The functional decision table preserves each complete imported source object beside its review. Positive plasma-membrane, clathrin-coated-pit, coat-assembly and endocytosis decisions rely on convergent human FCHO1 evidence. They do not require FCHO1 to be indispensable for every cargo or cell type. T-cell signaling and activation are retained as contextual, non-core roles.
PMID:20448150(https://pubmed.ncbi.nlm.nih.gov/20448150/) has a genuine author-hosted original and supplement. The supplement identifies human FCHO1 and mouse FCHo2 constructs. FCHO1 appears explicitly in Figure S1D localization, S2B coat dynamics, S3 knockdown comparisons and S5 expression comparisons; many main-paper experiments instead test FCHo2. The selected supplement Methods and captions were read, and actual PDF pages 15 and 20 (Figures S1 and S6) were viewed. This was a bounded read, not a claim that all supplemental movies or every panel were inspected.
The original reports FCHo1/2 depletion from coated-vesicle fractions. Figure S6E shows a combined FCHo1/2 signal, while the antibody Methods identify anti-FCHo2 Ra103. The FCHO1-specific scope of this negative result is unresolved here. Its imported NOT flag is preserved and its review is UNDECIDED; positive pit localization is not evidence of universal absence from detached vesicles. This is not a finding of curator misattribution.
PubMed explicitly links the 2025 Expression of Concern and subsequent Erratum to this report. Genuine notice metadata were recovered, but the bodies were inaccessible. The affected panels, correction scope and resolution are unknown; neither retraction nor resolution is inferred. The report is therefore marked DISPUTED. The notice caches’ automatic PRIMARY_RESEARCH classification does not make them experimental evidence. Independent 2012 and 2020 target evidence supports the positive annotations while these source-specific limits remain visible.
PMID:22484487(https://pmc.ncbi.nlm.nih.gov/articles/PMC3354769/) provides human FCHO1 surface-coat localization and maps AP-2 binding to its central linker. The Results sections “The linker region” and “The μHD,” Figure 1 and construct Methods distinguish human FCHO1 from mouse/rat AP-2 appendage reagents. The α-appendage platform dependence supports AP-2-complex binding. It does not turn the same experiment into a direct clathrin-binding or AP-2-activation assay. The Discussion and Figure 8 account of coat persistence after FCHO1/2 depletion limit universal obligatory-nucleator language. Zebrafish developmental findings are not presented as direct human developmental experiments.
PMID:32098969(https://pmc.ncbi.nlm.nih.gov/articles/PMC7042371/) supplies human wild-type/variant localization and coat-dynamics evidence (Figures 2 and 3), receptor-internalization and signaling results (Figure 4), and patient T-cell response observations (Figure 6). These support coat organization and a positive T-cell context. Direct FCHO1–CD3 binding was not established, and the detailed relationship between trafficking and signal strength remains unresolved. Preserved transferrin uptake in patient fibroblasts is an explicit counterpoint to universal dependence. The 2020 Author Correction corrects the Discussion’s account of prior work: Calzoni and colleagues had functional evidence, and their attributed defect concerned transferrin-receptor endocytosis in activated T-cell blasts, not all endocytosis. The correction contrasts that context with the study’s own preserved transferrin uptake and subtler effects. It states no experimental figure or data correction. The unmodified cache retains the old wording; that wording is not adopted here.
The 2012/2020 assessments also incorporate the database lane’s independently bounded main-text readings once. Neither lane claims a complete review of their supplemental images or movies. Paper clone names, “isoform b” wording and disease variants are not mapped to a unique natural splice-product function. All three imported alternative-product objects remain unchanged.
The resolved molecular anchor is AP-2 adaptor-complex binding, within a membrane-associated coat-organizing role involving endocytic partners. Coat assembly and clathrin-dependent endocytosis are supported contributions. The contextual T-cell findings add physiological scope without implying a new receptor-proximal catalytic activity. The feedback revision adds one IC annotation for the already-synthesized protein-membrane adaptor activity (GO:0043495), with both primary references. No process, product or supporting quotation is added.
Calzoni et al., PMID:30822429 is the prior study addressed by the 2020 correction. The complete main letter was read. Functional pre-transplant samples were available for patient P2: the main-text account of Figure E4A–B and Figure 1E reports reduced activation-induced proliferation, increased hypodiploid cells and fewer cycling cells despite preserved measured activation-marker induction. The Figure 1F/Figure E4C account reports impaired transferrin uptake in activated T-cell blasts but preserved TCR/CD3 internalization. This strengthens the human T-cell context while retaining the difference from the 2020 Jurkat Figure 4 receptor-trafficking/calcium result. Supplemental pixels and separate supplemental Methods were not reread. The new reference does not establish the molecular bridge by itself.
That bridge is supported by human FCHO1 in the 2012 Results, especially Figures 1–2 and Supplementary Figure S1k, together with 2020 Figures 2–3. Membrane binding and distinct AP-2/EPS15/ITSN interaction regions have measured localization and coat-recruitment consequences. The AP-2 alpha W840A reagent is not a FCHO1 allele. GO:0043495 has no typed ancestor/descendant relation to GO:0035612, GO:0097110, GO:1990782 or GO:0005515 in the checked official ontology response; activity as an adaptor is distinct from binding one partner. The added IC annotation is recorded separately in the feedback decisions.
UniProt O14526’s subunit section combines by-similarity support from mouse Q8K285 and the 2012 publication. Its clathrin association statement is considered, rather than erased by the negative direct-binding result for the isolated human linker; direct human clathrin binding is not required for the adaptor synthesis. The 2012 muHD Results actually assay intersectin association. The UniProt statement that FCHO1 is absent from mature coated vesicles is affirmative curated support with overlapping 2010 provenance, not a new FCHO1-specific experiment resolving the combined-blot/antibody limitation. The NOT annotation therefore remains UNDECIDED.