ライフサイエンスコーパス: endosome

1 eripheral membrane proteins of the recycling endosome.

2 for sorting and trafficking cargo out of the endosome.

3 ion of the receptor was found with the early endosome.

4 ne-remodeling functions, particularly at the endosome.

5 IFN-I can continue to signal from within the endosome.

6 ribution of vesicular transport in recycling endosomes.

7 ndent Mannose 6-Phosphate Receptor from late endosomes.

8 Clec2d localized to the plasma membrane and endosomes.

9 P-binding protein WIPI2 to virion-containing endosomes.

10 osomes, including early, late, and recycling endosomes.

11 hich diverts membrane flux through recycling endosomes.

12 BACE1 is endocytosed to early and recycling endosomes.

13 etromer-mediated retrograde trafficking from endosomes.

14 nhibiting Sanpodo trafficking towards acidic endosomes.

15 n the Rab11-related domain of slow recycling endosomes.

16 biquitinate agonist-activated GCGRs at early endosomes.

17 d treatment of pathogens internalized within endosomes.

18 assembly are not transferred out of Rab5 (+) endosomes.

19 ich prevents the maturation of early to late endosomes.

20 minimally expressed and mainly localized in endosomes.

21 ration of the ER into autophagosomes at late endosomes.

22 tment of Galpha(i/o) and beta-arrestin1/2 to endosomes.

23 ined Rab GTPase expression in early and late endosomes.

24 anelles, including the ER, mitochondria, and endosomes.

25 s of the enzymes PDI-3 and TRX-1 resident in endosomes.

26 for efficient post-Golgi transport of APP to endosomes.

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

28 from the internalized membrane and synaptic endosomes.

29 m synaptic vesicles and resemble trafficking endosomes.

30 the proper axonal transport of p75-positive endosomes.

31 mes while *0402 molecules traffic into early endosomes.

32 gi network, granules, or at the cell surface/endosomes.

33 ains drive ADBE and SV reformation from bulk endosomes.

34 crucial for ClC-5 activation by depolarizing endosomes.

35 X efficiently recruits ESCRT-III proteins to endosomes.

36 he ER and several organelles, including late endosomes.

37 s, and were delivered to DOPr-positive early endosomes.

38 ough asymmetric inheritance of Sara-positive endosomes.

39 ls of PI within the plasma membrane (PM) and endosomes.

40 ) complex that activates actin nucleation at endosomes.

41 in receptor 1 (hTfR1) into soluble shTfR1 in endosomes.

42 y was crucial for preventing Cl(-) exit from endosomes.

43 of intraluminal vesicles (ILVs) within late endosomes.

44 ble triggering of single-virus fusion within endosomes.

45 tudes, particularly at the acidic pH of late endosomes.

46 the virus envelope with the membrane of the endosome(2).

47 lipid receptors, which interact in the late endosome(9), are necessary for the membrane fusion and d

48 found to acquire a membrane envelope within endosomes, a phenomenon not reported for other viruses.

49 ing to full MOMP execution, which depends on endosomes accumulating on apoptotic mitochondria.

50 trafficking, MVB fusion, exosome uptake and endosome acidification.

51 The low pH of endosomes activates fusion by facilitating irreversible

52 TOR1-mediated peripheral positioning of late endosomes allows delivery of SRC proto-oncogene, nonrece

53 he membrane causing osmolysis to disrupt the endosome and allow viral escape.

54 so detected in the trans-Golgi network/early endosome and at the plasma membrane.

55 lum (ER) and thereby hampered its subsequent endosome and Golgi-associated degradation (EGAD).

56 sorting of MMP14 into the lumen of the late endosome and its proteolytic activation in lipid rafts.

57 T-0 to -III/VPS4) sequester receptors at the endosome and simultaneously deform the membrane to gener

58 internalization to a Rab5-positive signaling endosome and the further propagation of p75-dependent ne

59 afficking pathway within M6PR-positive large endosomes and (ii) most infectious VZV particles in conv

60 SLC34A2-ROS1 fusion oncoproteins resided on endosomes and activated the MAPK pathway.

61 Several proteins transit through endosomes and are exported in a Rab8-, Rab10-, and/or Ra

62 of GCC2 or M6PR impaired PS-ASO release from endosomes and decreased PS-ASO activity in human cells.

63 ibody-induced virus aggregation, fusion with endosomes and egress are inhibited.

64 ellularly and colocalized with CD63-positive endosomes and enhanced exosome secretion in differentiat

65 ited the recruitment of Rab5 GTPase-positive endosomes and enrichment of phosphatidylethanolamine in

66 pathway involving dynamin, clathrin, sorting endosomes and Golgi trafficking where the cargo is relea

67 et cells by sequestering incoming viruses in endosomes and in producing cells by leading to the produ

68 cking of internalized beta1 integrin to late endosomes and its ultimate degradation.

69 MET), and shunts their trafficking into late endosomes and lysosomal degradation.

70 ominantly localized to the membranes of late endosomes and lysosomes (LELs).

71 cation channel localized to the membranes of endosomes and lysosomes and is not present or functional

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

73 e found that TRPML1 channels present in late endosomes and lysosomes formed stable complexes with typ

74 Endosomes and lysosomes harbor Rab5 and Rab7 on their su

75 confocal imaging studies, we found that most endosomes and lysosomes in freshly isolated SMCs from ce

76 Ca(2+) released from endosomes and lysosomes into the cytosol through TRPML1

77 y within the acidic microenvironment of late endosomes and lysosomes of cancer cells (pH 5.4) and not

78 Adequate function of endosomes and lysosomes requires finely tuned luminal io

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

80 aggregates primarily accumulate within late endosomes and lysosomes, organelles that participate in

81 g the predominant phosphoinositide lipids at endosomes and lysosomes, whereas PI 4-phosphates, such a

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

83 f rapidly moving cellular structures such as endosomes and lysosomes.

84 ment protein pp150 is released from maturing endosomes and migrates to the nucleus, whereas other teg

85 GR endocytic trafficking through Rab5a early endosomes and Rab4a recycling endosomes, but also induce

86 l Wnt signaling proteins are housed on early endosomes and recruit nucleation sites to branch points.

87 we found that INPP4A partially localizes to endosomes and that loss of INPP4A in HAP1 cancer cells p

88 that SNX17 and EHD1 partially colocalize on endosomes and that this overlap further increases upon L

89 t Leu-725 enhances PC7 localization to early endosomes and that, together with Glu-719 and Glu-721, i

90 lysosomal proteins are targeted to the late endosomes and the ATP7A copper transporter is translocat

91 pair retrograde membrane trafficking between endosomes and the Golgi apparatus lead to neurodegenerat

92 erol accessible to a D4H probe, between late endosomes and the PM.

93 governing the continued GPCR signaling from endosomes and the structural aspects of the GPCR resensi

94 ize within the lumen of Rab7(+) and Lamp1(+) endosomes and their transport requires HOPS activity.

95 rithmic (mainly in flagellar pocket area and endosomes) and late stationary phase (mitochondrion).

96 g GTPase-containing EGO complex to signaling endosomes, and (3) TORC1 activity.

97 cortical ER marker Rtn1 accumulated at late endosomes, and a dramatic decrease in ER packaging into

98 embrane sorting, pH homeostasis in recycling endosomes, and cargo trafficking, and they also triggere

99 SERINC5 down-regulation, trafficking to late endosomes, and exclusion from newly synthesized viral pa

100 genesis of exosomes involves their origin in endosomes, and subsequent interactions with other intrac

101 the compartmentalized activation of TLR9 in endosomes, and use it to uncover unique aspects of TLR9-

102 ms by which non-enveloped viruses escape the endosome are poorly understood.

103 Endosomes are compositionally dynamic organelles that re

104 ascades are altered when early and recycling endosomes are disrupted by the expression of dominant-ne

105 , receptors that are internalized to sorting endosomes are sorted to different pathways, in part by s

106 er tegument proteins, including pp71, remain endosome associated in the cytoplasm.

107 We recently identified the endosome-associated recycling protein (EARP) complex and

108 differences in their binding to Trk-A in the endosomes at low pH, here, we further show differences i

109 w that Ad5-VII- particles are trapped in the endosome because they fail to increase VI exposure durin

110 very is especially useful for targets within endosomes because of the endosomal transport mechanisms

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

112 gh Rab5a early endosomes and Rab4a recycling endosomes, but also induced rapid deubiquitination of GC

113 enveloped viruses infect cells via fusion to endosomes, but controlling this process within living ce

114 Notably, T282M accumulated in endosomes, but its ability to form stable complexes foll

115 m autophagosome formation sites on recycling endosomes by causing increased binding to an alternative

116 dynamics of fusion and fission of recycling endosomes by controlling ubiquitination of the ESCRT-III

117 er with endocytic organelles (lysosomes/late endosomes) by forming membrane contact sites.

118 ed truncated form(s) of UBAP1 cause aberrant endosome clustering, pronounced endosome enlargement, an

119 a is lost from the SJ and becomes trapped on endosomes coated with the endosomal retrieval machinery

120 ows augmented trafficking to Rab4a recycling endosomes compared with the WT, thus affirming the role

121 Extracting virus:endosome conjugates from cells and exogenously triggerin

122 isolated influenza (A/Aichi/68; H3N2) virus:endosome conjugates from cells, immobilized them in a mi

123 Thus, Protrudin-mediated ER-endosome contact sites promote cell invasion by facilita

124 Thus, TMEM16K-containing ER-endosome contact sites represent clinically relevant pla

125 tion is instrumental for the formation of ER-endosome contacts, and their sterol transfer function.

126 TrkB and CaSR colocalize within late endosomes, cotraffic and coactivate GSK3, which serves a

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

128 The nanoparticle and enzyme reside in endosomes, creating engineered artificial organelles tha

129 viral assembly, such as Golgi- and recycling endosome-derived membranes.

130 in-97 and GCC88, shown previously to capture endosome-derived vesicles at the TGN, were individually

131 analysis to define the content of different endosome-derived vesicles destined for the trans-Golgi n

132 in protein 1, catalyzes fission and releases endosome-derived vesicles for recycling to the plasma me

133 In endocytosis and early endosome development, net VPS34CII-catalyzed PI3P produc

134 r data further motivate the need to identify endosome disrupting moieties which retain their activity

135 Nanogels modified with an endosome disrupting peptide failed to retain its native

136 This defective transit from the early endosome disrupts eventual recycling of beta1 integrins

137 genetic screen for mutations affecting early-endosome distribution in Aspergillus nidulans, we identi

138 a Rab5a DN that blocks trafficking at early endosomes eliminated agonist-induced GCGR deubiquitinati

139 ve (DN) that blocks trafficking at recycling endosomes enabled GCGR deubiquitination, whereas a Rab5a

140 use aberrant endosome clustering, pronounced endosome enlargement, and cytoplasmic accumulation of ub

141 Although many PX domains bind the canonical endosome-enriched lipid PtdIns3P, others interact with a

142 in proteolytic maturation of protein VI and endosome escape.

143 n VI must be released during entry to ensure endosome escape.

144 No large late endosomes filled with VZV particles were observed in Pom

145 MDAR-LTD, however, they are diverted to late endosomes for degradation.

146 (EGF), both ESCRT-I and Vps4 are retained at endosomes for dramatically extended periods of time, whi

147 reticulum (ER) protein STING translocates to endosomes for induction of interferon production, while

148 e Orai1 is trafficked to Rab 7-positive late endosomes for lysosomal degradation.

149 anism-SNX5-dependent PI3KC3-C1 activation at endosomes-for initiation of autophagy during viral infec

150 igration, and we find that interference with endosome formation or the Golgi apparatus impairs migrat

151 large quantities of SV constituents in large endosomes from which SVs reform.

152 ediated lipid transport in the regulation of endosome function.

153 gering fusion permits precise study of virus:endosome fusion kinetics.

154 hich increases plasma membrane fusion versus endosome fusion of SARS-CoV-2, attenuated IFITM3 restric

155 mal/lysosomal compartment and inhibits virus-endosome fusion.

156 Rab11A-containing recycling endosomes have been identified as a platform for intrace

157 ) between the endoplasmic reticulum (ER) and endosomes have emerged as important players in endosomal

158 eas the melanosome, the only color-producing endosome in mammals and birds, has been documented as a

159 ied the fusion of influenza virus virions to endosomes in a chemically controllable manner.

160 post-translationally stabilized on MAC+Rab5+ endosomes in a Rab5- and PI(3)P-dependent manner.

161 enylated proteins localize to TrkA-harboring endosomes in axons and promote receptor trafficking nece

162 ly mapped disulfide reduction exclusively in endosomes in Caenorhabditis elegans and identified that

163 ion of growth factor and nutrient signals at endosomes in cancer cells.

164 y affected trafficking through Rab5-positive endosomes in cells expressing each component of the 5-HT

165 P8 staining was preferentially found on late endosomes in N2a cells.

166 movement of AXL from the plasma membrane to endosomes in pancreatic cancer cells treated with the AX

167 k1 mediates transport of TrkB-BDNF-signaling endosomes in primary hippocampal neurons.

168 calcium rapidly decreases the size of early endosomes in primary human fibroblasts.

169 rimentally demonstrated to be delivered into endosomes in recipient cells and to activate endosomal T

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

171 f endoplasmic reticulum, integrins and Rab11 endosomes in the distal axon, whilst removing Protrudin'

172 ), we visualize a sterol flow between PM and endosomes in the fission yeast Schizosaccharomyces pombe

173 set of transmembrane proteins transiting the endosome, in addition to their roles in phospholipid rec

174 he retromer complex mediating recycling from endosomes, in a subset of axons.

175 ch as CD40, with RAB7 small GTPase on mature endosomes, in addition to signals emanating from the rec

176 on the cell surface and in various types of endosomes, including early, late, and recycling endosome

177 virus-induced, but not for basal, stress- or endosome-induced, autophagy.

178 Our findings thus reveal that late endosomes interact with RNA granules, translation machin

179 al distribution of the nanoparticle dose per endosome is independent of the initial administered dose

180 Thus, DOPr in endosomes is an endogenous mechanism and a therapeutic t

181 e of autophagosome precursors from recycling endosomes is mediated by DNM2-dependent scission of thes

182 2 is first targeted to the lumen of the late endosome (LE) en route to the cilia.

183 y, polyomavirus SV40 is sorted from the late endosome (LE) to the endoplasmic reticulum (ER) to cause

184 fficked through the exocytic pathway to late endosomes (LE) and lysosomes (Ly) (LE/Ly) to globally ma

185 ated PI(4,5)P(2) production in Rab7-positive endosomes leading to impaired Rab7 inactivation and incr

186 lipoprotein-associated APOL1 in trypanosome endosomes leads to eventual lysis of the parasite due to

187 tisense oligonucleotides (PS-ASOs) from late endosomes (LEs) is a rate-limiting step and a poorly def

188 tol phosphate 5-kinase i5 (PIPKIgammai5), an endosome-localized enzyme that produces phosphatidylinos

189 (ADAP2), gamma-interferon-inducible lysosome/endosome-localized thiolreductase (GILT), and lymphocyte

190 -modified liposomes also participated in the endosome/lysosome pathway (with high-efficiency BBB cros

191 on with Tom1 allow Tollip to facilitate late endosome/lysosome trafficking in response to mitochondri

192 Late endosomes, lysosomes, and endoplasmic reticulum were abu

193 e impaired endomembrane components including endosomes, lysosomes, endoplasmic reticulum and Golgi.

194 hat *0401 molecules traffic through the late endosome/lysosomes while *0402 molecules traffic into ea

195 sterol at membrane contacts between the late endosomes/lysosomes (LEL) and the endoplasmic reticulum

196 ined that a rapid accumulation of late stage endosomes/lysosomes precedes membrane permeabilisation,

197 sity lipoprotein-derived cholesterol in late endosomes/lysosomes, disruption of endocytic trafficking

198 entrates at contacts between the ER and late endosomes/lysosomes, where it interacts with GTP-Rab7.

199 LDLR) that promotes LDLR degradation in late endosomes/lysosomes.

200 ependent and does not associate with sorting endosome marker EEA1.

201 lls, mCherry-RavD colocalized with the early endosome marker EGFP-Rab5 as well as the PI(3)P biosenso

202 localized with the trans-Golgi network/early endosome markers.

203 During endosome maturation, Rab5 is replaced by Rab7, though th

204 In particular, we propose that the endosome may be more important than previously recognize

205 ther these components localize to an ER-late endosome MCS.

206 At these ER-late endosome MCSs, mitochondria are also recruited to form a

207 The intraluminal vesicles (ILVs) of endosomes mediate the delivery of activated signaling re

208 into distinct trachea and esophagus requires endosome-mediated epithelial remodeling involving the sm

209 omer and associated accessory factors on the endosome membrane drives clustering of retromer-bound in

210 e scaffold track the temporal development of endosome membrane markers, implying actin associations b

211 roposed that the tubular-vesicular recycling endosome membranes were a core platform on which the cri

212 7 activation and show severe defects in late endosome morphology and endosomal LDL trafficking, resul

213 I receptor DAF-4/BMPRII, along with impaired endosome morphology and mislocalization of DAF-4/BMPRII

214 rting of internalised cargos and directional endosome movement that itself actively promote CME event

215 re amphisomes formed through fusion of early endosomes, multivesicular bodies, and early autophagosom

216 While biogenesis of autophagosomes and late endosomes occurs continuously at axon terminals, non-deg

217 polysaccharide creates glycopeptides in the endosome of antigen-presenting cells.

218 orn snakes and show that the color-producing endosomes of all chromatophores are substantially affect

219 Peptide loading of MHCII in the endosomes of cells is controlled by the interplay of the

220 yve9) has been classically observed in early endosomes of different cells types where it regulates ve

221 on activate delta-opioid receptors (DOPr) in endosomes of nociceptors.

222 ited cells with nanobodies tethered to early endosomes or mitochondria changes the subcellular locati

223 o the cell surface, but not to mitochondria, endosomes, or lipid droplets.

224 es with ER and mitochondria, lipid droplets, endosomes, or plasma membrane, whereas disordered ER lip

225 ntially leading to a steady release from the endosomes over time.

226 sorting into the degradative multivesicular endosome pathway.

227 tein mainly expressed in early and recycling endosomes, plays an important role in regulating organel

228 human, and intracellularly colocalized with endosomes positive for a multivesicular bodies/exosomes

229 f UBAP1 leads to dysregulation of both early endosome processing and ubiquitinated protein sorting.

230 ALIX directly binds to ABA receptors in late endosomes, promoting their degradation.

231 results, we propose that early and recycling endosomes provide a platform for the integration of neur

232 of cargo protein traffic through prevacuolar endosome (PVE) compartments to the vacuole.

233 In mature endosomes, RAB7 directly interacts with TRAF6 E3 ubiquit

234 ng recruited preferentially to the recycling endosome rather than to the plasma membrane, our finding

235 ved regulator of H(+)-ATPase of vacuoles and endosomes (RAVE) complex, which binds to cytosolic V(1)

236 TMEM16K forms contact sites with endosomes, reconstituting split-GFP with the small GTPas

237 eting to the cell periphery and thereby late endosome recycling and had a major impact on YAP signali

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

239 other age-related programs supported by most endosome recycling.

240 d undergo vesicular fission from the sorting endosomes remain elusive.

241 is cleaved by cellular cathepsins in acidic endosomes, removing the glycan cap and exposing a bindin

242 V pseudovirus, and inhibit HPV exit from the endosome, resulting in loss of viral components from cel

243 ion of cargo-carrying transport tubules from endosomes, resulting in immature WPBs that lack endosoma

244 After entry into the endosome, sigma3 is proteolytically degraded and mu1 is

245 han ClC-5:S244L, but co-localized with early endosomes, suggesting decreased ClC-5:R345W membrane tra

246 ic reticulum and cis-Golgi, but not in early endosomes, suggesting the nonsense mutation affects ClC-

247 ith the sequestration of incoming virions in endosomes (target cell protection) and with the producti

248 PI(4,5)P(2) further retrieves Flower to bulk endosomes, terminating endocytosis.

249 Using endosomes that are confined by a local actin network as

250 macropinosome-derived CCR5-loaded signaling endosomes that are critical for CCL5-induced immunologic

251 ontinues to signal from a set of specialized endosomes that are crucial for T cell functions.

252 n formed contact sites with MT1-MMP-positive endosomes that contained the RAB7-binding Kinesin-1 adap

253 accumulated within large M6PR-positive late endosomes that were not degraded en route to the plasma

254 n the biogenesis of intralumenal vesicles at endosomes (the source of exosomes) revealed general and

255 in various compartments of the cell, such as endosomes, the cytosol, and the nucleus.

256 At lysosomes and endosomes, the Fab1 lipid kinase complex and the nutrien

257 Although Rab5 is known to work on early endosomes, this study showed that Rab5B plays a role in

258 We find that Orai1-SNPs escape late endosomes through endosomal pH regulation of interaction

259 switch from antiviral effector functions in endosomes to a PI3K amplification loop at the cell surfa

260 ther G protein-coupled receptors signal from endosomes to control important pathophysiological proces

261 alization and trafficking via early and late endosomes to down-regulation.

262 tendocytic sorting of nephrin from recycling endosomes to lysosomes for degradation.

263 VPS29:VARP binding inhibit trafficking from endosomes to the cell surface.

264 ficking via the retrograde route, from early endosomes to the Golgi apparatus.

265 facilitating translocation of MT1-MMP-laden endosomes to the plasma membrane, enabling both invadopo

266 r of the TBC family, TBC1D23 is critical for endosome-to-Golgi cargo trafficking by serving as a brid

267 and show that only Arl1 and Imh1 can restore endosome-to-TGN trafficking in ypt6-deleted cells.

268 Moreover, when endosome translocation or exocytosis was inhibited by de

269 bit similar defects in dynein-mediated early-endosome transport and nuclear distribution.

270 d mutant CHMP2B toxicity and implicate early endosome transport as a potential contributing pathway i

271 y but not the speed of dynein-mediated early-endosome transport is decreased, which correlates with a

272 Here, we examined the role of Golgi-endosome transport, specifically M6PR shuttling mediated

273 chain, and Hook, an adaptor protein in early endosome transport.

274 ytosol delivery of the siRNA payload without endosome trapping, as attested by fluorescence colocaliz

275 ma membrane and efficiently internalize into endosomes upon AngII stimulation.

276 ving decreased colocalization with the early endosome versus the Cys23 allele.

277 xport of integral membrane proteins from the endosome via retrograde and plasma membrane recycling pa

278 and C289W's residency with beta-arrestin2 in endosomes was greatly reduced, leading to decreased beta

279 he M6PR pathway (trans-Golgi network to late endosomes) was constrained in infected Pompe cells.

280 linked with GPCR trafficking or localized on endosomes, we identified signal-transducing adaptor mole

281 Recycling endosomes were elevated specifically in small spines aft

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

283 Additionally, SNX17-containing endosomes were larger in EHD1-depleted cells than in WT

284 and internalization, virions traffic to late endosomes where GP is cleaved by host cysteine proteases

285 endent endocytosis of mPRbeta into signaling endosome, where mPR interacts transiently with APPL1 and

286 LjVPY2 within the trans-Golgi network/early endosome, where they might function to regulate endocyti

287 s, the nanogel shells are degraded in acidic endosomes, where a proton sponge effect occurs instantan

288 ain, which causes Fab1 to shift to signaling endosomes, where it generates PI(3,5)P(2).

289 or (EGFR) is required for directing STING to endosomes, where it interacts with its downstream effect

290 ibutes from the plasma membrane to acidified endosomes, where it signals to maintain pain.

291 and instead enter Rab 11-positive recycling endosomes, where they are returned to the surface membra

292 Endogenous WDR44 labels a subset of tubular endosomes, which are closely aligned with the ER via bin

293 ntify Fab1 as a target of TORC1 on signaling endosomes, which are distinct from multivesicular bodies

294 protein TBC1 domain family member 5 to late endosomes, which controls the conversion of Rab7a from t

295 PKIgammai5 blocks Rab7a recruitment to early endosomes, which prevents the maturation of early to lat

296 caused a long-lasting activation of DOPr in endosomes, which provided sustained inhibition of nocice

297 sms result in immediate deterioration of the endosome, while others form pores in the membrane causin

298 membrane composition mimicking that of early endosomes, with PI(3)P enhancing membrane recruitment of

299 ly localizes to the postsynaptic density and endosomes within dendritic spines of CA2 neurons.

300 antly reduced the motility of BDNF-signaling endosomes without affecting the motility of other organe