FCHO1 is reviewed as a membrane-associated organizer of endocytic proteins, with one protein–membrane adaptor core supported by the human 2012 and 2020 studies. The existing clathrin-coat assembly and clathrin-dependent endocytosis terms describe its structural participation. This does not assume direct clathrin or CD3 binding, AP-2 core-subunit membership, universal dependence of endocytosis on FCHO1, or an inferred natural-isoform-specific mechanism.
The integrated review preserves all 37 imported rows (24 ACCEPT, eight KEEP_AS_NON_CORE, three MODIFY, one TOO_GENERAL and one UNDECIDED) and appends one IC NEW molecular-function row, for 38 rows total. The four remaining generic binding rows follow the user’s ClinGen curation instructions; DRAFT status records their advisories. No PENDING row remains. The same instructions prohibit new supporting quotations. All three natural splice-product objects are inherited exactly. Engineered fragments and disease variants are discussed at their measured scope without adding natural products or assigning product-specific functions.
The 2010 original and selected supplement evidence were recovered. Its Expression of Concern and Erratum are verified records, but their bodies, affected panels and resolution remain unavailable. No retraction or resolved-concern claim follows from that metadata. Source index 24 retains its NOT flag and UNDECIDED action: the combined FCHo1/2 coated-vesicle signal and the stated FCHO2 antibody leave FCHO1-specific negative-compartment scope unresolved. Positive pit localization alone does not prove absence from mature coated vesicles.
The 2020 Author Correction was read from the actual publisher body. It corrects the Discussion’s representation of earlier functional work and limits the prior transferrin-receptor observation to activated T-cell blasts; it does not state a figure or experimental-data correction. The original cache is preserved, while its superseded Discussion wording is not adopted. The 2012 original and 2020 original support the core with the source-specific limits recorded in the functional guide. No full sequential reading of every supplement, movie or figure is claimed.
The genuine automated research attempts failed (Falcon authentication HTTP 403; perplexity-lite fallback HTTP 401/insufficient_quota), with no provider report produced. The manual source records and journals document the evidence actually used. Raw diagnostic traces are excluded from delivery. All 30 selected normal files and the UniProt/GOA machine snapshots retain genuine bytes and modes; none was rewritten as part of interpretation.
The feedback revision adds an evidence-backed protein-membrane adaptor annotation, not a row added solely to remove a core-coverage warning. Human 2012 and 2020 experiments support its molecular role; the 2019 patient study supports a separate physiological context. The feedback decisions preserve exact changed-row/source joins and source locators. All imported actions and three natural splice products remain unchanged.
The Calzoni 2019 main letter was read directly: its P2 activated-blast transferrin defect coexists with preserved TCR/CD3 uptake. That result is distinguished from 2020 Jurkat TCR internalization/calcium responses. The correction is applied to the later article’s interpretation while both immutable caches remain intact. Reference-only citations follow the user’s no-new-quotation instruction; authored full-text-read flags describe separately recovered original evidence and need not equal the immutable cache’s acquisition flag.