The normal intake produced 75 annotations from 79 GOA rows after normal deduplication, two UniProt products and 50 reference entries. All original annotation fields, evidence, qualifiers, partners and product descriptions are retained. This review adds one experimentally supported molecular-function assertion, GO:0005200 structural constituent of cytoskeleton, and no biological-process assertion. The two recorded products are Q9BV73-1 and Q9BV73-2; the experiments are not mechanically assigned to both products or used to invent a functional isoform distinction.
The genuine Falcon research attempt timed out at its bounded limit; the genuine perplexity-lite fallback returned an insufficient-quota error. No provider report was produced. The conclusions below come from manual source reading, authentic selected caches, original articles retrieved separately, current source records and independent bounded peers. Downloaded publication, UniProt, GOA, Reactome and family files were not edited.
The applicable published ClinGen instruction explicitly authorizes supported generic binding as KEEP_AS_NON_CORE when no better supported activity is established. It permits evidence-based refinement and requires UNDECIDED for unresolved evidence. This is the user's project instruction, not a claimed repository-wide exception inferred from the action enum. NEK2 and SIK2 binding are refined to protein kinase binding; other positive associations retain their actual resolution.
Selected full Results, Discussion and Methods in PMID:36282799(https://doi.org/10.1371/journal.pbio.3001854) establish C-Nap1's own physical contribution. Functional endogenous human U2OS tagging and expansion microscopy reveal proximal centriole contacts, including bridges in a subset of interphase cells. Endogenous rootlet termini align with these assemblies. Truncations affect cohesion, and ectopic C-Nap1 partially restores cohesion after rootletin depletion. These are structural actions by C-Nap1, not merely the consequences of being a kinase substrate. The separate organelle-retargeting experiments demonstrate cohesive capacity; they do not establish native lysosomal, mitochondrial or Golgi localization. True phase separation and purified full-length rheology remain open.
The older human antibody-interference and dominant-negative experiments in PMID:11076968(https://doi.org/10.1083/jcb.151.4.837) independently support cohesion. They distinguish parental-centriolar proximity from the parent–procentriole connection, and do not establish an absolute requirement for every cell division. The original PMID:9647649(https://doi.org/10.1083/jcb.141.7.1563) assays human C-Nap1 localization and C-terminal-fragment association/phosphorylation with NEK2; the timing and consequence for cohesion were a working model. PMID:12140259(https://doi.org/10.1242/jcs.115.16.3275), read in its genuine Caltech-hosted full PDF, supplies cell-cycle-dependent phosphorylation/dissociation experiments and degradation controls. None assigns kinase catalysis to C-Nap1.
Live official GO definition and both ancestry directions were checked. GO:0005200 captures the demonstrated structural-integrity contribution and is not a protein-binding descendant. Its ancestors and descendants do not overlap any of the 75 seeded terms or proposed replacements. This justifies one precise NEW MF, rather than overwriting genuine partner-specific source assertions. The core uses existing cohesion and centrosomal protein-localization processes. The full current-main GO-CAM index has no exact Q9BV73 entry; that absence is recorded, not used as evidence for adding a process. The durable source extract includes the ontology checks and authentic response hashes.
Selected original full text was read externally where the normal cache was abstract-only. This includes the CEP135, centlein and CCDC102B papers, with assay limits recorded in their reference assessments. In particular, CEP135-to-C-Nap1 recruitment is not reversed, extract-based pull-down is not described as wholly purified binary binding, and a possible indirect CCDC102B/rootletin relationship is retained. The full author PDF for PMID:27623382(https://doi.org/10.1016/j.devcel.2016.07.013) supplies the human Girdin localization-dependency experiment separately from its nematode work.
PMID:27565344(https://doi.org/10.1016/j.cell.2016.07.025), in the normal full cache and a genuine author-hosted original PDF, includes endogenous Ninein–CEP250 co-IP in HeLa cells in Figure 3H. Its recombinant NPC-versus-neuronal constructs show differential association. The exact mapping of every construct to Q8N4C6-7 remains unresolved because Table S6 was not recovered. The positive human association is retained without declaring every isoform equivalent or inferring transgene species from the host cell. The conductin row retains its mouse O88566 partner rather than silently substituting human AXIN2.
The durable source extract contains eleven literal positive IntAct records for SIK2, OPTN and the SARS-CoV-2 mature chain, including exact participants, publication, taxa, assay, features, negative-interaction field, source query, resolvable accession URLs and raw-line hashes. These are target-record checks, not independent replication or a claim that every primary figure was read. Empty matches for other source queries are not treated as negative experiments.
Several papers centered on another centrosomal protein genuinely use C-Nap1 as a proximal marker. Their source-specific localization remains valid. The precise CEP250 supplementary record in PMID:21399614 and the IMP experiments attributed to PMID:23213374 were not resolved in the inspected material; no wrong-gene inference is made. Independent human studies directly support the biological localization/cohesion conclusions. The original source identities stay intact, and the citation-level uncertainty is explicit.
All 22 Reactome cytosol assertions retain their individual event references. The official human physical entity R-HSA-380263 maps Q9BV73 to cytosol; its literal identifier and compartment fields are included in the source extract. This supports a coarse curated location, without assigning every associated reaction's chemistry to CEP250. Initial placeholder Reactome reference titles were filled only from the exact genuine selected event-cache metadata.
The authentic authors' urinary-exosome database explicitly lists CEP250, NP_009117 and one peptide, with reference 2 pointing to PMID:19056867(https://doi.org/10.1681/ASN.2008040406). This resolves target-level detection. The existing exosome location is non-core; one-peptide identification does not establish secretion, vesicle topology or extracellular activity. Its literal row and RefSeq join are preserved in the source extract.
Three full primary papers were independently read for the cilium decisions. PMID:28005958(https://doi.org/10.1371/journal.pone.0168966) compares human full-length WT and A609V CEP250 in ARPE-19 cells, retaining endogenous CEP250, and measures cilium length. The separate native retinal localization is mouse. This supports a bounded non-core existing ciliary assertion, not a loss/rescue demonstration of initiation or a measured assembly rate.
PMID:23789104(https://doi.org/10.1242/bio.20134457) really does test C-Nap1 in human RPE1 cells despite its Cep123-focused title. Formation and maintenance protocols report positive effects with depletion and cell-stress controls. PMID:28100636(https://doi.org/10.1091/mbc.E16-05-0325) finds normal ciliation in validated null cells and shows an off-target ciliation effect for its reused Conroy 2012 reagent. The unrecovered 2013 Table S2 prevents equating those reagents. The exact non-motile-assembly assertion remains UNDECIDED; the earlier experiment is not erased or declared disproved. The PAINT cilium-assembly assertion is likewise unresolved in physiological scope. Target self-inclusion is legitimate, and knockout nonessentiality alone does not refute an ancestral participation judgment.
Current mouse Q60952 source records identify retinal inner-segment and light-detection provenance in PMID:30998843 and spindle-pole provenance in PMID:19117032. Genuine normal abstracts were obtained, but the exact full assays remain unavailable. These precise transfers remain UNDECIDED. Positive retinal phenotype does not establish the light-to-signal reaction; conversely, abstract-only access does not justify an experimental removal. Human basal-body/proximal-centriolar evidence independently supports the broader location.
Externally read full selected text is not mislabeled unavailable merely because a repository cache contains only an abstract. Each PMID assessment records what was actually inspected. Access to a selected Results/Methods section is not described as a complete supplementary-data audit. Failed HTTP, CAPTCHA and provider responses remain failed receipts in the preparation packet, not publication caches.
The final source capture uses actual published main 6ae4685964aa1aae16bfec2647cab2ccfed750f6, following an initial capture at 2b6a4561b112799f115b70c8fdbf46494a1fb143. Existing source bytes are identical across those captures. All existing source-cache bytes were reused exactly; the original machine assertions and both products are unchanged. The author-supplied evidence JSON is explicitly a deterministic extraction/manual interpretation artifact. It is not a generated provider report. Short verbatim anchors identify the structural NEW/core assertion, unique kinase-binding evidence, independent centrosomal recruitment, and both sides of the ciliary evidence conflict. The repeated structural excerpt totals fourteen words from PMID:36282799; every source remains within twenty-five words across the authored YAML and notes. The separate quote audit counts repeated anchors explicitly. No scientific conclusion is based on a fabricated source, guessed PANTHER node, or assumed activity inherited from an interaction partner.
This dated entry supersedes the earlier interpretation where specified and preserves the original notes above. The authentic GOA file contains 77 data rows, normally deduplicated to 75 source assertions; the opening entry's count of 79 was incorrect. Both machine products, all source objects, and all downloaded caches remain unchanged.
The cilium-assembly IMP from PMID:28005958 is now UNDECIDED. Selected full Methods and Figure 4 establish a human WT-versus-A609V overexpression comparison in ARPE-19 cells, with IT6 tagging and endogenous protein retained PMID:28005958. Increased endpoint length is a valid phenotype, but it does not resolve assembly versus disassembly or a change in their rates. No directional regulatory replacement is inferred. The null-cell findings in PMID:28100636 constrain essentiality without proving absence of every assembly contribution. This corrects the earlier non-core acceptance of that precise process assertion; the other two unresolved ciliary assertions remain unchanged.
Both light-detection transfers remain UNDECIDED after explicit reconsideration of the reviewer's proposed electronic-overannotation action. The official GO:0050908 definition concerns receiving light and converting it into a molecular signal; its typed ancestry includes light detection and a part_of link to visual perception. The exact current mouse Q60952 donor is an IMP from PMID:30998843(https://pubmed.ncbi.nlm.nih.gov/30998843/), rather than a protein-class-to-process mapping. The verified abstract reports ERG loss together with retinal thinning. Such coupled endpoints leave open whether reduced responses reflect degeneration, a separate proximal detection contribution, or both. A structural contribution to a detection step is possible; being a centrosomal structural protein is not a disqualification. Renewed bounded publisher access did not recover the full experiments. Thus neither a concrete propagation defect nor absence of a relevant experiment has been established. This uncertainty concerns the specific biological role as well as source access, not whether the retinal phenotype exists. Exact donor fields, term paths and response hashes are in the source evidence.
The two outer-segment transfers remain non-core with an explicit antibody-specificity boundary: the P60 mouse retinal experiment in PMID:28005958 uses commercial AB_2076918, and its inspected Methods/Figure 4 legend do not report a knockout or peptide-block control for that panel. The human transfection experiment is separate. All 22 Reactome cytosol reasons now identify R-HSA-380263 as the compartment pedigree within the same source; this is not independent replication of the location.
The hierarchy extract now distinguishes pure is_a ancestry of GO:0005200 (molecular-function root, structural molecule activity, and itself) from the broader is_a/part_of related closure. The original BP entries are genuine consequences of the explicit GO:0005200 part_of GO:0007010 edge, not MF is_a ancestors or fabricated API output. Fresh official queries confirm that neither scoped closure overlaps the 75 source terms or their proposed replacements. The existing structural NEW and core are unchanged.
Finally, the fetched PTHR23159 metadata's InterPro-derived LLM name is not an asserted official PANTHER family label. The official PANTHER name is CENTROSOMAL PROTEIN 2. The machine metadata is preserved; no family ID or label is authored into the review. No biological-process NEW, cache replacement, or global policy change is made by this follow-up.