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1 reduces amyloid precursor protein sorting to intraluminal vesicles.
2 hat the EGFR complex is sequestered in these intraluminal vesicles.
3 mber of enlarged LE/MVBs densely packed with intraluminal vesicles.
4 rane proteins and the formation of endosomal intraluminal vesicles.
5 here it plays a key role in the formation of intraluminal vesicles and in lipid sorting.
6  in that the organelles are enlarged and the intraluminal vesicles are almost completely absent and t
7         We also found increased formation of intraluminal vesicles coupled with enhanced release of e
8 nery that assists with cargo recruitment and intraluminal vesicle formation in MVBs.
9 nt biological processes, including endosomal intraluminal vesicle formation, HIV budding and cytokine
10               A mechanistic role for Vps4 in intraluminal vesicle (ILV) formation has been unclear.
11 function at the endosome in the formation of intraluminal vesicles (ILVs) containing cargo proteins d
12            This requires EGFR sorting to the intraluminal vesicles (ILVs) of multi-vesicular endosome
13 ble for sorting ubiquitinated receptors into intraluminal vesicles (ILVs) of multivesicular bodies (M
14  (ESCRT)-0, -I, -II, and -III complexes into intraluminal vesicles (ILVs) of multivesicular bodies (M
15 port (ESCRT) machinery, and then sorted into intraluminal vesicles (ILVs) of multivesicular bodies (M
16 ent, ESCRT/ALIX-dependent incorporation onto intraluminal vesicles (ILVs) of MVBs.
17 s of either protein blocks EGFR sorting into intraluminal vesicles (ILVs) of the multivesicular body.
18 nes caused APP redistribution from endosomal intraluminal vesicles (ILVs) to the endosomal limiting m
19 ed, targeted to endosomes, internalized into intraluminal vesicles (ILVs), and excreted in exosomes.
20 n the endosomal system, through formation of intraluminal vesicles (ILVs), which are subsequently rel
21 osed EGFR before the receptor is sorted onto intraluminal vesicles (ILVs).
22 ecruited to sort the ubiquitinated Ypq1 into intraluminal vesicles (ILVs).
23 d budding, which results in the formation of intraluminal vesicles (ILVs).
24 zed in punctate, dot-like structures, likely intraluminal vesicles (ILVs).
25 , endosomes are enlarged and fail to acquire intraluminal vesicles (ILVs).
26 K9 function leads to decreased number of the intraluminal vesicles in MVBs and diminished release of
27 rane remodeling and the release of endosomal intraluminal vesicles into multivesicular bodies.
28          In eukaryotic cells, the budding of intraluminal vesicles (IVLs) is mediated by the endosoma
29  sorting of amyloid precursor protein to the intraluminal vesicles of endosomes and enhances amyloid-
30 he inclusions, indicating their origins from intraluminal vesicles of late endosomes and of a lysosom
31 eveal that the localization of MHC-II on the intraluminal vesicles of multivesicular antigen processi
32  Here we show that SIMPLE resides within the intraluminal vesicles of multivesicular bodies (MVBs) an
33 e neck of caveolae, microvilli/filopodia and intraluminal vesicles of multivesicular bodies (MVBs).
34 ery controls the incorporation of cargo into intraluminal vesicles of multivesicular bodies.
35   When EGF.EGFR complexes accumulated in the intraluminal vesicles of the late endosome, phosphorylat
36 s that RAB7 is not required for formation of intraluminal vesicles of the LE/MVB, since RAB7-deficien
37                             The formation of intraluminal vesicles was not significantly detected in
38 osomes are nano-sized endosome-derived small intraluminal vesicles, which are important facilitators
39                                      Loading intraluminal vesicles with specific miRNAs and releasing
40 c analysis suggests that, instead of forming intraluminal vesicles with the help of Vps4, ESCRT-III/S
41 ult in the arrested accumulation of enlarged intraluminal vesicles within synaptic boutons.

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