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1 ormation but not for Optn recruitment to the phagophore.
2 the ULK1 autophagy initiation complex to the phagophore.
3 equires activation of the ULK complex at the phagophore.
4 -induced centrosomal GABARAP delivery to the phagophore.
5 he mobilization of membranes to generate the phagophore.
6  barrier in the transition to the cup-shaped phagophore.
7 folds for assembly of the ULK complex at the phagophore.
8 which in turn initiates the formation of the phagophore.
9 organization of Atg9 vesicles into the early phagophore.
10 f the Atg12-5-16L1 complex to Wipi2-positive phagophores.
11 n of these vesicles and their fusion to form phagophores.
12 CP1-positive autophagosome precursors called phagophores.
13           Forming the autophagosome from the phagophore, a cup-shaped double-membrane vesicle, is a c
14  is regulated for efficient formation of the phagophore, an isolation membrane that sequesters the pe
15  a very early event in the generation of the phagophore and in the process of macroautophagy.
16 ositive structures interact dynamically with phagophores and autophagosomes without being incorporate
17 lead to impairment in isolation membrane (or phagophore) and autophagosome formation, maturation, or
18 xpansion of the autophagosome precursor, the phagophore, and give the first real-time, observation-ba
19 of the initial sequestering compartment, the phagophore, and is proposed to play a key role in membra
20 RAPPIII complex directs this Ypt1 GEF to the phagophore assembly site (PAS) that is involved in autop
21 fects the recruitment of mitochondria to the phagophore assembly site (PAS), a critical step in the p
22                   Most of them reside at the phagophore assembly site (PAS), although the function of
23 tg17-Atg31-Atg29 complex translocates to the phagophore assembly site (PAS), where an autophagosome f
24 utophagy begins with the organization of the phagophore assembly site (PAS), where most of the AuToph
25 through what mechanism Atg9 functions at the phagophore assembly site (PAS).
26                COG subunits localized to the phagophore assembly site and interacted with Atg (autoph
27 that TRAPPIII binds to COPII vesicles at the phagophore assembly site and that COPII vesicles may pro
28 s that are dependent on PtdIns(3)P for their phagophore assembly site association.
29  conjugation systems, Atg8 and Atg16, to the phagophore assembly site is affected.
30 the Rab GTPase Ypt1 that is recruited to the phagophore assembly site when macroautophagy is induced.
31         Additionally, the pexophagy-specific phagophore assembly site, organized by the dual interact
32 tant, Atg8 is inefficiently recruited to the phagophore assembly site, which is involved in autophago
33 ed the initial protein assembly steps at the phagophore assembly site.
34 ely downstream of the Atg1 kinase complex at phagophore assembly sites.
35 R-mitochondria contact sites are involved in phagophore assembly.
36 ly unknown; we confirm roles for Gyp1 at the phagophore-assembly site, Atg24 in cargo engulfment, Atg
37  the autophagy pathway via interactions with phagophore-associated ATG8-like proteins.
38 ere we show that Bcl-2 directly binds to the phagophore-associated protein GABARAP.
39                            During autophagy, phagophores capture portions of cytoplasm and form doubl
40       A vesicle, possibly a precursor of the phagophore, contains translocated m-IL-1beta and later t
41 ocess whereby newly formed membranes, termed phagophores, engulf parts of the cytoplasm leading to th
42 ve and nonselective autophagy at the step of phagophore expansion at the PAS.
43  well appreciated that autophagy begins with phagophore formation and expansion through lipid acquisi
44 remodeling thus emerges as a viable route to phagophore formation.
45 x, activation of CAMKK2, AMPK, and ULK1, and phagophore formation.
46 d specifically for pexophagy at the stage of phagophore formation.
47 ion facilitates membrane flow to the PAS for phagophore formation.
48 ance mechanism in which the double-membraned phagophore grows and engulfs cytosolic material.
49 xpand the initial sequestering membrane, the phagophore; however, essentially nothing is known about
50                        mAtg9 is recruited to phagophores independent of early autophagy proteins, suc
51            STX13 was present on LC3-positive phagophores induced by rapamycin and was highly enriched
52  and plays a previously unrecognized role in phagophore initiation from ER exit sites.
53 ates LC3-II production and maturation of the phagophore into the autophagosome, by facilitating the r
54 nction and participates in the maturation of phagophores into closed autophagosomes.
55                                          The phagophore is largely devoid of integral membrane protei
56           The origin of the cup shape of the phagophore is poorly understood.
57 iated Atg12-5-16L1 complex to Wipi2-positive phagophores is crucial for producing microtubule-associa
58                                              Phagophore maturation is a key step in the macroautophag
59                                In yeast, the phagophore nucleates from a cluster of 20-30 nm diameter
60 g31-Atg29 subcomplex of Atg1 is critical for phagophore nucleation at the PAS.
61        The intermediate membrane, termed the phagophore or isolation membrane, is a cup-like structur
62 o play a key role in membrane transport; the phagophore presumably expands by vesicular addition to f
63                             Growth along the phagophore rim marks the progress of both organelle expa
64 st three vesicles need to fuse to induce the phagophore shape, consistent with experimental observati
65 brane, and in their homotypic fusion to form phagophore structures.
66 rmation of a cup-shaped structure called the phagophore that matures into the autophagosome.
67 d by the formation of an isolation membrane (phagophore) that engulfs cytoplasmic constituents, leadi
68  fusion of the edges of the double-membraned phagophores to form autophagosomes.
69        However, the number of Wipi2-positive phagophores was not decreased in Optn-deficient cells.
70 proceeds by the growth of a double-membraned phagophore, which engulfs cytosol and other substrates.
71 s are formed by the elongation and fusion of phagophores, which can be derived from preautophagosomal
72 d transport is then used to feed the growing phagophore with pre-selected cargoes and debris derived

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