This guide records the evidence actually inspected for the 2026-10-24 augmentation. Normal publication archives remain unchanged. Original access may exceed an abstract-only normal cache; conversely, an available supplement does not establish access to the main article. No publication quotations were added. The earlier quotations retained in the review record retain their inherited provenance and do not imply that each underlying experiment was repeated or fully accessible.
Original article, DOI 10.1080/15548627.2017.1389356; PMC article; actual author-repository PDF.
Read the main Results, Discussion and operative Methods in the normal original and the 16-page author manuscript. The inspected figure pixels are Figure 3 (PDF page 6, journal page 27), Figure 4 (page 7/page 28), and Figure 7 (page 11/page 32). Figures 1, 2 and 5 were assessed through main text and captions, without separate pixel inspection. The follow-up independent assessment additionally inspected Figure 6 pixels (PDF page 9, journal page 30). Supplementary movies and other supplementary bodies were not inspected.
Original article, DOI 10.1016/j.molcel.2016.08.021; actual publisher supplement, 32 pages; actual main Figure 6 image.
The original main article remains inaccessible. Publisher/API identity metadata, the supplement cover, DOI and article identifier agree. The normal cache remains abstract-only. The original supplement's relevant Results/captions and Methods were read, including Protein expression and purification, In vitro pulldown, immunogold localization, liposome preparation/reconstitution and lipid mixing. Supplementary Figures S3, S4 and S6 and main Figure 6 pixels were inspected. The main Figure 6 operative Results and caption were not recovered; the image alone is not a substitute for that access.
Human-fragment binding, full-length human cell association and worm biochemical reconstitution are distinct evidence scopes. None establishes identical activity for both human splice isoforms. The inherited vesicle-membrane-tethering proposal remains UNDECIDED; this is an unresolved experimental attribution, not a claim that the biological tethering model is false.
Original article, DOI 10.1038/ng.2497; PMC original.
Read the main Results concerning patient muscle/fibroblast autophagy (normal archive lines 104–122, especially 118–120), together with imaging and drug-treatment Methods (220–230). Results/Figures 3–4 support impaired clearance and reduced LC3/LAMP1 colocalization in human patient cells. Rapamycin and bafilomycin experiments distinguish induction from downstream clearance. Figure pixels were not independently inspected. These are cellular loss-of-function results, not purified tethering experiments.
Original article, DOI 10.1016/j.cell.2010.04.034.
Only the normal abstract and bibliographic metadata were available for this assessment. The inherited quotations remain unchanged, and the reviewer reference flag records unavailable main full text. Current human fusion/clearance judgments are supported independently by the actual originals described above. No claim is made that this assessment inspected the 2010 operative experiments.
Original article, DOI 10.1038/s42003-021-01830-x; PMC original.
The primary article XML was read, including Results, relevant main captions, Discussion and Methods for full-length human EPG5 expression/purification and binding. Full-length human 2579-residue EPG5 expressed in Sf9 cells has an elongated architecture and preferential GABARAP-family binding. The human-cell knockout/recruitment experiments concern induced mitophagy conditions. Figure 7 presents a membrane-engagement model; it is not an isolated membrane-bridging assay. Main figure pixels and supplementary bodies were not independently inspected in this augmentation. The proposed two-factor/multivalent LIR interpretation must be read alongside the 2025 study below.
Original article, DOI 10.1080/15548627.2024.2447213; PMC original.
Read the primary XML Methods, operative Results/Discussion and main captions. Figures 1–2 combine a 7.85 Å cryo-EM map of purified human EPG5 with domain-wise structural models. The LIR-containing loop is unresolved and modeled; it is not a directly resolved contact. Tandem-peptide NMR supports contact with the canonical GABARAPL1 docking site but does not itself identify which tandem LIR is bound. Figure 3C, using full-length human EPG5 in engineered HEK293 cells, distinguishes WT/W567A association from severely impaired W550A/double-mutant association. These results revise the speculative multivalent interpretation of the 2021 work. No isolated human membrane-bridging assay was established. Main figure pixels, supplementary bodies and simulations were not independently inspected or rerun.
Both structural papers received genuine normal publication fetches into separate additive files. They were not substituted for, or written into, existing normal caches.
PANTHER family PTHR31139; official PAINT downloads; human UniProt Q9HCE0.
The actual family tree and MSA were inspected. Human leaf PTN002525333 has the exact displayed 2579-residue Q9HCE0 sequence. It descends from PTN001579556 (the recovered cytoplasmic IBD) and PTN001259269 (the recovered lysosomal IBD). Target self-evidence is valid descendant support. The wider family includes distinct branches; a family label is not assumed to imply uniform EPG5-specific function.
The inspected current IBD export contains the two location assertions and no negated record on this target path. A separate NOT export was not recovered. Current QuickGO retains the autophagosome-lysosome-fusion IBA, and the actual tree confirms human/fish descendants, but the corresponding fusion IBD is absent from the inspected current export. The fish record returns IBA rather than its underlying experimental ZFIN record. That traceability gap is documented separately from biological acceptance based on direct human original evidence.
Current QuickGO definitions and is_a/part_of ancestry were checked for SNARE binding, lysosomal membrane, autophagosome-lysosome fusion and endosome to lysosome transport. The two processes are not ancestor/descendant duplicates. Vesicle membrane tethering activity is a valid current molecular function; uncertainty concerns the precise human evidence, not the identifier. No distinct molecular function is imposed on the endocytic-delivery core.
The GO:7770062 assertion discussed above is an inherited curator-authored proposal, now retired: true with its UNDECIDED assessment retained. It is not an active NEW assertion and was never an imported GOA row. Retirement withdraws our proposal while preserving its exact source fields and quotations; it does not assert an upstream GOA withdrawal or biological absence of tethering. There are now 15 active records and one retired historical proposal. The two inherited human binding proposals and the added LC3/GABARAP-binding proposal remain active, and the unresolved human membrane-bridging question remains explicit.
The direct full-length human binding experiments in PMID:33674710 Figure 2 and PMID:39809444 Figure 3C support GO:0032182 ubiquitin-like protein binding, now recorded as a NEW molecular annotation. The term covers LC3/GABARAP-family partners; it does not assert conjugating-enzyme activity. Searches of the retrieved current ontology for LC3 and GABARAP binding did not return a more specific term.
GO:0030674 and GO:0043495 were checked explicitly. Human assembled-SNARE binding and EPG5-dependent complex association support a coordinated fusion model, but do not distinguish direct two-partner linkage from recognition, stabilization or localization. The functional interpretation remains in the core narrative and experimental question; the specific SNARE-binding molecular term is retained. The 2021 and 2025 membrane geometry figures are mechanistic models, and their modeled unresolved segments are not direct measurements of membrane bridging.
Current GO:1990786 definition and ancestry were retrieved on 2026-10-24. Its direct parents are GO:1990784 response to dsDNA and GO:1901699 cellular response to nitrogen compound. This broad response term includes changes in gene expression and does not specify a DNA receptor or immune-signaling pathway. The parent term is examined for scope, not proposed for annotation.
In the actual PMID:29130391 original, Results “EPG5 role in the transport of DNA and RNA vectors,” Methods “Baculovirus infection” and Figure 6B use dsDNA BacMam RAB5A/RAB7-GFP vectors in human healthy-donor and PT1 fibroblasts. Figure 6 reports positive-cell percentages, combining multiple trafficking and expression steps; the RNA-vector comparator is also impaired. Methods “Toll-like receptor stimulation” instead uses single-stranded ODN for the separate cytokine/NFKB experiments. Neither those signaling results nor the composite vector assay settles whether the dsDNA observation is a host response to a stimulus or delivery and expression of a template. The broad term and positive trafficking evidence also do not establish categorical over-annotation. This accessible-evidence ambiguity is recorded as UNDECIDED, with the exact scope question retained for a curator. No additional supplemental body was inspected in this follow-up.
