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1 docytosis and low-pH-triggered fusion in the early endosome.
2 alization of the receptor was found with the early endosome.
3 found that both of them are localized in the early endosome.
4 ulting in an accumulation of the TfR1 in the early endosome.
5 nding of PE molecules in the membrane of the early endosome.
6 ggesting an important role for TSPAN9 in the early endosome.
7 g cells, and were delivered to DOPr-positive early endosomes.
8 egulating the formation of branched actin on early endosomes.
9 ork, whereas others suggested an origin from early endosomes.
10 PN-1 greatly reduced Lifeact accumulation on early endosomes.
11 tive trafficking between plasma membrane and early endosomes.
12 s, and LPS is released into the cytosol from early endosomes.
13 cking to Rab7-labeled late endosomes but not early endosomes.
14 lays long lifetimes, all features typical of early endosomes.
15 b5-GTP, and its recruitment to Rab5-positive early endosomes.
16 33 deubiquitinate agonist-activated GCGRs at early endosomes.
17 tine, unlike retromer components that act on early endosomes.
18 the cytoplasmic domain of beta1 integrin in early endosomes.
19 -operate to support bi-directional motion of early endosomes.
20 traffic of HAS3 from the plasma membrane to early endosomes.
21 ng Hook protein as general motor adapters on early endosomes.
22 periphery and reduced virion localization to early endosomes.
23 zed with both NOD1 and RIP2 in EEA1-positive early endosomes.
24 s essential for in vitro homotypic fusion of early endosomes.
25 sosomes because of a failure to recycle from early endosomes.
26 microtubule-based long-distance motility of early endosomes.
27 t the MHC-II-Ii complex away from March-I(+) early endosomes.
28 AP3 localized to the trans-Golgi network and early endosomes.
29 te receptor to become trapped in clusters of early endosomes.
30 sorted into recycling tubules emerging from early endosomes.
31 lysosomes while *0402 molecules traffic into early endosomes.
32 in-dependent endocytosis and accumulation of early endosomes.
33 responsible for terminating Ras activity on early endosomes.
34 olymers colocalized with transferrin-labeled early endosomes.
35 of early endosome antigen 1 (EEA1)-positive early endosomes.
36 cropinosomes often interacting with EEA-1(+) early endosomes.
37 d to only partially inhibit ASLV fusion with early endosomes.
38 of the synaptobrevin-like v-SNARE Snc1 from early endosomes.
39 crotubules, but were generally distinct from early endosomes.
40 ondrial quality control mediated by Rab5 and early endosomes.
41 leading to its accumulation in EEA1-positive early endosomes.
42 upports the formation of F-actin networks on early endosomes.
43 ion of DISLL enhances the exit of BACE1 from early endosomes, a pathway mediated by GGA1 and retromer
44 d that retrograde cargo TGN-38 is trapped in early endosomes after depletion of SNX-3 (a retromer com
46 lmitoylated peptide also passed rapidly from early endosome Ag-1-positive endosomes to RAS-related GT
48 here that peroxisomes move by hitchhiking on early endosomes, an organelle that directly recruits the
50 both an increased stability at the pH of the early endosome and efficient degradation at lower pH in
51 enin also prolonged TNF association with the early endosome and enhanced caspase-8 activation in apop
52 w glucose variation-induced stress regulated early endosome and lysosome formation via endocytosis of
53 s accumulate abnormal endosomes positive for early endosome and recycling endosome markers that are n
54 mannose-phosphate receptor-positive tubular early endosomes and a reduction in Notch signaling capac
55 iptional regulator RNF11, which localizes to early endosomes and appears additionally in the cell nuc
57 ermal growth factor receptor (EGFR) from the early endosomes and degradation of EGFR after EGF stimul
58 ARRDC3 primarily localizes to EEA1-positive early endosomes and directly interacts with the beta2AR
59 by finding that F13 was largely confined to early endosomes and failed to colocalize with B5 in the
60 by tubular-vesicular carriers that bud from early endosomes and fuse with a corresponding acceptor c
61 transport in which peroxisomes hitchhike on early endosomes and identify PxdA as the novel linker pr
62 rs from the TGN, perinuclear accumulation of early endosomes and impaired transferrin endocytosis.
63 overexpression reduced NTR1 localization in early endosomes and increased expression of proteins rel
64 tination, promoted BACE1 accumulation in the early endosomes and late endosomes/lysosomes, and decrea
66 new tools to quantify peripherally localized early endosomes and measure the rapid recycling of integ
67 e proteins, IFITMs), on the pH regulation in early endosomes and on the efficiency of acid-dependent
69 osphate (PIP3) on B cell receptor-containing early endosomes and proper sorting into the MHC class II
70 ted GCGR endocytic trafficking through Rab5a early endosomes and Rab4a recycling endosomes, but also
71 mine/siRNA polyplexes initially appearing in early endosomes and rapidly moving to other compartments
72 nonical Wnt signaling proteins are housed on early endosomes and recruit nucleation sites to branch p
73 RNAs are internalized by a specific class of early endosomes and show preferential association with e
74 2A, whereupon it quickly translocates to the early endosomes and subsequently routes to the lysosomes
75 PTH) stimulation, the PTHR internalizes into early endosomes and subsequently traffics to the retrome
76 hat KIF13A and KIF13B bind preferentially to early endosomes and that KIF1A and KIF1Bbeta bind prefer
77 ed that Leu-725 enhances PC7 localization to early endosomes and that, together with Glu-719 and Glu-
79 now show that HCMV is initially retained in early endosomes and then moves sequentially to the trans
81 d activation of Rab5 to cause enlargement of early endosomes and to disrupt retrograde axonal traffic
83 pathway used, all these viruses converge in early endosomes and use multivesicular bodies for cell e
84 resent in all endocytic compartments between early endosomes and vacuoles, shares features of Vam3p a
85 ation by two Sec1/Munc-18 proteins, Vps45 in early endosomes and Vps33 in early and late endosomes/va
86 ssemblies of clathrin and caveolin, Rab5a in early endosomes, and alpha-actinin, often in relationshi
87 due to delayed transit time of EGFR through early endosomes, and cells preferentially proliferate.
89 beta1 integrin is internalized, traffics to early endosomes, and is returned to the plasma membrane
90 the Golgi/trans-Golgi network (TGN), in the early endosomes, and on the plasma membrane, yet the cel
91 rins, attenuates integrin translocation into early endosomes, and reduces delayed mitogen-activated p
94 t complex after stimulation with EGF, as was early endosome antigen 1 (EEA1), a factor responsible fo
95 n HSP, Mecp2 KO neurons have lower levels of early endosome antigen 1 (EEA1), a protein involved in A
96 ed colocalization of G. bethesdensis with an early endosome antigen 1 (EEA1)-positive compartment, fo
97 ripheral Rab5 puncta and a reduced number of early endosome antigen 1 (EEA1)-positive early endosomes
98 27a), and, to some extent, early endosomes (early endosome antigen 1), indicating a lack of integrit
102 ed, the transit time of EGF receptor through early endosomes are accelerated, mitogenic MAPK-ERK1/2 s
105 fficking of plasma membrane receptors to the early endosomes as well as inhibit phagocytosis of the b
106 subcellular localization of the receptor in early endosomes associated with EEA-1 (early endosome an
107 imultaneous time-lapse imaging, we find that early endosome-associated PxdA localizes to the leading
108 A (A. nidulans FTS homologue) disrupts HookA-early endosome association and inhibits early endosome m
109 association requires FhipA and HookA, FhipA-early endosome association is independent of HookA and F
110 ith early endosomes, thus differing from the early endosome association of the cargo adapter HookA (H
111 rly endosomes, and interestingly, while FtsA-early endosome association requires FhipA and HookA, Fhi
112 in endothelial cells, possibly by fusing in early endosomes at higher pH or by other, unknown mechan
113 s of vezA causes an abnormal accumulation of early endosomes at the hyphal tip, where microtubule plu
115 interaction between dynein-dynactin and the early-endosome-bound HookA is significantly decreased.
116 P21 dynamically localizes with EEA1-positive early endosomes but is also found in EEA1-negative endos
117 with the model that VSV initiates fusion in early endosomes but releases its core into the cytosol a
118 ansports various cellular cargoes, including early endosomes, but how dynein binds to its cargo remai
119 osome-related organelles obtain cargoes from early endosomes, but the fusion machinery involved and i
120 loss of VezA, HookA associates normally with early endosomes, but the interaction between dynein-dyna
121 EGFR-AMSH was efficiently internalized into early endosomes, but, importantly, the rates of ligand-i
122 t a model proposing that traffic jams in the early endosome can act as an upstream pathogenic hub in
123 some maturation appears to control a pool of early endosomes capable of fusing with autophagosomes wh
124 nein is able to physically interact with the early endosome cargo, but dynein-mediated early endosome
126 Our data suggest that TSPAN9 modulates the early endosome compartment to make it more permissive fo
127 ed in the accumulation of EEA1/Rab5-positive early endosomes concomitant with a decrease in Rab7-posi
128 X, an increased amount of ZAP70 localized to early endosomes consistent with the role of monoubiquiti
130 cells resulted in prolonged EGFR activity in early endosomes, delayed EGFR degradation, increased EGF
131 hemocytes and nephrocytes, and localizes to early endosomes despite the lack of a clear Vps3 homolog
135 rom a genetic screen for mutations affecting early-endosome distribution in Aspergillus nidulans, we
137 d binding protein 27a), and, to some extent, early endosomes (early endosome antigen 1), indicating a
138 ssociated with the trans-Golgi network (TGN)/early endosome (EE) and tracked along filamentous actin,
139 s required for maturation of TLR3 containing early endosome (EE) into LE, the compartment that fuses
140 ssential for kinesin-3- and dynein-dependent early endosome (EE) motility in the fungus Ustilago mayd
141 rt between the trans-Golgi network (TGN) and early endosome (EE) requires Drs2, a phospholipid transl
143 n caused significant accumulation of ASOs in early endosomes (EEs) and reduced localization in LEs an
144 , and the endoplasmic reticulum (ER) rely on early endosomes (EEs) for intracellular movement in a fu
145 ow that long-distance retrograde motility of early endosomes (EEs) is necessary to trigger transcript
148 enetic ablation of the Hook complex adapting early endosomes (EEs) to dynein but absolutely requires
149 hereas a Rab5a DN that blocks trafficking at early endosomes eliminated agonist-induced GCGR deubiqui
150 tein implicated in translocation of Hsc70 to early endosomes for clathrin removal during retrograde t
152 n of the protein from the plasma membrane to early endosomes, for tubule formation, and for CaMV infe
153 ither for membrane scission (shibire) or for early endosome formation (Rab5, Vps45, and Rabenosyn-5).
156 l imaging suggests that MoVps17 can regulate early endosome fusion and budding as well as endocytosis
158 lized endosomal compartments, beginning with early endosomes harboring Rab5 and its effector EEA1.
159 that form at the PM and trans-Golgi network/early endosomes have emerged as the prominent vesicle ty
162 elevation of external pH can raise the pH in early endosomes in a cell type-dependent manner and ther
163 nd dissociation of signalling molecules from early endosomes in a dense cytoplasm with single-molecul
164 have demonstrated that RME-8 associates with early endosomes in a phosphatidylinositol 3-phosphate (P
165 t SNX27 binds several beta integrin tails in early endosomes in a PI3 (phosphatidylinositide 3)-kinas
166 n organelle distribution: Golgi outposts and early endosomes in distal dendritic branches are reduced
172 le in cargo sorting and vesicle budding from early endosomes, in most cases leading to cargo fusion w
173 y showed a dissociation of payloads from the early endosome indicating translocation of the chimeric
174 e interaction occurs independently of dynein-early endosome interaction and requires the C-terminal d
175 h dynein and dynactin independently of HookA-early endosome interaction but dependent on the N-termin
178 d loss of HookA significantly weakens dynein-early endosome interaction, causing a virtually complete
179 bility of RME-8 to associate with PI(3)P and early endosomes is largely abolished when residues Lys(1
180 ors of beta1/beta2-integrin recycling in the early endosome, is decreased in Klf5(Delta/Delta) haemat
184 argos, including mitochondria, Rab5-positive early endosomes, late endosomes/lysosomes, and TrkA-, Tr
185 r bacterium Ehrlichia chaffeensis resides in early endosome-like vacuoles and circumvents lysosomal f
186 in PxdA that is necessary and sufficient for early endosome localization and peroxisome distribution
188 an cells without affecting other organelles (early endosomes, lysosomes, the Golgi apparatus, the end
189 we observed that C5b-9 colocalizes with the early endosome marker EEA1 and that, in the presence of
190 ian cells, mCherry-RavD colocalized with the early endosome marker EGFP-Rab5 as well as the PI(3)P bi
191 ized GPRC6A was mainly co-localized with the early endosome marker Rab5 and the long loop recycling e
195 plasma membrane as expected, but also in the early endosome membrane, and that internalized receptors
198 AVE/SCAR and Arp2/3 regulate endocytosis and early endosome morphology in diverse tissues of C. elega
199 ements require ATP and involve bidirectional early endosome motility, indicating that microtubule-ass
200 he early endosome cargo, but dynein-mediated early endosome movement away from the hyphal tip occurs
201 kA, as a factor required for dynein-mediated early endosome movement in the filamentous fungus Asperg
206 ions are amphisomes formed through fusion of early endosomes, multivesicular bodies, and early autoph
207 inding of SNX31 with beta1 integrin tails in early endosomes occurs between the FERM domain and the m
209 RA, zfyve9) has been classically observed in early endosomes of different cells types where it regula
210 pletion did not alter the delivery of SFV to early endosomes or change their pH or protease activity.
211 ome-edited cells with nanobodies tethered to early endosomes or mitochondria changes the subcellular
213 , Strip acts as a molecular platform for the early endosome organization that has important roles in
214 tely 5,000-fold, whereas transferrin uptake, early endosome organization, and dynein-dependent moveme
215 the phosphatidylinositol-3-phosphate pool in early endosomes; phosphatidylinositol-3,4-biphosphate an
217 ediated fusion between Golgi-derived SGs and early endosomes precedes the maturation of the SGs, as r
218 tion of UBAP1 leads to dysregulation of both early endosome processing and ubiquitinated protein sort
219 internalizing surface pMHC-II in March-I(+) early endosomes promotes degradation of "old" pMHC-II an
220 (a) detection of the enzyme in EEA1-positive early endosomes, Rab7-positive late endosomes/multivesic
221 ure has ever been identified at the level of early endosomes, raising a question about their role.
225 In MDCK 3D cultures, CLIC4 is expressed on early endosome, recycling endosome and apical transport
226 that once internalized, M1 mAChRs traffic to early endosomes, recycling endosomes and late endosomes.
227 1 was recruited to the cell surface from the early endosome-recycling complex pathway, its knockdown
228 - and branched actin-mediated trafficking on early endosome regulates apical delivery during early lu
230 lised into early endosomes, where the master early endosome regulator Rab5b promotes STAT5 phosphoryl
231 , IFITM2 and IFITM3 localize to the late and early endosomes, respectively, as well as the lysosome.
233 ed infection by several viruses that fuse in early endosomes (SFV, SINV, CHIKV, and vesicular stomati
235 n and caused prolonged TLR4 retention at the early endosome, suggesting that TLR4 transport from earl
236 port than ClC-5:S244L, but co-localized with early endosomes, suggesting decreased ClC-5:R345W membra
238 oplasmic reticulum and cis-Golgi, but not in early endosomes, suggesting the nonsense mutation affect
239 suggested that TRAM and TLR2 co-localize in early endosomes, supporting the hypothesis that signalin
241 NG gene, which encodes a trans-Golgi network/early endosome (TGN/EE)-localized E3 ubiquitin ligase.
242 ole required neither the trans-Golgi network/early endosome (TGN/EE)-localized vacuolar H(+)-ATPase a
246 the retromer complex, a sorting platform on early endosomes that promotes recycling of surface recep
247 ow demonstrate that polysomes associate with early endosomes that undergo kinesin 3- and dynein-depen
248 a) antibody to be localized to Rab5-positive early endosomes, the trans-Golgi network, and subsequent
249 ch shortens the transit time of EGFR through early endosomes, thereby limiting mitogenic MAPK signals
250 ings demonstrate that NOD1 detects PG within early endosomes, thereby promoting RIP2-dependent autoph
252 venger receptors and subsequently escape the early endosome through a pH-triggered disassembly mechan
253 In contrast, if antigens were delivered to early endosomes through CD40 or CD11c, BDCA1(+) DCs were
254 manner but are not obviously associated with early endosomes, thus differing from the early endosome
255 trafficking vesicles that dock and fuse with early endosomes, thus overriding the default pathway to
256 OC-1 to -3, mediate protein sorting from the early endosome to lysosomes and lysosome-related organel
258 in-3 complex, which transports TLRs from the early endosome to the late endolysosomal compartments.
259 mal acid hydrolases requires traffic through early endosomes to late endosomes followed by transient
261 own about the regulators of Ag delivery from early endosomes to lysosomal compartments where the prop
263 Rab14 and PI(3)P to direct the maturation of early endosomes to Rab9/CD63-containing late endosomes.
266 all Rab GTPase mediating fast recycling from early endosomes to the plasma membrane, and enhanced the
267 ided evidence that retrograde transport from early endosomes to the trans-Golgi network is required f
269 x2 and found that depletion of UNC50 blocked early endosome-to-Golgi trafficking and induced lysosoma
273 onstrated that the IRT1 protein localizes to early endosomes/trans-Golgi network (EE/TGN) and is cons
274 ociated mutant CHMP2B toxicity and implicate early endosome transport as a potential contributing pat
279 equency but not the speed of dynein-mediated early-endosome transport is decreased, which correlates
280 enhanced localization of HIV-1 with TLR8(+) early endosomes, triggered a pro-inflammatory response,
286 tive intracellular staining of lysosomes and early endosomes via subtle changes in fluorescence emiss
289 irmed that while VP2 is shed from virions in early endosomes, virus particles still consisting of VP5
292 activity of Rab5, the key GTPase regulating early endosomes, was required for p75 death signaling.
294 Y1 and LjVPY2 within the trans-Golgi network/early endosome, where they might function to regulate en
296 internalize polymersomes by endocytosis into early endosomes, where they are disassembled by the low
297 of PIPKIgammai5 blocks Rab7a recruitment to early endosomes, which prevents the maturation of early
298 However, 5-NT altered the distribution of early endosomes with a concomitant impairment of reoviru
299 lipid membrane composition mimicking that of early endosomes, with PI(3)P enhancing membrane recruitm
300 arance of large TrkA puncta in enlarged Rab5-early endosomes within the cytoplasm, suggesting delayed