Cytoplasmic dynein 2 intermediate chain 1 (WDR60; FAP163 homolog), human.
Falcon deep research succeeded (DYNC2I1-deep-research-falcon.md; the first attempt with the 600 s default timed out, and the rerun with --timeout 2400 succeeded). Its summary agrees with the publication-based review below. The review's supporting quotes come from the cached publications.
The 56 historical source assertions and their machine metadata are preserved exactly. Current ordinary fetching reconciled all 56 contexts one-to-one, with no added or retired assertion. The accepted review has 33 ACCEPT, 10 MODIFY, 12 KEEP_AS_NON_CORE and one REMOVE; no NEW annotation is proposed. This entry supersedes the earlier generic-removal recommendation for NUDC and the earlier tear-proteomics over-annotation judgment without rewriting the historical notes above.
The two NUDC associations are refined to protein-folding chaperone binding. Literal human interaction records identify the participants, and independently purified human NUDC suppresses reporter aggregation in PMID:21530541. This describes the partner class, not folding by DYNC2I1 or a demonstrated NUDC-dependent folding pathway for DYNC2I1. TCTEX1D2 and DYNC2I2 pairs are separately refined to light-chain and intermediate-chain binding. The project-specific CLINGEN policy retains supported generic binding as non-core when no justified specific term is available; it does not require removal merely for genericity.
The nuclear NAS decision rests on the actual dynein-1 reagents and nuclear figure caption in PMID:36973253, together with a target-name survey of the original and six supplements. It does not infer impossibility from nuclear topology. The same paper reports mouse Wdr34 among selected Y2H hits; that is positive dynein-2-related evidence, but it does not establish WDR60 nuclear localization. Absence from the selected hit list is not an exhaustive negative binding experiment. By contrast, the original tear-proteomics Table II positively identifies WDR60, so extracellular detection is retained as non-core without inferring secretion, contamination or extracellular function.
The seven PAINT assertions have literal IBD joins on the reconstructed PTHR16022 target lineage, with exact official-sequence agreement. The target appearing among its own experimental descendants is expected. Broad cytoskeleton/cytoplasmic-dynein-complex assertions are refined to the supported cytoplasmic dynein complex. Broad intraflagellar transport is refined to intraciliary retrograde transport. The tip assertions are core-relevant states of the principal transport cycle, with their Reactome-model provenance preserved; no new human residence-time or velocity measurement is asserted. Ciliary base and tip, and cilium assembly and retrograde transport, are each nonredundant pairs under current typed ancestry.
The single integrated core distinguishes the intermediate chain's light-chain binding from its contribution to complex-level motor activity. DYNC2I1 does not supply ATP-driven force. The accepted structural evidence uses recombinant human subunits in insect cells and docking to an algal IFT train; those contexts are not conflated. The human RPE1 knockout study explicitly lacked reliable quantitative IFT measurements, used crosslinking for anti-HA coimmunoprecipitation, and showed distinct WDR60 and WDR34 phenotypes. No autonomous axonemal polymerization or universal loss of cilia is inferred. One official displayed Q8WVS4 product has 1,066 residues. Engineered fragments, disease alleles and knockouts are not natural alternative products.
The earlier successful Falcon report and all of its artifacts remain unchanged. The current configured Falcon attempt failed with HTTP 403; the genuine fallback attempt failed with HTTP 401 and an insufficient-quota response. No replacement provider report was fabricated. Existing publication bytes and availability flags remain unchanged, including short full-text representations; newly obtained fuller copies were used as separately accessed research evidence and were not silently substituted. Only the genuinely fetched, independently used PMID:21530541 cache is proposed as a new publication file. Three additional normal-fetched metadata sources were not needed for the decisions and remain private.
The source guide gives primary locators, actual read scopes and access limits. The portable evidence audit reproduces the database joins from saved raw inputs. The original notes remain an exact prefix. All 27 inherited row excerpts and eight inherited note excerpts are retained. Four old core excerpts are removed as part of the authorized consolidation of the overlapping cores; no new source quotation is introduced, and no claim is made that the historical excerpt totals fall below a new-quotation budget.
The same dynein-2 mechanism is represented by three complementary binding activities: light-chain, heavy-chain and intermediate-chain binding. Motor contribution, ciliary locations and transport/assembly processes remain on the integrated first entry. The other two entries expose the established interfaces without duplicating those processes or asserting autonomous motor activity.
The tear HDA detection remains non-core after checking the publisher's actual Table II and collection/identification methods. The source guide now links directly to that table. No secretion mechanism or contaminant origin is asserted. The ciliary-tip location remains explicitly the curated transport-cycle state; constitutive residence is not implied. The retrograde refinement now links its specific human WDR60 experimental anchor, while preserving the inherited broader IFT excerpt. The male-germ-cell NAS removal explains the contextual role of its existing quotation. A reference-only support link also resolves the cilium review-source advisory.
All 56 imported source assertions, actions, official-product fields and 27 inherited annotation excerpts are unchanged. There are 33 ACCEPT, 10 MODIFY, 12 KEEP_AS_NON_CORE and one REMOVE, with no NEW annotations or new quotations. Prior core excerpt removals remain unchanged.