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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
47                               APPL1, but not early endosome Ag 1, deficiency impairs IRF3 target gene
48 lmitoylated peptide also passed rapidly from early endosome Ag-1-positive endosomes to RAS-related GT
49 cipates in the trafficking and tubulation of early endosomes along microtubules.
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
55 ized in the Golgi stack, trans-Golgi network/early endosome and tonoplast.
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
58                           USP2a localizes to early endosomes and associates with EGFR, stabilizing th
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
69 ation-induced stress-stimulated formation of early endosomes and lysosomes.
70 e proteins, IFITMs), on the pH regulation in early endosomes and on the efficiency of acid-dependent
71           PACS-2 co-localizes with ADAM17 on early endosomes and PACS-2 knockdown decreases the recyc
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
74 multivesicular body pathway, retained APP in early endosomes and reduced Abeta(40) production.
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
79                        We localized AFTPH to early endosomes and the trans-Golgi network (TGN) in uns
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
82 ), suggesting brief receptor localization in early endosomes and transfer to late endosomes.
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.
88           Both FhipA and FtsA associate with early endosomes, and interestingly, while FtsA-early end
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
91 ed NTR1 traffics from the plasma membrane to early endosomes, and then recycles.
92                     At CCVs, CvpB binding to early endosome- and autophagy-derived PI(3)P and the con
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
96 A with VEGFR-2 is localized within the EEA1 (early endosome antigen 1) endosomal compartment.
97  27a), and, to some extent, early endosomes (early endosome antigen 1), indicating a lack of integrit
98 or in early endosomes associated with EEA-1 (early endosome antigen 1).
99 th transferrin and EGF receptors (EGFRs) and early endosome antigen 1, but not with LAMP1 protein.
100 es transient oxidation on or close to RAB5+/ early endosome antigen 1- endosomes.
101 ero-oligomers including Bax, Troponin C, and Early Endosome Antigen 1.
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
104                                              Early endosomes are essential for regulating cell signal
105                                              Early endosomes are transported bidirectionally by cytop
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
116 early endosome clustering, and Rab5-positive early endosomes become smaller and scattered.
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
128                 Strip knockdown disturbs the early endosome clustering, and Rab5-positive early endos
129 atients also accumulated large RAB5-positive early endosomes compared to controls.
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
133                      TSPAN9 was localized to early endosomes containing internalized alphavirus, and
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
136 pergillus nidulans, as a factor critical for early endosome distribution.
137  genome-wide screen for mutants defective in early-endosome distribution.
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
144       We show that shortly after uptake into early endosomes (EE), CpG and siRNA parts of the conjuga
145               Unlike B2AR, which traffics to early endosomes (EE), LHR internalizes to distinct pre-e
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
150                                              Early endosomes (EEs) mediate protein sorting, and their
151                               PS-ASOs exited early endosomes (EEs) rapidly after internalization and
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
155 Hook homologues were found to link dynein to early endosomes for their transport.
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).
158 lasma membrane to the lysosomal membrane via early endosome formation.
159 ly binds to and activates Rabex-5, promoting early-endosome formation.
160 l imaging suggests that MoVps17 can regulate early endosome fusion and budding as well as endocytosis
161                                    Phagosome-early endosome fusion required PI(3)P, yet did not depen
162 lized endosomal compartments, beginning with early endosomes harboring Rab5 and its effector EEA1.
163                  Different subpopulations of early endosomes have been described, raising the questio
164 brane, although the TGN also functions as an early endosome in plants.
165 t from the Golgi and the trans-Golgi network/early endosome in the seed coat epidermis.
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
168  of poly(I:C) to effect signaling by TLR3 in early endosomes in a mechanism that involves FPRL1.
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
172 8aa transmembrane smORF peptide localised to early endosomes in Drosophila macrophages.
173 ndosomal trafficking through somatodendritic early endosomes in L1-mediated axon growth.
174 uggesting that dense granules originate from early endosomes in MKs.
175 nteraction between dynein and the Hook-bound early endosomes in vivo.
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
180 HookA is a novel linker important for dynein-early endosome interaction in vivo.
181                                        HookA-early endosome interaction occurs independently of dynei
182 d loss of HookA significantly weakens dynein-early endosome interaction, causing a virtually complete
183 mechanism that initiates PAR1 sorting at the early endosome is not known.
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
186 t pHs characteristic of the plasma membrane, early endosome, late endosome, and lysosome.
187                                CLN3-positive early endosomes, late endosomes and cholesterol/sphingol
188 nto phagolysosomes by sequential fusion with early endosomes, late endosomes, and lysosomes.
189 ires sequential fusion of the phagosome with early endosomes, late endosomes, and lysosomes.
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
193 cted contribution of the trans-Golgi network/early endosome-localized V-ATPase to vacuolar pH.
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
197              We identify a specific stage of early endosome maturation that is regulated by beclin 1,
198                                           As early endosomes mature, the SAND-1/CCZ-1 complex acts as
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
201 s and colocalizes with the Golgi membrane or early endosome membrane.
202 on of TSPAN9 inhibited virus fusion with the early endosome membrane.
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
207 equency but not the speed of dynein-mediated early endosome movement.
208 pA complex are important for dynein-mediated early endosome movement.
209 ion, causing a virtually complete absence of early endosome movement.
210 ookA-early endosome association and inhibits early endosome movement.
211 s in dynein-mediated nuclear positioning and early endosome movement.
212 inding of SNX31 with beta1 integrin tails in early endosomes occurs between the FERM domain and the m
213 f function, thus affecting actin dynamics in early endosomes of BLOC-1-deficient cells.
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.
216  long-range movement of peroxisomes, but not early endosomes or nuclei.
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
221 somes (EE), LHR internalizes to distinct pre-early endosomes (pre-EEs) for its recycling.
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.
226                The bidirectional movement of early endosomes randomly distributes polysomes, which ma
227 ex and uncovered a new function for Vps13 in early endosome recycling and Neo1 localization.
228                     We further show that the early-endosome recycling route and its control though th
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
233 and alters the subcellular enrichment of the early endosome regulator RAB-5.
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.
236            Membrane microcompartments of the early endosomes serve as a sorting and signaling platfor
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
241            Apm2 and Apm1 colocalize at Golgi/early endosomes, suggesting that they do not associate w
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
245 r its recognition at the trans-Golgi network/early endosomes (TGN/EE) for vacuolar targeting.
246       In plants, the trans-Golgi network and early endosomes (TGN/EE) function as the central junctio
247        Thus FhipA is more directly linked to early endosomes than HookA and FtsA.
248 owth factor receptor (EGFR) occurs from APPL early endosomes that mature into early EEA1 endosomes.
249                    Within the small group of early endosomes that move away from the hyphal tip in th
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
260 he exocytosis (not endocytosis) of NHE3 from early endosome to plasma membrane.
261 in-3 complex, which transports TLRs from the early endosome to the late endolysosomal compartments.
262 fficking apparatus that sorts cargo from the early endosome to the trans-Golgi network.
263 mal acid hydrolases requires traffic through early endosomes to late endosomes followed by transient
264 lts is that ArfGAP3 regulates transport from early endosomes to late endosomes.
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
268 h enhanced recycling of VE-cadherin-positive early endosomes to the IEJ.
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
272 cifically blocking retrograde transport from early endosomes to the trans-Golgi network.
273 x2 and found that depletion of UNC50 blocked early endosome-to-Golgi trafficking and induced lysosoma
274        To identify host factors required for early endosome-to-Golgi trafficking of STx2, we performe
275                                              Early endosome-to-Golgi transport allows the toxins to e
276        A new study investigates why directed early endosome trafficking is so frequently interrupted,
277 onstrated that the IRT1 protein localizes to early endosomes/trans-Golgi network (EE/TGN) and is cons
278      Here we develop a mathematical model of early endosome transport in Ustilago maydis.
279                                         When early endosome transport is abolished, POs and LDs drift
280  enhanced localization of HIV-1 with TLR8(+) early endosomes, triggered a pro-inflammatory response,
281                          CvpB association to early endosome triggers vacuolation and clustering, lead
282                                              Early endosomes undergo retrograde transport (clustering
283              We show that DTX3L localizes to early endosomes upon CXCR4 activation and interacts dire
284 ed with TLR4, CD14, and dynamin into Rab5(+) early endosomes upon LPS treatment.
285 tive intracellular staining of lysosomes and early endosomes via subtle changes in fluorescence emiss
286 n-dependent sequestration into Rab5-positive early endosomes via the ESCRT machinery.
287       RIN3 recruited CD2AP to RAB5a-positive early endosomes via these interaction sites.
288 irmed that while VP2 is shed from virions in early endosomes, virus particles still consisting of VP5
289        The rapid transit of BACE1 S498D from early endosomes was coupled with reduced levels of amylo
290                      Albumin accumulation in early endosomes was independent of FcRn-binding affinity
291                           SNX17 localizes to early endosomes where it directly binds NPX(Y/F) motifs
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.
294               Prolactin is internalised into early endosomes, where the master early endosome regulat
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
299 ed in the accumulation of endocytosed APP in early endosomes with reduced APP processing.
300 arance of large TrkA puncta in enlarged Rab5-early endosomes within the cytoplasm, suggesting delayed

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