ライフサイエンスコーパス: late endosome

1 eceptor down-regulation and recycling at the late endosome.

2 ll integral membrane protein of the lysosome/late endosome.

3 ment of elevated pH, likely derived from the late endosome.

4 veloped viruses that enter cells through the late endosome.

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

6 protein that captures vesicles inbound from late endosomes.

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

8 ty greatly reduced cortactin localization to late endosomes.

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

10 5 were trafficked sequentially from early to late endosomes.

11 Internalized BCR localized normally to late endosomes.

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

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

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

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

16 to early endosomes, recycling endosomes and late endosomes.

17 mimicked gradual acidification from early to late endosomes.

18 arly/recycling endosomes and subsequently to late endosomes.

19 ys via distinct intracellular trafficking to late endosomes.

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

21 t endogenous GMFG localized within early and late endosomes.

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

23 regulates transport from early endosomes to late endosomes.

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

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

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

27 requires multiple fusion events at early and late endosomes.

28 reas Rab7(dominant negative) trapped RGS4 in late endosomes.

29 in virus internalization and trafficking to late endosomes.

30 ag at an intermediate step between early and late endosomes.

31 s, but not on Rab7, which is associated with late endosomes.

32 hat activated FLS2 receptors are targeted to late endosomes.

33 sion and membrane dynamics between early and late endosomes.

34 GFP was accumulated in early, recycling, and late endosomes.

35 CRT III) machinery, and then with markers of late endosomes.

36 verse cell types that accumulated as dilated late endosomes.

37 alization in early endosomes and transfer to late endosomes.

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

39 suggest a rationale for phlebovirus entry in late endosomes.

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

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

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

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

44 hanisms, including physical sequestration in late endosomes.

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

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

47 mportant regulator for AMSH3 function at the late endosomes.

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

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

50 sitide-interacting domain (ML1N) to activate late endosome and lysosome (LEL)-localized transient rec

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

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

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

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

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

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

57 zed with markers of the trans-Golgi network, late endosomes and alpha-granules.

58 567 residue of ezrin was rephosphorylated in late endosomes and at the plasma membrane at later times

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

60 CLN3-positive early endosomes, late endosomes and cholesterol/sphingolipid-enriched pla

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

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

63 ion of cholesterol and glycosphingolipids in late endosomes and early lysosomes.

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

65 (DM), and influences DM localization within late endosomes and exosomes.

66 that Rush controls trafficking from early to late endosomes and from late endosomes to lysosomes by m

67 anisms control cytosolic protein delivery to late endosomes and identify a microautophagy-like proces

68 Gag localization at the plasma membrane and late endosomes and increased the accumulation of HIV-1 G

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

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

71 also promoted trafficking of mutant NPC1 to late endosomes and lysosomes and rescued the aberrant st

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

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

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

75 Phagosomal fusion with late endosomes and lysosomes enhances proteolysis, causi

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

77 autophagosomes gain competence to fuse with late endosomes and lysosomes is not known.

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

79 glioside and unesterified cholesterol within late endosomes and lysosomes of neurons in selective bra

80 s colocalizes with Rab7, Rab9, and Lamp-1 in late endosomes and lysosomes to a similar extent.

81 f beta1 integrin to the degradation pathway (late endosomes and lysosomes) rather transport along rec

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

83 f LRRK2 (Lrrk) localizes to the membranes of late endosomes and lysosomes, physically interacts with

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

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

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

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

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

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

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

91 urnover, CAV1 is ubiquitinated and sorted to late endosomes and lysosomes.

92 tein is required for cholesterol efflux from late endosomes and lysosomes.

93 well as overexpressed TMEM106B localizes to late endosomes and lysosomes.

94 inting to a defect in the transition between late endosomes and lysosomes.

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

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

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

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

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

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

101 tubular connections between MT1-MMP-positive late endosomes and the plasma membrane in contact with t

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

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

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

105 lowed the axonal transport of autolysosomes, late endosomes, and lysosomes and caused their selective

106 ges that increases resistance of phagosomes, late endosomes, and lysosomes to membrane damage.

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

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

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

110 Thus, although both early and late endosomes appear to support cross presentation in h

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

112 ection depends on processing in the early to late endosome as well as in the lysosome prior to nuclea

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

114 t DC receptors that are targeted to early or late endosomes at distinct efficiencies.

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

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

117 t-negative Rab GTPases that affect early and late endosome biogenesis and maturation influenced reovi

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

119 interference had little effect on lysosomes/late endosomes but severely inhibited axonal transport o

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

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

122 The limiting membrane of late endosomes can fuse with the plasma membrane, leadin

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

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

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

126 TbRab7 defines discrete late endosomes closely juxtaposed to the terminal p67(+)

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

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

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

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

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

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

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

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

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

136 The delivery of autophagic cargo to late endosomes for complete or partial degradation has a

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

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

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

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

141 MP into invasive pseudopodia, primarily from late endosomes, from which it was delivered to the plasm

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

143 early endosome/multivesicular bodies to the late endosome-Golgi for surface expression or to the lys

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

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

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

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

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

149 in recycling tubules largely failed to reach late endosomes in HeLa cells, whereas other CIE cargo pr

150 nd Scar homolog (WASH) on MT1-MMP-containing late endosomes in invasive breast carcinoma cells.

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

152 arly endosomes are distinguished from static late endosomes in order to study Aspergillus nidulans en

153 annin treatment, which induces the fusion of late endosomes in plants, resulted in enlarged FLY1-YFP

154 that acidic pHs comparable to those seen in late endosomes induce a structural change in the capsid

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

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

157 hology, but the transition between early and late endosomes is sharp, as only in a minor proportion o

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

159 While virions reached early and late endosomes, ISVPs did not and instead escaped the en

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

161 ously undescribed role for Cul3 complexes in late endosome (LE) maturation.

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

163 otein, L1, are necessary for escape from the late endosome (LE).

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

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

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

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

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

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

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

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

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

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

174 promoted PDC differentiation, and increased late endosome localization of autoantigen in PDCs and mo

175 trin also caused caveolin-1 to accumulate on late endosome/lysosomal membranes.

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

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

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

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

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

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

182 links mTORC1 to a critical component of the late endosome/lysosome, the V-ATPase.

183 no acids direct mTORC1 to the surface of the late endosome/lysosome, where mTORC1 becomes receptive t

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

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

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

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

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

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

190 Targeting of caveolin-1 to late endosome/lysosomes is not observed normally, and th

191 somal pH gradient also trapped caveolin-1 on late endosome/lysosomes.

192 accumulation of unesterified cholesterol in late endosomes/lysosomes (LE/L) and impaired export of c

193 kdown impaired the fusion of phagosomes with late endosomes/lysosomes and high levels of active Rab34

194 ation and accumulation of BACE1 in early and late endosomes/lysosomes as well as at the cell membrane

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

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

197 AVP, thus demonstrating that escape from the late endosomes/lysosomes is a critical step for improvin

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

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

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

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

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

203 410S at acidic pH, a reduced LDL delivery to late endosomes/lysosomes, and an increased release in th

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

205 mitochondria, Rab5-positive early endosomes, late endosomes/lysosomes, and TrkA-, TrkB-, and APP-posi

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

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

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

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

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

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

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

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

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

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

216 rgoes exocytosis through egress of LNPs from late endosomes/lysosomes.

217 which colocalizes with active alpha5beta1 in late endosomes/lysosomes.

218 tive (EEA-1(+)) early endosomes or LAMP-1(+) late endosomes/lysosomes.

219 active-conformation alpha5beta1 integrin to late endosomes/lysosomes.

220 ponsible for recruiting the motor complex to late endosomes/lysosomes.

221 biquitination of CD98 and routing of CD98 to late endosomes/lysosomes.

222 ment of fob in the fusion of phagosomes with late endosomes/lysosomes.

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

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

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

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

227 5, an early endosome marker, but not Rab7, a late endosome marker.

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

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

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

234 ue to the recently reported dysregulation of late endosome movement by ORP1L knockdown.

235 d early and recycling endosome movement, but late endosome movement is unaffected, and mitotic spindl

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

237 oluble cytosolic proteins to the vesicles of late endosomes/multivesicular bodies (MVBs).

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

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

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

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

242 umulated in the intraluminal vesicles of the late endosome, phosphorylation of the receptor was not s

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

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

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

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

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

248 The strong fusion-enhancing effect of BMP, a late endosome-resident lipid, is consistent with the mod

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

250 and Rab7 GTPases, associated with early and late endosomes, respectively.

251 m recycling tubules to EEA1 compartments and late endosomes, resulting in reduced surface levels.

252 ll integral membrane protein of the lysosome/late endosome (SIMPLE) account for the rare autosomal-do

253 small integral membrane protein of lysosome/late endosome (SIMPLE) cause autosomal dominant, Charcot

254 ogression of endocytosed cargo and increases late endosome size.

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

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

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

258 cruited to membranes already at the stage of late endosomes still lacking vacuolar morphology, but th

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

260 d showed greater association with markers of late endosomes than phagosomes containing wild-type M. t

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

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

263 residence time of molecules in endosomes or late endosomes, thus potentially increasing the likeliho

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

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

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

267 icking from early to late endosomes and from late endosomes to lysosomes by modulating the activity o

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

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

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

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

272 ycling of mannose 6-phosphate receptors from late endosomes to the trans Golgi network.

273 nsport of mannose 6-phosphate receptors from late endosomes to the trans-Golgi network.

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

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

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

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

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

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

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

281 1 at the plasma membrane and is recruited to late endosomes upon Avr4 trigger, also depending on BAK1

282 ition, pah1Delta vacuoles were devoid of the late endosome/vacuolar Rab Ypt7p, the phosphatidylinosit

283 This early-to-late endosome/vacuole transition is coupled to dynein-de

284 45 in early endosomes and Vps33 in early and late endosomes/vacuoles contributes to the wide domain o

285 RabS(Rab7) mediates homotypic fusion of late endosomes/vacuoles in a homotypic fusion- and vacuo

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

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

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

289 These late endosomes were not functional lysosomes as they wer

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

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

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

293 One family member, IFITM3, localizes to late endosomes, where reoviruses undergo proteolytic dis

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

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

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

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

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

299 and within or in association with early and late endosomes, with some nuclear co-localization observ

300 ells, but only those that traverse early and late endosomes yield a productive infection.