of late endosomes or lysosomes (LE/Lys) is crucial for prop

246 ng compartments were initially thought to be late endosomes or multivesicular bodies, but it has sinc

247 rt from the trans-Golgi network (TGN) to the late endosome/prevacuolar compartment (PVC) and for TGN

248 ana) ALIX directly binds to ABA receptors in late endosomes, promoting their degradation.

249 TRPV2 colocalized with Rab7, a late endosome protein, in addition to TrkA and activated

250 n-independent mannose 6-phosphate receptor), late endosomes (Ras-associated binding protein 27a), and

251 release of fluorescent oligonucleotides from late endosomes rather than other intracellular compartme

252 virus [VSV]), while viruses that fuse in the late endosome (recombinant VSV-Lassa and VSV-Junin), inc

253 targeting to the cell periphery and thereby late endosome recycling and had a major impact on YAP si

254 Our findings identify the late endosome recycling pathway as a key mechanism that

255 and uncoating involving low pH in early and late endosomes, respectively.

256 for vacuolar degradation occurs through the late endosome route and depends on FYVE DOMAIN PROTEIN R

257 typal member of the Reoviridae, utilizes the late endosome-specific lipid lysobisphosphatidic acid fo

258 CGs are refilled with granzyme B at the late endosome stage and polarize to subsequent synapses

259 arrested endocytic traffic progression at a late-endosome stage.

260 concomitant with a decrease in Rab7-positive late endosomes, suggesting a delay in early-to-late endo

261 show that the Nef-Alix interaction occurs in late endosomes that are enriched in internalized CD4.

262 ssociation of axonal RNA granules with Rab7a-late endosomes that provides a platform for local transl

263 icles accumulated within large M6PR-positive late endosomes that were not degraded en route to the pl

264 At the level of late endosomes, they are depleted of membrane-stabilizin

265 We find that Orai1-SNPs escape late endosomes through endosomal pH regulation of intera

266 IFITM2 and IFITM3 and their association with late endosomes, thus augmenting LV core endosomal escape

267 Overproduction of Btn2p, involved in late endosome to Golgi protein transport, or its paralog

268 hich control the trafficking of MT1-MMP from late endosome to the plasma membrane and play an importa

269 nternalization and trafficking via early and late endosomes to down-regulation.

270 14) enzymatic recovery/recycling through the late endosomes to enable disengagement of tissue inhibit

271 Autophagy promoted HCV trafficking from late endosomes to lysosomes, thus providing a link with

272 receptor recycling and receptor targeting to late endosomes to regulate signaling output after asymme

273 bed delivery of cargo via autophagosomes and late endosomes to SiNP-filled cathepsin B/L-containing l

274 f NPC1 disrupts cholesterol trafficking from late endosomes to the endoplasmic reticulum and plasma m

275 rions through the endosomal system, and from late endosomes to the trans-Golgi-network, before nuclea

276 ing of these tethering complexes to early or late endosomes to time fusion events in the endo/lysosom

277 some/multivesicular bodies (MVB), transitory late endosome/ tonoplast, tonoplast, plastids, mitochond

278 es whereby dynein has been shown to regulate late endosome trafficking of EGFR with the Rab7 GTPase.

279 ic reticulum Mn(2+) transporter Spf1 and the late endosome/trans-Golgi Nramp metal transporter Smf2.

280 ctin network formation in vitro and early-to-late endosome transport in vivo also depend on the F-act

281 tely required, much like actin, for early-to-late-endosome transport and multivesicular endosome form

282 1 at the plasma membrane and is recruited to late endosomes upon Avr4 trigger, also depending on BAK1

283 45 in early endosomes and Vps33 in early and late endosomes/vacuoles contributes to the wide domain o

284 infection of viruses that enter through the late endosome was relatively resistant to TSPAN9 depleti

285 Colocalization of Munc13-4 and syntaxin 7 at late endosomes was demonstrated by high-resolution and l

286 osome-associated membrane protein 1-positive late endosomes was evaluated with confocal microscopy.

287 of the M6PR pathway (trans-Golgi network to late endosomes) was constrained in infected Pompe cells.

288 Previously, we reported that late endosomes were implicated in tau secretion.

289 These late endosomes were not functional lysosomes as they wer

290 ment and internalization, virions traffic to late endosomes where GP is cleaved by host cysteine prot

291 FR signaling response by the transit-time to late endosomes where it is switched-off by high PTP1B ac

292 facilitates PS-ASO trafficking from early to late endosomes where it may also contribute to PS-ASO re

293 TMEM16F is located in late endosomes, where it facilitates the generation of m

294 Uncoating of naked virions occurs in late endosomes, whereas eHAV undergoes ALIX-dependent tr

295 ating protein TBC1 domain family member 5 to late endosomes, which controls the conversion of Rab7a f

296 of cholesterol in multivesicular bodies and late endosomes, which inhibits the fusion of intralumina

297 eased the intracellular processing of ICs in late endosomes, which is associated with decreased synth

298 Rab7 promotes fusion of autophagosomes and late endosomes with lysosomes in yeast and metazoan cell

299 on machinery, alpha-factor still proceeds to late endosomes with the same kinetics.

300 uential exposure to the pH of both early and late endosomes, with each step corresponding to changes