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1 ted degradation of the viral proteins by the autolysosome.
2 d lipid accumulation within greatly enlarged autolysosomes.
3 l-associated membrane protein 2/p62 positive autolysosomes.
4 mpanied by robust accumulation of undegraded autolysosomes.
5 lting in a time-dependent formation of giant autolysosomes.
6 in the formation of mitochondria-containing autolysosomes.
7 res and lipid droplets within giant neuronal autolysosomes.
8 les called autophagosomes and degrades it in autolysosomes.
9 o distinguish early autophagic vacuoles from autolysosomes.
10 ic four- to fivefold increase in the size of autolysosomes.
11 gy protein 5) implicated in the formation of autolysosomes.
12 its active, GTP-locked form associates with autolysosomes.
13 lipidated LC3 protein, and the formation of autolysosomes.
14 d monodansylcadaverine staining for late AVs/autolysosomes.
15 s oncogene display late stages of autophagy, autolysosomes.
16 ream accumulation of autophagic vacuoles and autolysosomes.
17 cells, Tsc2-deficient neurons have increased autolysosome accumulation and autophagic flux despite mT
18 unctional relevance of doxorubicin-triggered autolysosome accumulation, we studied animals with dimin
19 ted as a result of a selective impairment of autolysosome acidification and cathepsin activation.
20 , which accumulate enlarged lysosomes and/or autolysosomes also but exhibit very low levels of acid h
22 RHOA is sequestered via p62 (SQSTM1) within autolysosomes and fails to localize to the plasma membra
24 gy markedly diminished the sizes of enlarged autolysosomes and lowered their content of GM2 gangliosi
25 features, including increased autophagosomes/autolysosomes and nuclear convolution at early stages, a
26 iated localization of the oncoprotein to the autolysosomes and subsequent degradation mediated by the
27 somal tubules and vesicles that extrude from autolysosomes and ultimately mature into functional lyso
29 e, markedly increased autophagosomes but not autolysosomes (assessed as punctate dual fluorescent mCh
31 esults suggest that ARV induces formation of autolysosome but does not induce complete autophagic flu
32 he degradation of the autophagosome cargo in autolysosomes, but the regulation of autophagy in respon
33 Lipids are localized in autophagosomes and autolysosomes by double immunofluorescence analyses in w
36 omes to lysosomes, and impaired clearance of autolysosomes, combined with reduced neuron viability an
37 king accumulation of LC3 and LAMP-1 positive autolysosomes containing undigested cytoplasmic contents
38 vacuoles in the exocrine glands are enlarged autolysosomes containing undigested cytoplasmic material
39 ion and a lower number of autophagosomes and autolysosomes during both basal and starvation-induced a
43 a, an autophagy protein that is critical for autolysosome function and clearance, is required for Pur
44 ant role in both autophagosome formation and autolysosome fusion, in induction of LC3II, a marker of
45 lutionarily conserved Wnt pathway to inhibit autolysosome generation, thereby leading to evasion of t
46 l features of early and late autophagosomes (autolysosomes), had little or no overlap with ubiquitin,
47 es, and these autophagosomes can mature into autolysosomes; however the autophagosomes are very small
48 de new evidence for the participation of the autolysosome in LD metabolism and demonstrate a novel ro
50 of autophagosomes and their maturation into autolysosomes in the absence of increased cell death.
52 acidification slowed the axonal transport of autolysosomes, late endosomes, and lysosomes and caused
53 ochrome c oxidase), autophagosome (p62), and autolysosome (lysosomal associated membrane protein 2) p
54 teins and other autophagic substrates within autolysosomes/lysosomes and reduced intraneuronal amyloi
55 mes while increasing numbers of normal-sized autolysosomes/lysosomes with reduced content of undigest
57 rient deprivation, active cathepsin-positive autolysosomes rather than LC3-II-positive autophagosomes
59 mal trafficking of EGFR and the formation of autolysosomes responsible for the degradation of interna
60 usion with mature autophagosomes to generate autolysosomes that degrade autophagic materials; therefo
61 les cells to degrade pieces of themselves in autolysosomes to enable their survival in times of stres
65 and bulk ubiquitinated cytosolic proteins to autolysosomes where they were proteolytically converted
67 nstead promote the generation of degradative autolysosomes, which are the endpoint compartments of au
68 ponents and then fuse with lysosomes to form autolysosomes, which degrade their contents to regenerat
69 ion of lysosomes with autophagosomes to form autolysosomes, which is crucial for the completion of th
70 cence, and eliminates giant lipid-containing autolysosomes while increasing numbers of normal-sized a
71 biting cathepsin-mediated proteolysis within autolysosomes with cysteine- and aspartyl-protease inhib
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