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1 found that both of them are localized in the early endosome.
2 ulting in an accumulation of the TfR1 in the early endosome.
3 the plasma membrane or lysosome, but not the early endosome.
4 ment of actin in regulating processes at the early endosome.
5 thin the cell, for example the ER, golgi and early endosome.
6 nding of PE molecules in the membrane of the early endosome.
7 ggesting an important role for TSPAN9 in the early endosome.
8 docytosis and low-pH-triggered fusion in the early endosome.
9 d to only partially inhibit ASLV fusion with early endosomes.
10 s, and LPS is released into the cytosol from early endosomes.
11 cking to Rab7-labeled late endosomes but not early endosomes.
12 lays long lifetimes, all features typical of early endosomes.
13 b5-GTP, and its recruitment to Rab5-positive early endosomes.
14 tine, unlike retromer components that act on early endosomes.
15 the cytoplasmic domain of beta1 integrin in early endosomes.
16 -operate to support bi-directional motion of early endosomes.
17 traffic of HAS3 from the plasma membrane to early endosomes.
18 ng Hook protein as general motor adapters on early endosomes.
19 periphery and reduced virion localization to early endosomes.
20 zed with both NOD1 and RIP2 in EEA1-positive early endosomes.
21 of the synaptobrevin-like v-SNARE Snc1 from early endosomes.
22 s essential for in vitro homotypic fusion of early endosomes.
23 sosomes because of a failure to recycle from early endosomes.
24 microtubule-based long-distance motility of early endosomes.
25 t the MHC-II-Ii complex away from March-I(+) early endosomes.
26 AP3 localized to the trans-Golgi network and early endosomes.
27 te receptor to become trapped in clusters of early endosomes.
28 sorted into recycling tubules emerging from early endosomes.
29 the apical cell surface and moves rapidly to early endosomes.
30 ggesting that cathepsin L cleavage occurs in early endosomes.
31 crotubules, but were generally distinct from early endosomes.
32 isms deliver cargo into different subsets of early endosomes.
33 ated structures and the no-insert isoform on early endosomes.
34 fficient recycling of Rab7 from lysosomes to early endosomes.
35 ellular trafficking of both mitochondria and early endosomes.
36 and appeared conjointly with alpha-toxin in early endosomes.
37 ondrial quality control mediated by Rab5 and early endosomes.
38 leading to its accumulation in EEA1-positive early endosomes.
39 upports the formation of F-actin networks on early endosomes.
40 egulating the formation of branched actin on early endosomes.
41 ork, whereas others suggested an origin from early endosomes.
42 PN-1 greatly reduced Lifeact accumulation on early endosomes.
43 cropinosomes often interacting with EEA-1(+) early endosomes.
44 tive trafficking between plasma membrane and early endosomes.
45 ion of DISLL enhances the exit of BACE1 from early endosomes, a pathway mediated by GGA1 and retromer
46 d that retrograde cargo TGN-38 is trapped in early endosomes after depletion of SNX-3 (a retromer com
48 lmitoylated peptide also passed rapidly from early endosome Ag-1-positive endosomes to RAS-related GT
50 here that peroxisomes move by hitchhiking on early endosomes, an organelle that directly recruits the
51 both an increased stability at the pH of the early endosome and efficient degradation at lower pH in
52 enin also prolonged TNF association with the early endosome and enhanced caspase-8 activation in apop
53 w glucose variation-induced stress regulated early endosome and lysosome formation via endocytosis of
54 s accumulate abnormal endosomes positive for early endosome and recycling endosome markers that are n
56 mannose-phosphate receptor-positive tubular early endosomes and a reduction in Notch signaling capac
57 iptional regulator RNF11, which localizes to early endosomes and appears additionally in the cell nuc
59 ermal growth factor receptor (EGFR) from the early endosomes and degradation of EGFR after EGF stimul
60 ARRDC3 primarily localizes to EEA1-positive early endosomes and directly interacts with the beta2AR
61 fter activation, receptors are trafficked to early endosomes and either recycled or sorted to lysosom
62 by finding that F13 was largely confined to early endosomes and failed to colocalize with B5 in the
63 by tubular-vesicular carriers that bud from early endosomes and fuse with a corresponding acceptor c
64 transport in which peroxisomes hitchhike on early endosomes and identify PxdA as the novel linker pr
65 rs from the TGN, perinuclear accumulation of early endosomes and impaired transferrin endocytosis.
66 overexpression reduced NTR1 localization in early endosomes and increased expression of proteins rel
67 tination, promoted BACE1 accumulation in the early endosomes and late endosomes/lysosomes, and decrea
68 endocytic trafficking, causing clustering of early endosomes and leading to the accumulation of endoc
70 e proteins, IFITMs), on the pH regulation in early endosomes and on the efficiency of acid-dependent
72 osphate (PIP3) on B cell receptor-containing early endosomes and proper sorting into the MHC class II
73 mine/siRNA polyplexes initially appearing in early endosomes and rapidly moving to other compartments
75 RNAs are internalized by a specific class of early endosomes and show preferential association with e
76 2A, whereupon it quickly translocates to the early endosomes and subsequently routes to the lysosomes
77 PTH) stimulation, the PTHR internalizes into early endosomes and subsequently traffics to the retrome
78 hat KIF13A and KIF13B bind preferentially to early endosomes and that KIF1A and KIF1Bbeta bind prefer
80 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 the Golgi/trans-Golgi network (TGN), in the early endosomes, and on the plasma membrane, yet the cel
90 rins, attenuates integrin translocation into early endosomes, and reduces delayed mitogen-activated p
93 t complex after stimulation with EGF, as was early endosome antigen 1 (EEA1), a factor responsible fo
94 n HSP, Mecp2 KO neurons have lower levels of early endosome antigen 1 (EEA1), a protein involved in A
95 ed colocalization of G. bethesdensis with an early endosome antigen 1 (EEA1)-positive compartment, fo
97 27a), and, to some extent, early endosomes (early endosome antigen 1), indicating a lack of integrit
99 th transferrin and EGF receptors (EGFRs) and early endosome antigen 1, but not with LAMP1 protein.
102 ed, the transit time of EGF receptor through early endosomes are accelerated, mitogenic MAPK-ERK1/2 s
103 We exploit the ease with which highly motile early endosomes are distinguished from static late endos
106 ed to nascent dense granules from contiguous early endosomes as MKs mature or functions in dense gran
107 fficking of plasma membrane receptors to the early endosomes as well as inhibit phagocytosis of the b
108 subcellular localization of the receptor in early endosomes associated with EEA-1 (early endosome an
109 imultaneous time-lapse imaging, we find that early endosome-associated PxdA localizes to the leading
110 A (A. nidulans FTS homologue) disrupts HookA-early endosome association and inhibits early endosome m
111 association requires FhipA and HookA, FhipA-early endosome association is independent of HookA and F
112 ith early endosomes, thus differing from the early endosome association of the cargo adapter HookA (H
113 rly endosomes, and interestingly, while FtsA-early endosome association requires FhipA and HookA, Fhi
114 in endothelial cells, possibly by fusing in early endosomes at higher pH or by other, unknown mechan
115 s of vezA causes an abnormal accumulation of early endosomes at the hyphal tip, where microtubule plu
117 interaction between dynein-dynactin and the early-endosome-bound HookA is significantly decreased.
118 P21 dynamically localizes with EEA1-positive early endosomes but is also found in EEA1-negative endos
119 with the model that VSV initiates fusion in early endosomes but releases its core into the cytosol a
120 ansports various cellular cargoes, including early endosomes, but how dynein binds to its cargo remai
121 which plays an important regulatory role in early endosomes, but not on Rab7, which is associated wi
122 osome-related organelles obtain cargoes from early endosomes, but the fusion machinery involved and i
123 loss of VezA, HookA associates normally with early endosomes, but the interaction between dynein-dyna
124 EGFR-AMSH was efficiently internalized into early endosomes, but, importantly, the rates of ligand-i
125 t a model proposing that traffic jams in the early endosome can act as an upstream pathogenic hub in
126 some maturation appears to control a pool of early endosomes capable of fusing with autophagosomes wh
127 nein is able to physically interact with the early endosome cargo, but dynein-mediated early endosome
130 Our data suggest that TSPAN9 modulates the early endosome compartment to make it more permissive fo
131 ed in the accumulation of EEA1/Rab5-positive early endosomes concomitant with a decrease in Rab7-posi
132 X, an increased amount of ZAP70 localized to early endosomes consistent with the role of monoubiquiti
134 cells resulted in prolonged EGFR activity in early endosomes, delayed EGFR degradation, increased EGF
135 hemocytes and nephrocytes, and localizes to early endosomes despite the lack of a clear Vps3 homolog
138 d binding protein 27a), and, to some extent, early endosomes (early endosome antigen 1), indicating a
139 ssociated with the trans-Golgi network (TGN)/early endosome (EE) and tracked along filamentous actin,
140 s required for maturation of TLR3 containing early endosome (EE) into LE, the compartment that fuses
141 ssential for kinesin-3- and dynein-dependent early endosome (EE) motility in the fungus Ustilago mayd
142 rt between the trans-Golgi network (TGN) and early endosome (EE) requires Drs2, a phospholipid transl
143 TGN) to the cell surface and to and from the early endosomes (EE) requires active protein sorting dec
146 rn to the plasma membrane (PM) directly from early endosomes (EE; fast recycling) or they can traffic
147 n caused significant accumulation of ASOs in early endosomes (EEs) and reduced localization in LEs an
148 , and the endoplasmic reticulum (ER) rely on early endosomes (EEs) for intracellular movement in a fu
149 ow that long-distance retrograde motility of early endosomes (EEs) is necessary to trigger transcript
152 enetic ablation of the Hook complex adapting early endosomes (EEs) to dynein but absolutely requires
153 tein implicated in translocation of Hsc70 to early endosomes for clathrin removal during retrograde t
154 f CD74 is to translocate HLA-DR molecules to early endosomes for reloading with peptides prior to rec
156 n of the protein from the plasma membrane to early endosomes, for tubule formation, and for CaMV infe
157 ither for membrane scission (shibire) or for early endosome formation (Rab5, Vps45, and Rabenosyn-5).
160 l imaging suggests that MoVps17 can regulate early endosome fusion and budding as well as endocytosis
162 lized endosomal compartments, beginning with early endosomes harboring Rab5 and its effector EEA1.
166 elevation of external pH can raise the pH in early endosomes in a cell type-dependent manner and ther
167 nd dissociation of signalling molecules from early endosomes in a dense cytoplasm with single-molecul
169 have demonstrated that RME-8 associates with early endosomes in a phosphatidylinositol 3-phosphate (P
170 t SNX27 binds several beta integrin tails in early endosomes in a PI3 (phosphatidylinositide 3)-kinas
171 n organelle distribution: Golgi outposts and early endosomes in distal dendritic branches are reduced
176 le in cargo sorting and vesicle budding from early endosomes, in most cases leading to cargo fusion w
177 y showed a dissociation of payloads from the early endosome indicating translocation of the chimeric
178 e interaction occurs independently of dynein-early endosome interaction and requires the C-terminal d
179 h dynein and dynactin independently of HookA-early endosome interaction but dependent on the N-termin
182 d loss of HookA significantly weakens dynein-early endosome interaction, causing a virtually complete
184 bility of RME-8 to associate with PI(3)P and early endosomes is largely abolished when residues Lys(1
185 ors of beta1/beta2-integrin recycling in the early endosome, is decreased in Klf5(Delta/Delta) haemat
190 argos, including mitochondria, Rab5-positive early endosomes, late endosomes/lysosomes, and TrkA-, Tr
191 r bacterium Ehrlichia chaffeensis resides in early endosome-like vacuoles and circumvents lysosomal f
192 in PxdA that is necessary and sufficient for early endosome localization and peroxisome distribution
194 an cells without affecting other organelles (early endosomes, lysosomes, the Golgi apparatus, the end
195 we observed that C5b-9 colocalizes with the early endosome marker EEA1 and that, in the presence of
196 ized GPRC6A was mainly co-localized with the early endosome marker Rab5 and the long loop recycling e
199 under mildly acidic conditions mimicking the early endosome, mature virions release pentons and perip
200 plasma membrane as expected, but also in the early endosome membrane, and that internalized receptors
203 AVE/SCAR and Arp2/3 regulate endocytosis and early endosome morphology in diverse tissues of C. elega
204 ements require ATP and involve bidirectional early endosome motility, indicating that microtubule-ass
205 he early endosome cargo, but dynein-mediated early endosome movement away from the hyphal tip occurs
206 kA, as a factor required for dynein-mediated early endosome movement in the filamentous fungus Asperg
212 inding of SNX31 with beta1 integrin tails in early endosomes occurs between the FERM domain and the m
214 pletion did not alter the delivery of SFV to early endosomes or change their pH or protease activity.
215 occur minimally in EEA-1-positive (EEA-1(+)) early endosomes or LAMP-1(+) late endosomes/lysosomes.
217 , Strip acts as a molecular platform for the early endosome organization that has important roles in
218 tely 5,000-fold, whereas transferrin uptake, early endosome organization, and dynein-dependent moveme
219 the phosphatidylinositol-3-phosphate pool in early endosomes; phosphatidylinositol-3,4-biphosphate an
220 a dense granule defect in mice, to show that early endosomes play a direct role in dense granule biog
222 ediated fusion between Golgi-derived SGs and early endosomes precedes the maturation of the SGs, as r
223 internalizing surface pMHC-II in March-I(+) early endosomes promotes degradation of "old" pMHC-II an
224 (a) detection of the enzyme in EEA1-positive early endosomes, Rab7-positive late endosomes/multivesic
225 ure has ever been identified at the level of early endosomes, raising a question about their role.
229 In MDCK 3D cultures, CLIC4 is expressed on early endosome, recycling endosome and apical transport
230 that once internalized, M1 mAChRs traffic to early endosomes, recycling endosomes and late endosomes.
231 1 was recruited to the cell surface from the early endosome-recycling complex pathway, its knockdown
232 - and branched actin-mediated trafficking on early endosome regulates apical delivery during early lu
234 lised into early endosomes, where the master early endosome regulator Rab5b promotes STAT5 phosphoryl
235 , IFITM2 and IFITM3 localize to the late and early endosomes, respectively, as well as the lysosome.
237 ed infection by several viruses that fuse in early endosomes (SFV, SINV, CHIKV, and vesicular stomati
238 cargo from the plasma membrane into specific early endosome subpopulations is required for its approp
239 n and caused prolonged TLR4 retention at the early endosome, suggesting that TLR4 transport from earl
240 ns in dense granule biogenesis directly from early endosomes, suggesting that dense granules originat
242 suggested that TRAM and TLR2 co-localize in early endosomes, supporting the hypothesis that signalin
243 NG gene, which encodes a trans-Golgi network/early endosome (TGN/EE)-localized E3 ubiquitin ligase.
244 ole required neither the trans-Golgi network/early endosome (TGN/EE)-localized vacuolar H(+)-ATPase a
248 owth factor receptor (EGFR) occurs from APPL early endosomes that mature into early EEA1 endosomes.
250 the retromer complex, a sorting platform on early endosomes that promotes recycling of surface recep
251 ow demonstrate that polysomes associate with early endosomes that undergo kinesin 3- and dynein-depen
252 a) antibody to be localized to Rab5-positive early endosomes, the trans-Golgi network, and subsequent
253 ch shortens the transit time of EGFR through early endosomes, thereby limiting mitogenic MAPK signals
254 ings demonstrate that NOD1 detects PG within early endosomes, thereby promoting RIP2-dependent autoph
255 venger receptors and subsequently escape the early endosome through a pH-triggered disassembly mechan
256 In contrast, if antigens were delivered to early endosomes through CD40 or CD11c, BDCA1(+) DCs were
257 manner but are not obviously associated with early endosomes, thus differing from the early endosome
258 trafficking vesicles that dock and fuse with early endosomes, thus overriding the default pathway to
259 OC-1 to -3, mediate protein sorting from the early endosome to lysosomes and lysosome-related organel
261 in-3 complex, which transports TLRs from the early endosome to the late endolysosomal compartments.
263 mal acid hydrolases requires traffic through early endosomes to late endosomes followed by transient
265 own about the regulators of Ag delivery from early endosomes to lysosomal compartments where the prop
266 Rab14 and PI(3)P to direct the maturation of early endosomes to Rab9/CD63-containing late endosomes.
267 th the AP-3 clathrin adaptor complex, act at early endosomes to sort components required for melanin
269 all Rab GTPase mediating fast recycling from early endosomes to the plasma membrane, and enhanced the
270 arly retromer-mediated retrieval of APP from early endosomes to the TGN, resulted in the accumulation
271 ided evidence that retrograde transport from early endosomes to the trans-Golgi network is required f
273 x2 and found that depletion of UNC50 blocked early endosome-to-Golgi trafficking and induced lysosoma
277 onstrated that the IRT1 protein localizes to early endosomes/trans-Golgi network (EE/TGN) and is cons
280 enhanced localization of HIV-1 with TLR8(+) early endosomes, triggered a pro-inflammatory response,
285 tive intracellular staining of lysosomes and early endosomes via subtle changes in fluorescence emiss
288 irmed that while VP2 is shed from virions in early endosomes, virus particles still consisting of VP5
292 rimary, resting NK cells on endocytosis into early endosomes where its receptor, CD158d, resides.
293 RTM3 co-localizes with both APP and BACE1 in early endosomes, where BACE1 processing of APP occurs.
295 internalize polymersomes by endocytosis into early endosomes, where they are disassembled by the low
296 inated by the E3 ubiquitin ligase March-I in early endosomes, whereas biosynthetically immature MHC-I
297 ose receptor targeted antibody conjugates to early endosomes, whereas DEC205 targeted antigen primari
298 However, 5-NT altered the distribution of early endosomes with a concomitant impairment of reoviru
300 arance of large TrkA puncta in enlarged Rab5-early endosomes within the cytoplasm, suggesting delayed
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