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1 ciated with the intralumenal vesicles of the multivesicular endosomes.
2 by the localization of MR1 molecules in the multivesicular endosomes.
3 e cancer cells were principally derived from multivesicular endosomes.
4 cs with the formation of luminal vesicles in multivesicular endosomes.
5 ana, which localizes to the cytoplasm and to multivesicular endosomes.
6 containing late endosomes/lysosomes, but not multivesicular endosomes.
7 utant cells, resulting in the restoration of multivesicular endosomes.
8 e-to-lysosome transport intermediates called multivesicular endosomes.
9 delivery of internalised viral particles to multivesicular endosomes.
10 budding of the endosomal membrane generates multivesicular endosomes.
11 0-nm extracellular vesicles that derive from multivesicular endosomes.
12 originate from maturation of endosomes into multivesicular endosomes (also known as multivesicular b
14 chain of T. gondii AP-1 (a) was localized to multivesicular endosomes and the limiting and luminal me
16 omet tails had the morphological features of multivesicular endosomes as revealed by electron microsc
17 during the ostensibly disparate processes of multivesicular endosome biogenesis, cytokinesis, and ret
19 Membrane contact sites between the ER and multivesicular endosomes/bodies (MVBs) play important ro
20 R) are trafficked through a subpopulation of multivesicular endosomes/bodies (MVBs) that are distinct
21 and-receptor complexes through the early and multivesicular endosomes followed by segregation of the
24 cling fate, routing the receptor to modified multivesicular endosomes (MVBs) and lysosomal compartmen
27 tein sorting into vesicles that bud into the multivesicular endosome (MVE) en route to the vacuole.
29 y been identified as important components of multivesicular endosomes (MVEs) and are involved in the
33 of a large enveloped DNA virus engaging the multivesicular endosome sorting machinery to enable infe
34 gion and in vesicles and tubules surrounding multivesicular endosomes, suggesting impaired recycling
35 as accompanied by protein sorting defects at multivesicular endosomes that divert the exosomal marker
36 ation of intralumenal vesicles that bud into multivesicular endosomes, the ESCRT-II complex initiates
37 tioning into intralumenal vesicles (ILVs) of multivesicular endosomes underlies such cellular process
39 ial for the formation of luminal vesicles in multivesicular endosomes, we now show that Vps4 function
40 ses RAB27A and RAB27B regulate exocytosis of multivesicular endosomes, which lead to exosome secretio
41 lar vesicles that originate by the fusion of multivesicular endosomes with the plasma membrane [1-8].
42 icular bodies) with subsequent fusion of the multivesicular endosomes with the plasma membrane, it re
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