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1 f mitochondria (mitophagy), and peroxisomes (pexophagy).
2 ance is degradation via selective autophagy (pexophagy).
3 bers is through an autophagic process called pexophagy.
4 (PEX2) is the causative agent for mammalian pexophagy.
5 s sequestered within vacuoles as a result of pexophagy.
6 peroxisomal and is required specifically for pexophagy.
7 ks pexophagy, and its overexpression induces pexophagy.
8 e is necessary but not sufficient to trigger pexophagy.
9 heir delivery to the autophagy machinery for pexophagy.
10 pAtg30, mediates peroxisome selection during pexophagy.
11 tions, at least one of which is required for pexophagy.
12 pecies-induced pejvakin-LC3B interaction and pexophagy.
13 Cvt pathway and efficient autophagy but not pexophagy.
14 oxisomes in the process of being engulfed by pexophagy.
15 d the targeted degradation of peroxisomes by pexophagy.
16 storis, Gsa9 is required for glucose-induced pexophagy.
17 appears to be required for an early event in pexophagy.
18 de proteins that might provide signal(s) for pexophagy.
19 with OPTN is a key feature of OPTN-mediated pexophagy.
20 ated peroxisome membrane proteins to prevent pexophagy.
21 f the autophagic machinery for OPTN-mediated pexophagy.
22 as growth and division, rather than impaired pexophagy.
23 o types of selective autophagy, ER-phagy and pexophagy.
24 endently localises to peroxisomes and drives pexophagy.
26 -resolved mapping of peroxisome turnover and pexophagy across development, metabolism, and disease.
27 e shown that these proteins are required for pexophagy and autophagy in P. pastoris and the Cvt pathw
29 y, including cytoplasm-to-vacuole targeting, pexophagy and mitophagy, and mammalian genetic screens h
30 of cellular recycling mechanisms (autophagy, pexophagy and ribosome breakdown) in maintaining cell vi
31 verlap of macroautophagy with the process of pexophagy and with the biosynthetic cytoplasm-to-vacuole
32 ame this protein Atg36 as its absence blocks pexophagy, and its overexpression induces pexophagy.
37 ignal transduction pathway are necessary for pexophagy but not for pexophagosome formation or other n
40 study, we investigated the role of Sar1p in pexophagy by expressing dominant-negative mutant forms o
42 n Atg11/FIP200 interaction motif to modulate pexophagy by virtue of its conserved phospho-metabolite
43 of Atg26 and Vac8 functions under different pexophagy conditions demonstrates that not only pexophag
44 ains also displayed defects in autophagy and pexophagy, degradative pathways that share protein machi
45 We find that overexpressing USP30 prevents pexophagy during amino acid starvation, and its depletio
48 Lc3b cDNAs completely restored sound-induced pexophagy, fully prevented the development of oxidative
50 ion of peroxisomal membrane proteins signals pexophagy; however, the E3 ligase responsible for mediat
52 , and xenophagy, has also been implicated in pexophagy in HEK-293 cells, the underlying mechanisms re
54 eling, provide evidence for the existence of pexophagy in plants, and indicate that peroxisome destru
57 endently localized to peroxisomes to promote pexophagy in several physiological conditions, illustrat
60 ctive autophagic degradation of peroxisomes (pexophagy) in auditory hair cells from wild-type, but no
62 ophagy conditions demonstrates that not only pexophagy inducers, such as glucose or ethanol, but also
64 shes a versatile platform for dissecting how pexophagy integrates with mitochondrial quality control
68 hat the function of sterol glucoside (SG) in pexophagy is both species and peroxisome inducer specifi
70 ne via interaction with peroxins, and during pexophagy it colocalizes transiently at the preautophago
71 terminal half of overexpressed OPTN triggers pexophagy, likely by oligomerizing with endogenous OPTN.
72 , regulation of division and protein import, pexophagy, matrix protein degradation, solute transport,
73 r hydrolase, aminopeptidase I (API), whereas pexophagy mediates the delivery of excess peroxisomes fo
75 ls that activate this pathway do not trigger pexophagy on their own, suggesting that this MAPK cascad
77 stinct from endoplasmic reticulum-autophagy, pexophagy, or mitophagy, despite the close association b
83 We find that latent activation of the yeast pexophagy receptor Atg36 by the casein kinase Hrr25 in r
85 gest that pejvakin acts as a redox-activated pexophagy receptor/adaptor, thereby identifying a previo
91 ome turnover by autophagy-related processes (pexophagy), termed micropexophagy and macropexophagy, is
93 regulator, is also necessary for regulating pexophagy, the selective autophagic degradation of perox
94 size of peroxisomes before their turnover by pexophagy, the selective autophagy of peroxisomes, and f
96 rols the selective autophagy of peroxisomes (pexophagy) through the assembly of a receptor protein co
97 e for NIX, not only in mitophagy but also in pexophagy, thus illustrating the interconnection between
98 rgo rapid, selective autophagic degradation (pexophagy) when the metabolic pathways they contain are
99 on of both mitochondria and peroxisomes (via pexophagy), whereas Hog1 functions specifically in mitop