ライフサイエンスコーパス: endosome

1 orresponding changes in cargo sorting at the endosome.

2 of PE molecules in the membrane of the early endosome.

3 vice that orchestrates cargo export from the endosome.

4 and causes its accumulation in the recycling endosome.

5 ed with membrane fusion in the low pH of the endosome.

6 nly partially inhibit ASLV fusion with early endosomes.

7 EGF-like trafficking through EEA1-containing endosomes.

8 sogenic trimers in the acidic environment of endosomes.

9 dent active alpha5beta1-integrin to assorted endosomes.

10 e budding of intralumenal vesicles (ILVs) at endosomes.

11 tay at the plasma membrane or are trapped in endosomes.

12 rapidly altered by Rab11A-positive recycling endosomes.

13 n microscopy, and optimize their delivery to endosomes.

14 the recycling of SK2 channels from recycling endosomes.

15 e synaptobrevin-like v-SNARE Snc1 from early endosomes.

16 similarly in canonical phagosomes as well as endosomes.

17 vian sarcoma and leukosis virus (ASLV), with endosomes.

18 P intermediate (GPCL) generated in host cell endosomes.

19 ules, but were generally distinct from early endosomes.

20 or close to RAB5+/ early endosome antigen 1- endosomes.

21 the recycling processes of SK2 channels from endosomes.

22 ists act preferentially via caveolae-derived endosomes.

23 layed until EphA2 has been internalized into endosomes.

24 on occurring only after receptor uptake into endosomes.

25 dL with retromer-coated vacuolar and tubular endosomes.

26 de within intracellular compartments such as endosomes.

27 l quality control mediated by Rab5 and early endosomes.

28 k, and subsequently Rab11-positive recycling endosomes.

29 cell types that accumulated as dilated late endosomes.

30 n GIPC1 to facilitate transport to recycling endosomes.

31 ynapses that were large and lacked recycling endosomes.

32 lowing them to bind receptors and traffic to endosomes.

33 s and selectively inhibited CLR signaling in endosomes.

34 eotide CpG, were present as cargo in IRAP(+) endosomes.

35 that promotes the pausing of SHR-associated endosomes.

36 e Rab can coordinate recycling and fusion on endosomes.

37 n reported to regulate cholesterol levels in endosomes.

38 an influx of superoxide anion in the ensuing endosomes.

39 apparatus, presumably through the recycling endosomes.

40 osomes often interacting with EEA-1(+) early endosomes.

41 here it associates with early and re-cycling endosomes.

42 ciated protein (GABARAP)+ autophagosomes and endosomes.

43 agocytic pathway, tPCs mature by fusing with endosomes.

44 c reticulum (ER) and mitochondria as well as endosomes.

45 DISLL enhances the exit of BACE1 from early endosomes, a pathway mediated by GGA1 and retromer, whic

46 at the tips of these filopodia, while APPL1 endosomes accumulate at the base.

47 s in the trafficking and tubulation of early endosomes along microtubules.

48 pologically equivalent processes at both the endosome and the plasma membrane and are consistently re

49 hat the ESCRTs can function at both the late endosome and the vacuole membrane to mediate cargo sorti

50 /DNA complexes segregate from L1 in the late endosome and travel to the nucleus, IFN-gamma treatment

51 s necessary for beta-arrestin recruitment to endosomes and Akt signaling and lays the foundation for

52 is required for beta-arrestin recruitment to endosomes and Akt signaling.

53 CpGs) engage Toll-Like Receptor 9 (TLR-9) in endosomes and are well described stimulators of the inna

54 lopodia formation and MYO6 motor function at endosomes and at the plasma membrane.

55 ains endosomal recycling, thereby preventing endosomes and autophagosomes from reaching lysosomes.

56 ellular localization, with CD63 primarily in endosomes and CD9 on the plasma membrane.

57 ts at the intersection of autophagosomes and endosomes and contributes to cellular homeostasis by med

58 h factor receptors (EGFR) from early to late endosomes and enhanced activation of EGFR signalling upo

59 endophilin-A2 and endophilin-B1 to enlarged endosomes and formation of highly dynamic filamentous ne

60 e transport of BACE1 from early to recycling endosomes and have identified essential roles for the so

61 logy that is specific to AD and that affects endosomes and induces the progressive failure of lysosom

62 ts phosphatidylinositol 3-kinase activity on endosomes and is critical for endosome maturation, viabi

63 recycling numerous cell-surface cargoes from endosomes and is structurally and functionally related t

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

65 ncomplete because the pH range of 4-7 in the endosomes and lysosomes does not provide complete cleava

66 basis, the established early involvement of endosomes and lysosomes in amyloid precursor protein (AP

67 Rupture of endosomes and lysosomes is a major cellular stress condi

68 of newly synthesized transmembrane cargos to endosomes and lysosomes is thought to occur at the TGN t

69 loaded drug almost exclusively traffics into endosomes and lysosomes upon intracellular uptake, and o

70 intracellular pH that delineates individual endosomes and lysosomes, and the therapeutic intracellul

71 cells within minutes and then transported to endosomes and lysosomes.

72 rs but not on the types of organelle such as endosomes and lysosomes.

73 branes of intracellular compartments such as endosomes and lysosomes.

74 bringing about clustering and fusion of late endosomes and lysosomes.

75 fected the albumin distribution between late endosomes and lysosomes.

76 tin-8 (encoded by LGALS8), detects permeated endosomes and marks them for autophagic degradation, whe

77 ular transport and then fuse with lysosomes, endosomes and multivesicular bodies through mechanisms t

78 omain and leucine zipper 1 (APPL1) signaling endosomes and MYO6+ expression causes a dramatic relocal

79 eins, IFITMs), on the pH regulation in early endosomes and on the efficiency of acid-dependent fusion

80 ery rely on their ability to shuttle between endosomes and plasma membranes, as well as on their late

81 e (PIP3) on B cell receptor-containing early endosomes and proper sorting into the MHC class II antig

82 iRNA polyplexes initially appearing in early endosomes and rapidly moving to other compartments withi

83 eraction with effectors, its localization to endosomes and recycling vesicles, and hence important fo

84 Exosomes are generated within endosomes and released when these fuse with the plasma m

85 s and Shrub overexpression similarly elevate endosomes and result in the arrested accumulation of enl

86 sicular bodies but involves enclosure within endosomes and secretory lysosomes.

87 ist, CGRP8-37, accumulated in CLR-containing endosomes and selectively inhibited CLR signaling in end

88 re internalized by a specific class of early endosomes and show preferential association with epiderm

89 calized at the plasma membrane as well as in endosomes and soluble in the apoplast.

90 a membrane proteins (cargo) are delivered to endosomes and sorted by endosomal sorting complex requir

91 alpha1B-adrenergic receptor transfer to late endosomes and that Rab9 regulates this process and parti

92 ases and transferred to the cell nucleus via endosomes and the cytoplasm.

93 Contacts between endosomes and the endoplasmic reticulum (ER) promote end

94 diating retrograde vesicle transport between endosomes and the trans-Golgi network.

95 , DAT robustly targeted to retromer-positive endosomes, and DAT/retromer colocalization was observed

96 b7(+) SGs, followed by a merge with Rab11(+) endosomes, and depended on Ca(2+) binding to Munc13-4.

97 dogenous proteins, live imaging of dendritic endosomes, and interference approaches against the endos

98 s between the surface membrane and recycling endosomes, and is presumably triggered by changes in the

99 sidered as hallmarks of the plasma membrane, endosomes, and lysosomes, these compartments contain oth

100 compartments, including secretory granules, endosomes, and lysosomes.

101 sequential fusion with early endosomes, late endosomes, and lysosomes.

102 ke place at ER contact sites with the Golgi, endosomes, and mitochondria.

103 attenuates integrin translocation into early endosomes, and reduces delayed mitogen-activated protein

104 ith tubulovesicular structures, likely to be endosomes, and with sparse multivesicular bodies and lys

105 ansmembrane protein 3 (IFITM3) is a cellular endosome- and lysosome-localized protein that restricts

106 Mecp2 KO neurons have lower levels of early endosome antigen 1 (EEA1), a protein involved in AMPA-ty

107 ocalization of G. bethesdensis with an early endosome antigen 1 (EEA1)-positive compartment, followed

108 nsient oxidation on or close to RAB5+/ early endosome antigen 1- endosomes.

109 igomers including Bax, Troponin C, and Early Endosome Antigen 1.

110 that CD74 NTF-induced structural changes of endosomes are not directly involved in these processes.

111 tiology of anti-PE autoimmunity and, because endosomes are of central importance in almost all types

112 Endosomes are the major protein-sorting hubs of the endo

113 ontrol pain transmission and identify CLR in endosomes as a therapeutic target for pain.

114 Here we identified IRAP(+) endosomes as major cellular compartments for the early s

115 and transferrin receptor internalization to endosomes as well as traffic of agonist-occupied MC4R to

116 Here, we show that endosome-associated VPS9a, the conserved guanine-nucleot

117 98D BACE1 mutant was trafficked to recycling endosomes at a faster rate compared with wild-type BACE1

118 CE1 is predominantly accumulated within late endosomes at the synapses of AD-related mutant human APP

119 IRAP stabilized CpG-containing endosomes by interacting with the actin-nucleation facto

120 del proposing that traffic jams in the early endosome can act as an upstream pathogenic hub in AD.

121 that C99, in addition to its localization in endosomes, can also be found in MAM, where it is normall

122 re, that interventions designed to unjam the endosome carry high therapeutic promise.

123 induced through chemical adjustments in the endosome, causing alleviation of autoinhibition and rece

124 In endosomes, CD74 undergoes sequential degradation by diff

125 e/lysosomes (ClC-3a and ClC-3b) or recycling endosome (ClC-3c).

126 Dil-oxLDL and rMBSA taken up into MSC endosomes colocalized with Mtb phagosomes, thus suggesti

127 hosphate (PI3P) in vivo and acts in the late endosome compartment.

128 monstrated with EEA1 but not RBSN-containing endosomes, consistent with preferential EGF-like traffic

129 Our results implicate failure of the ER-endosome contact process in axonopathy and suggest that

130 yme spastin and the ESCRT protein IST1 at ER-endosome contacts drives endosomal tubule fission.

131 Endosomes containing D2LR and PDGFRbeta are then transpo

132 ing Sorting Nexin 16 and a reduction in late endosomes containing Rab11.

133 Whether GPCRs in endosomes control pathophysiological processes in vivo a

134 Following maturation, these endosomes deliver mitochondria to lysosomes for degradat

135 MoVps17 is localized to endosomes depending on the activity of phosphatidylinosi

136 Exosomes are endosome-derived nanovesicles that are involved in cellu

137 GFP-HSV nor localization of TLR9 in CD71(+) endosomes, directing us to investigate downstream events

138 ombined in trans with a previously described endosome-disrupting agent composed of the pore-forming p

139 o plays a distinct role in the regulation of endosome dynamics during fungal development and plant in

140 PS-ASOs exited early endosomes (EEs) rapidly after internalization and became

141 ablation of the Hook complex adapting early endosomes (EEs) to dynein but absolutely requires p25 in

142 zyme 1 (BACE-1), is the primary cause of the endosome enlargement in AD and the earliest initiator of

143 afficking from the PM to the nucleus via the endosome-ER network.

144 Rab7 to transition ERBB2 from early to late endosome for degradation.

145 ations, such as to enable cargo release from endosomes for cellular delivery, or as cancer therapeuti

146 intracellular sorting of AMPARs toward late endosomes for degradation.

147 cAMP enhanced the acidification of endosomes for Fe(II) release to the LIP likely through R

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

149 ated in myriad cellular processes, including endosome formation, fusion of autophagosomes/amphisomes

150 nd NUMBL resulted in a partial block of late endosome formation, resulting in sustained ERBB2 signali

151 rs are retrogradely transported in signaling endosomes from distal axons to cell bodies, where they a

152 monstrate a requirement for normal recycling endosome function in AMPAR-dependent synaptic function a

153 lum-resident VAP proteins that regulate late endosome function under regulation of Rab7-GTP.

154 indings, we propose that GPCR signaling from endosomes functions as a biologic noise filter to enhanc

155 ing suggests that MoVps17 can regulate early endosome fusion and budding as well as endocytosis.

156 We focused on validating endosome/Golgi-localized hits specific for STx2 and foun

157 Within DC endosomes, HIV-1 somehow evades detection by the pattern

158 t regulates innate immunity to adenovirus in endosomes.IMPORTANCE Early region 3 proteins encoded by

159 ion of external pH can raise the pH in early endosomes in a cell type-dependent manner and thereby de

160 sociation of signalling molecules from early endosomes in a dense cytoplasm with single-molecule reso

161 PICK1 recruits Ago2 to recycling endosomes in dendrites, where it inhibits miRNA-mediated

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

163 demonstrate that NHE9 localizes to recycling endosomes in hBMVECs where it raises the endosomal pH.

164 The role of endosomes in receptor signal transduction is a long-stan

165 ecules with the spatial resolution of single endosomes in specific cells in Caenorhabditis elegans.

166 hantavirus allows us to propose a model for endosome-induced reorganization of the hantaviral glycop

167 membrane is rapidly endocytosed, targeted to endosomes, internalized into intraluminal vesicles (ILVs

168 ect protein export from the ER lumen or from endosomes into the cytosol, suggesting that the inhibiti

169 omains of the toxins translocate from low-pH endosomes into the cytosol.

170 h dynein to drive the transport of signaling endosomes into the soma.

171 equired for transport (ESCRT) machinery into endosome intralumenal vesicles (ILVs) for degradation.

172 The endosome is increasingly recognized as an important cros

173 o discover how Nsg1 and Nsg2 localization to endosomes is regulated in primary rat hippocampal neuron

174 endocytic uptake, the d-peptide, once in the endosome, is significantly more prone to escape than its

175 agolysosomes by sequential fusion with early endosomes, late endosomes, and lysosomes.

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

177 mpairs its trafficking by trapping it in the endosomes, leading to impaired insulin signaling and ins

178 e observed that the recruitment of host late endosomes (LEs) and lysosomes is reduced in uis4(-) para

179 enclosed endocytotic organelles, mainly late endosomes (LEs).

180 GFP-TOR can associate with endosome-like structures in ROP2-overexpressing plants,

181 erium Ehrlichia chaffeensis resides in early endosome-like vacuoles and circumvents lysosomal fusion

182 C) and is localized at ESCRT-I-positive late endosomes likely through its PI3P and actin binding SH3Y

183 are associated with bypass of recognition by endosome-localized deubiquitylases - including Doa4 whic

184 en human and mouse, is localized to the late endosome/lysosome and interacts with the lysosomal v-ATP

185 splayed increased expression of Rab7, a late endosome/lysosome-associated small GTPase.

186 e analyses suggest a key role for miR-153 in endosome/lysosome-related pathways during amelogenesis.

187 ntion of L2 and the viral genome in the late endosome/lysosome.

188 These vesicles (M7Vs) are distinct from endosomes, lysosomes, and other familiar vesicles or org

189 ls without affecting other organelles (early endosomes, lysosomes, the Golgi apparatus, the endoplasm

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

191 t to exogenous PCSK9-mediated degradation in endosomes/lysosomes and showed reduced LDL internalizati

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

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

194 Moreover, we show that p97 helps clear late endosomes/lysosomes ruptured by endocytosed tau fibrils.

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

196 at acidic pH, a reduced LDL delivery to late endosomes/lysosomes, and an increased release in the med

197 , and inhibited by chemical ablation of late endosomes/lysosomes, suggesting a lysosomal secretory pa

198 IONs are internalized and accumulate in late endosomes/lysosomes, while aminolipid-SPIONs reside at t

199 causing the accumulation of pMHC inside late endosomes/lysosomes.

200 some marker Rab5 and the long loop recycling endosome marker Rab11 and to a much lesser extent with t

201 PRC6A was mainly co-localized with the early endosome marker Rab5 and the long loop recycling endosom

202 11 and to a much lesser extent with the late endosome marker Rab7.

203 r NCS1, whereas recruitment of the recycling endosome marker VAMP3 was unaffected.

204 Rab2, is also required for autophagosome and endosome maturation and proper lysosome function in Dros

205 s and endolysosomal membrane dynamics during endosome maturation and sorting.

206 Endosome maturation requires a coordinated change in the

207 se activity on endosomes and is critical for endosome maturation, viability, and dendrite growth of n

208 - and retromer-mediated Glut4 retrieval from endosomes may represent a step in the Glut4 pathway vuln

209 ROP2-overexpressing plants, indicating that endosomes mediate ROP2 effects on TOR activation.

210 ex, thereby enabling retromer recruitment to endosome membranes and GLUT1 plasma membrane translocati

211 ed by endosomal trafficking, suggesting that endosomes might provide new strategies for manipulating

212 e weakly acidic environment contained within endosomes of hematopoietic and parenchymal cells, whereu

213 Taking advantage of the naturally large endosomes of the C. elegans coelomocyte, we visualized c

214 atal Fc receptor (FcRn) expressed within the endosomes of the syncytiotrophoblastic membrane.

215 Blocking aberrant signaling from endosomes or reducing BMP activity ameliorates the sever

216 of synaptic growth receptors from signaling endosomes or to reduce BMP signaling reduce pathology in

217 ptide is associated with membranes in, e.g., endosomes (or lysosomes) in the cytosol.

218 Within the endosome, particles undergo a series of stepwise disasse

219 low the endocytosed virus to escape from the endosome, pass through the cell cytoplasm, and deliver t

220 dherin complexes to pericentriolar recycling endosomes (PCREs).

221 osphatidylinositol-3-phosphate pool in early endosomes; phosphatidylinositol-3,4-biphosphate and the

222 om the trans-Golgi network (TGN) to the late endosome/prevacuolar compartment (PVC) and for TGN homot

223 nce for physiological roles of the recycling endosome protein GRASP1 in glutamatergic synapse functio

224 f/FIP3, a Rab11 effector, mediates recycling endosome (RE)-based vesicle delivery to the cytokinesis

225 transported via Rab11A-containing recycling endosomes (RE) and use both microtubules (MT) and actin.

226 uncovered a new function for Vps13 in early endosome recycling and Neo1 localization.

227 We further show that the early-endosome recycling route and its control though the Vam6

228 osome, we find that disrupting the recycling endosome reduces ciliary polycystin-2 and causes its acc

229 evidence that PI3P located at early/sorting endosomes regulates the postsynaptic clustering of gephy

230 into early endosomes, where the master early endosome regulator Rab5b promotes STAT5 phosphorylation.

231 from the endolysosomal pathway to recycling endosomes represents an important transport step in the

232 responds to directed exocytosis of recycling endosomes (REs) containing these integrins and their fib

233 ecretory pathway and accumulate in recycling endosomes (REs) located in dendrites and spines before r

234 to traffic through Rab11-positive recycling endosomes (REs), suggesting a model in which F and M tra

235 translocation is caused by alkalinization of endosomes resulting from inhibition of proton pumping ac

236 ne increased DAT exit from retromer-positive endosomes significantly.

237 1 protein dissociates and is degraded in the endosome, some L1 protein remains associated with the vi

238 However, the mechanisms that regulate endosome sorting of BACE1 are poorly understood.

239 detected DAT targeting to classic recycling endosomes, suggesting that internalized DAT targets to e

240 ishes Daple's ability to bind PI3-P-enriched endosomes that engage dynein motor complex for long-dist

241 At pH 5, as it occurs in the endosome, the alignment of LAH4-L1 at a peptide/lipid ra

242 ibody to be localized to Rab5-positive early endosomes, the trans-Golgi network, and subsequently Rab

243 receptors and subsequently escape the early endosome through a pH-triggered disassembly mechanism.

244 , indicating that multimerization of MYO6 on endosomes through binding to GIPC is required for this c

245 cking vesicles that dock and fuse with early endosomes, thus overriding the default pathway to the Go

246 omplex, which transports TLRs from the early endosome to the late endolysosomal compartments.

247 Transmembrane proteins are sorted from endosomes to avoid lysosomal degradation.

248 not only at the plasma membrane but also in endosomes to control complex processes in vivo.

249 P8-37 Our results show that CLR signals from endosomes to control pain transmission and identify CLR

250 ficking pathways: autophagy and rerouting of endosomes to lysosomes.

251 d electron tomograms of Arabidopsis thaliana endosomes to measure cargo escape from budding ILVs.

252 te-receptor-dependent LTP recruits recycling endosomes to spines, enhances synaptic recycling of AMPA

253 overed that yeast has a recycling route from endosomes to the cell surface that functions efficiently

254 a new pathway that delivers cholesterol from endosomes to the endoplasmic reticulum, where it is este

255 rt transport of LDL-derived cholesterol from endosomes to the endoplasmic reticulum, where it was con

256 plex, which mediates recycling of cargo from endosomes to the Golgi.

257 iate the retrograde transport of CI-MPR from endosomes to the TGN independently of the core retromer

258 complex involved in retrograde transport of endosomes to the trans-Golgi apparatus.

259 t mannose 6-phosphate receptor (CI-MPR) from endosomes to the trans-Golgi network (TGN), is thought t

260 plex has been linked to cargo retrieval from endosomes to the trans-Golgi network.

261 Therefore, retromer-mediated endosome-to-Golgi retrieval of cation-independent mannos

262 found that depletion of UNC50 blocked early endosome-to-Golgi trafficking and induced lysosomal degr

263 To identify host factors required for early endosome-to-Golgi trafficking of STx2, we performed a vi

264 ing Golgi membrane protein that serves as an endosome-to-Golgi trafficking receptor for the toxin.

265 Early endosome-to-Golgi transport allows the toxins to evade d

266 III core protein Shrub has a central role in endosome-to-multivesicular body membrane trafficking, wi

267 Although endosome-to-plasma membrane recycling is critical for ma

268 CI-MPR through recognition of a specific WLM endosome-to-TGN sorting motif.

269 teins leads to a pronounced defect in CI-MPR endosome-to-TGN transport.

270 biogenesis of tubular profiles required for endosome-to-TGN transport.

271 e role of retromer in the sequence-dependent endosome-to-trans-Golgi network (TGN) transport of the c

272 CRT-III subunits polymerize rapidly on yeast endosomes, together with the recruitment of at least two

273 ntrin Cdc31, in trans-Golgi network (TGN) to endosome traffic and TGN homotypic fusion.

274 ormation, as are some trans-Golgi network-to-endosome trafficking genes.

275 Endosome transport by transcytosis is the primary mechan

276 ced localization of HIV-1 with TLR8(+) early endosomes, triggered a pro-inflammatory response, and in

277 rotein hemagglutinin (HA), the low pH in the endosome triggers a transition from the metastable prefu

278 g infectious entry, acidification within the endosome triggers uncoating of the human papillomavirus

279 FNs were only expressed from TLRs present on endosomes, type III IFNs could be induced by TLRs that r

280 in trafficking of Toll-like receptors to the endosome (Unc93b1(-/-) mice).

281 main that is delivered into the cytosol from endosomes via a translocation domain after receptor-medi

282 ndent sequestration into Rab5-positive early endosomes via the ESCRT machinery.

283 The rapid transit of BACE1 S498D from early endosomes was coupled with reduced levels of amyloid pre

284 Albumin accumulation in early endosomes was independent of FcRn-binding affinity, but

285 BAIAP3 localized to endosomes was required for Golgi trans-Golgi network 46

286 with the role of BLOC-1 in sorting from the endosome, we find that disrupting the recycling endosome

287 localizes to and functions in the dendritic endosome, we set out to discover how Nsg1 and Nsg2 local

288 gulators of Neo1 trafficking and activity at endosomes, we first identified mutants with impaired rec

289 Since SIEL and SHR associate with endosomes, we suggest that KinG serves as a linker betwe

290 ter endocytosis, transmembrane cargo reaches endosomes, where it encounters complexes dedicated to op

291 D-L1 at the plasma membrane and in recycling endosomes, where it prevents PD-L1 from being targeted f

292 tdIns(3)P, plays a role in localizing IDE to endosomes, where the enzyme reportedly encounters physio

293 Prolactin is internalised into early endosomes, where the master early endosome regulator Rab

294 s with KSR1 and Rab11, a marker of recycling endosomes, whereas p-ERK associates predominantly with a

295 d human papillomavirus virion uncoats in the endosome, whereupon conformational changes result in a d

296 f SK2 channels from both early and recycling endosomes while filamin A probably aids the recycling of

297 7 promotes fusion of autophagosomes and late endosomes with lysosomes in yeast and metazoan cells, ac

298 Following fusion of the S. aureus-associated endosomes with lysosomes, alkalinization of the acidic e

299 DAT also targeted rab7-positive endosomes with slow, linear kinetics that were unaffecte

300 Fusion of mature endosomes with the lysosome-like vacuole also requires R