CEP57

Summary: Human translokin was recovered in an NS5A two-hybrid screen.

Reason: The authentic PMID:15607035 abstract explicitly identifies translokin among human liver-library positives against hepatitis C virus NS5A derivatives. The preserved P27958-PRO_0000037576 identifier is the annotated NS5A chain in the current UniProt viral polyprotein. The exact clone, viral strain and responsible NS5A truncation were not recovered from the full target table, and the abstract does not list translokin among the subsequent purified-protein confirmations. Retain the curated low-resolution association at the screen scope under the campaign binding instruction; do not infer an antiviral role or a demonstrated native human complex.

Summary: A mapped interaction with MYC supports transcription-factor binding.

Reason: Source-linked IntAct records for PMID:20195357 join exact human Q86XR8 and P01106. They retain sufficient-binding-region features for CEP57 residues 76–116 and MYC residues 370–454 in this interaction-region screen. MYC is a DNA-binding transcription factor, so GO:0140297 conveys the partner class. Fragment interaction is not evidence that full-length CEP57 regulates MYC transcription or has DNA-binding activity itself. Exact record identifiers, methods and features are retained in the source-evidence extract.

Proposed replacements: DNA-binding transcription factor binding

Summary: The original HI-NGS table contains the CEP57–RALBP1/Q15311 pair.

Reason: PMID:21516116 Supplementary Table 2 lists the exact Entrez pair 9702–10928 on PDF page 17; the two columns were visually checked, and current UniProt GeneID mappings join the preserved accessions. This is source-specific human two-hybrid interaction evidence. Retain it as non-core under the supported-binding instruction, without transferring the partner activity to CEP57 or claiming a physiological trafficking complex. The IntAct query lacked this publication pair, which was an access gap rather than negative evidence.

Summary: The original HI-NGS table contains the CEP57–GCC1/Q96CN9 pair.

Reason: PMID:21516116 Supplementary Table 2 lists the exact Entrez pair 9702–79571 on PDF page 16; the two columns were visually checked, and current UniProt GeneID mappings join the preserved accessions. This is source-specific human two-hybrid interaction evidence. Retain it as non-core under the supported-binding instruction, without transferring the partner activity to CEP57 or claiming a physiological trafficking complex. The IntAct query lacked this publication pair, which was an access gap rather than negative evidence.

Summary: A source-linked human screen supports association with KRT13/A1A4E9.

Reason: Exact IntAct source records join Q86XR8 to the preserved partner accession and PMID:25416956, with positive human two-hybrid records and their assay stages. The durable extract preserves taxon, method, participant features and interaction identifiers. Retain this supported association as non-core under the campaign instruction; it does not establish a native complex, a regulatory effect, or the partner's own molecular activity in CEP57. Repeated pooling, array and validation records are stages of the screen, not independent biological replications; blank feature fields do not establish a nucleotide or mutation state.

Summary: A source-linked human screen supports association with KRT15/P19012.

Reason: Exact IntAct source records join Q86XR8 to the preserved partner accession and PMID:25416956, with positive human two-hybrid records and their assay stages. The durable extract preserves taxon, method, participant features and interaction identifiers. Retain this supported association as non-core under the campaign instruction; it does not establish a native complex, a regulatory effect, or the partner's own molecular activity in CEP57. Repeated pooling, array and validation records are stages of the screen, not independent biological replications; blank feature fields do not establish a nucleotide or mutation state.

Summary: A source-linked human screen supports association with RALBP1/Q15311.

Reason: Exact IntAct source records join Q86XR8 to the preserved partner accession and PMID:25416956, with positive human two-hybrid records and their assay stages. The durable extract preserves taxon, method, participant features and interaction identifiers. Retain this supported association as non-core under the campaign instruction; it does not establish a native complex, a regulatory effect, or the partner's own molecular activity in CEP57. Repeated pooling, array and validation records are stages of the screen, not independent biological replications; blank feature fields do not establish a nucleotide or mutation state.

Summary: A source-linked human screen supports association with KRT31/Q15323.

Reason: Exact IntAct source records join Q86XR8 to the preserved partner accession and PMID:25416956, with positive human two-hybrid records and their assay stages. The durable extract preserves taxon, method, participant features and interaction identifiers. Retain this supported association as non-core under the campaign instruction; it does not establish a native complex, a regulatory effect, or the partner's own molecular activity in CEP57. Repeated pooling, array and validation records are stages of the screen, not independent biological replications; blank feature fields do not establish a nucleotide or mutation state.

Summary: A source-linked human screen supports association with KRT40/Q6A162.

Reason: Exact IntAct source records join Q86XR8 to the preserved partner accession and PMID:25416956, with positive human two-hybrid records and their assay stages. The durable extract preserves taxon, method, participant features and interaction identifiers. Retain this supported association as non-core under the campaign instruction; it does not establish a native complex, a regulatory effect, or the partner's own molecular activity in CEP57. Repeated pooling, array and validation records are stages of the screen, not independent biological replications; blank feature fields do not establish a nucleotide or mutation state.

Summary: A source-linked human screen supports association with GCC1/Q96CN9.

Reason: Exact IntAct source records join Q86XR8 to the preserved partner accession and PMID:25416956, with positive human two-hybrid records and their assay stages. The durable extract preserves taxon, method, participant features and interaction identifiers. Retain this supported association as non-core under the campaign instruction; it does not establish a native complex, a regulatory effect, or the partner's own molecular activity in CEP57. Repeated pooling, array and validation records are stages of the screen, not independent biological replications; blank feature fields do not establish a nucleotide or mutation state.

Summary: A source-linked human screen supports association with MAGEA2B/Q96E03.

Reason: Exact IntAct source records join Q86XR8 to the preserved partner accession and PMID:25416956, with positive human two-hybrid records and their assay stages. The durable extract preserves taxon, method, participant features and interaction identifiers. Retain this supported association as non-core under the campaign instruction; it does not establish a native complex, a regulatory effect, or the partner's own molecular activity in CEP57. Repeated pooling, array and validation records are stages of the screen, not independent biological replications; blank feature fields do not establish a nucleotide or mutation state.

Summary: A source-linked human screen supports association with CEP63/Q96MT8.

Reason: Exact IntAct source records join Q86XR8 to the preserved partner accession and PMID:25416956, with positive human two-hybrid records and their assay stages. The durable extract preserves taxon, method, participant features and interaction identifiers. Retain this supported association as non-core under the campaign instruction; it does not establish a native complex, a regulatory effect, or the partner's own molecular activity in CEP57. Repeated pooling, array and validation records are stages of the screen, not independent biological replications; blank feature fields do not establish a nucleotide or mutation state.

Summary: A source-linked human screen supports association with MIA2/Q96PC5.

Reason: Exact IntAct source records join Q86XR8 to the preserved partner accession and PMID:25416956, with positive human two-hybrid records and their assay stages. The durable extract preserves taxon, method, participant features and interaction identifiers. Retain this supported association as non-core under the campaign instruction; it does not establish a native complex, a regulatory effect, or the partner's own molecular activity in CEP57. Repeated pooling, array and validation records are stages of the screen, not independent biological replications; blank feature fields do not establish a nucleotide or mutation state.

Summary: A source-linked human screen supports association with TFIP11/Q9UBB9.

Reason: Exact IntAct source records join Q86XR8 to the preserved partner accession and PMID:25416956, with positive human two-hybrid records and their assay stages. The durable extract preserves taxon, method, participant features and interaction identifiers. Retain this supported association as non-core under the campaign instruction; it does not establish a native complex, a regulatory effect, or the partner's own molecular activity in CEP57. Repeated pooling, array and validation records are stages of the screen, not independent biological replications; blank feature fields do not establish a nucleotide or mutation state.

Summary: The GCC1 pair is supported in a variant-interaction assay.

Reason: PMID:31515488 source-linked records contain human CEP57–GCC1 association and a mutation-with-no-effect feature at GCC1 position 274 (rs34887879). That feature is on Q96CN9, not on CEP57. Retain the tested association with this scope; do not infer a CEP57 disease mutation or a Golgi function merely from the partner. Exact record fields are preserved in the evidence extract.

Summary: The TFIP11 pair is supported in a variant-interaction assay.

Reason: PMID:31515488 source-linked records contain human CEP57–TFIP11 association with mutation-with-no-effect features on TFIP11 positions 8 and 688 (rs34764403 and rs149764032). Preserve the original Q9UBB9 partner and these tested contexts. They are not CEP57 mutations and do not assign spliceosomal activity to CEP57.

Summary: The HRAS pair supports small-GTPase binding.

Reason: Exact human Q86XR8–P01112 two-hybrid records are linked to PMID:32814053. HRAS is a small GTPase, supporting the current GO:0031267 partner-class term. The record does not establish nucleotide-state preference, GEF/GAP activity, or a RAS signaling function for CEP57. The requested historical Ras-binding identifier resolved to this current term in the official ontology response; the original source term is unchanged.

Proposed replacements: small GTPase binding

Summary: The FGFR3 pair supports receptor-tyrosine-kinase binding.

Reason: Exact human Q86XR8–P22607 two-hybrid records are linked to PMID:32814053. FGFR3 is a receptor tyrosine kinase, so GO:0030971 is more informative than generic binding. This screen does not demonstrate receptor activation, phosphorylation of CEP57, or mediation of downstream FGFR3 signaling. The FGF2 trafficking experiments are separate evidence and are not substituted for this source.

Proposed replacements: receptor tyrosine kinase binding

Summary: A source-linked human screen supports association with SPRED1/Q7Z699.

Reason: Exact IntAct source records join Q86XR8 to the preserved partner accession and PMID:32814053, with positive human two-hybrid records and their assay stages. The durable extract preserves taxon, method, participant features and interaction identifiers. Retain this supported association as non-core under the campaign instruction; it does not establish a native complex, a regulatory effect, or the partner's own molecular activity in CEP57. Repeated pooling, array and validation records are stages of the screen, not independent biological replications; blank feature fields do not establish a nucleotide or mutation state.

Summary: A source-linked human screen supports association with the preserved Q9Y649 protein record (GW128).

Reason: Exact IntAct source records join Q86XR8 to the preserved partner accession and PMID:32814053, with positive human two-hybrid records and their assay stages. The durable extract preserves taxon, method, participant features and interaction identifiers. Retain this supported association as non-core under the campaign instruction; it does not establish a native complex, a regulatory effect, or the partner's own molecular activity in CEP57. Repeated pooling, array and validation records are stages of the screen, not independent biological replications; blank feature fields do not establish a nucleotide or mutation state.

Summary: BioPlex supports CEP57–CEP63 complex association.

Reason: The exact source-linked PMID:33961781 record identifies tagged human CEP57 bait and CEP63 prey in an affinity-purification/co-immunoprecipitation context. Retain the association with its complex-level resolution; it does not alone establish a purified binary contact, stoichiometry or an enzyme activity. Independent mechanistic studies support the centrosomal relationship but do not change this original screen provenance.

Summary: The neural centrosome study supports association with CEP63.

Reason: The exact source-linked PMID:35709258 record contains the preserved human CEP63–CEP57 pair with anti-bait co-immunoprecipitation. This supports a native complex association at non-core annotation resolution, without making CEP57 the catalytic or disease-effector activity of other proteins in the study. The record is retained separately from BioPlex and the purified fragment experiments.

Summary: Nuclear localization is supported in the mouse ortholog expression experiment.

Reason: PMID:12954732 actual Methods and Results describe mouse Tsp57 constructs and a full-length GFP fusion in CV-1 cells that distributes to cytoplasm and nucleus. Preserve the human combined electronic assertion and Q8CEE0/Ensembl provenance at contextual, non-core scope. This is conserved localization evidence, not a direct endogenous human nuclear-function assay. The abstract and body differ in numbering the putative NLS deletion; no NLS-number claim or product-specific assignment is made.

Summary: Nuclear localization is supported in the mouse ortholog expression experiment.

Reason: PMID:12954732 actual Methods and Results describe mouse Tsp57 constructs and a full-length GFP fusion in CV-1 cells that distributes to cytoplasm and nucleus. Preserve the human ISS assertion and Q8CEE0/Ensembl provenance at contextual, non-core scope. This is conserved localization evidence, not a direct endogenous human nuclear-function assay. The abstract and body differ in numbering the putative NLS deletion; no NLS-number claim or product-specific assignment is made.

Summary: The broad cytoplasmic location is compatible with ortholog and target evidence.

Reason: The mouse/Ensembl and UniProt subcellular sources are preserved. Full-length mouse Tsp57 localizes to cytoplasm as well as nucleus in PMID:12954732; human CEP57 also has a cytosolic pool in the current HPA record. Keep the broad location as non-core while the centrosomal and microtubule locations carry the more informative functional context.

Summary: The exact original Golgi-localization assay remains inaccessible.

Reason: PMID:10942595 describes a 25-protein GFP localization survey in a human cell line. Its authentic abstract does not identify the CEP57 construct, target image, marker or Golgi assignment, and bounded publisher/full-text searches did not recover that source-specific result. Preserve the experimental IDA and use UNDECIDED; later centrosomal localization does not disprove a Golgi pool or establish a mistaken original annotation.

Summary: Inherited centrosomal activity agrees with CEP57 structural work.

Reason: PAINT PTN001064019 is an ancestral functional inference, not a pairwise similarity transfer. Target self-inclusion among descendant sources is legitimate. Human centrosomal imaging, direct PCNT anchoring and defects in PCM organization after CEP57 depletion independently corroborate active structural work at the centrosome. The complete PAINT ancestral-node history was not reconstructed; neither donor count nor the target being a donor is treated as a failure.

Summary: Current HPA immunofluorescence supports the centrosome assignment.

Reason: The exact current HPA CEP57 record (ENSG00000166037/Q86XR8) classifies centrosome as its main location with supported reliability. This agrees with independent human STED localization around proximal mother centrioles. Preserve the original immunofluorescence-curation source without claiming to have re-examined every HPA image.

Summary: The original centrosome annotation is independently corroborated in human cells.

Reason: Preserve the original PMID:14654843 IDA. The source study identity and accessible text were checked, but its exact CEP57 peptide/imaging output was not independently re-extracted. Human target-specific STED and perturbation experiments in PMID:30804344 establish CEP57 at the proximal mother-centriole/inner-PCM region. This supports the biological location while keeping the independent corroboration distinct from the original proteomic provenance.

Summary: The original centrosome annotation is independently corroborated in human cells.

Reason: Preserve the original PMID:21399614 IDA. The source study identity and accessible text were checked, but its exact CEP57 peptide/imaging output was not independently re-extracted. Human target-specific STED and perturbation experiments in PMID:30804344 establish CEP57 at the proximal mother-centriole/inner-PCM region. This supports the biological location while keeping the independent corroboration distinct from the original proteomic provenance.

Summary: Combined electronic centrosome support agrees with target experiments.

Reason: Preserve ARBA00029136, mouse Q8CEE0, Ensembl and SL-0048 source identifiers. Independent human CEP57 imaging and PCM interaction studies support this broad centrosome location. No isoform-specific distribution is inferred from the unqualified source row.

Summary: Current HPA records a cytosolic CEP57 pool.

Reason: The exact current HPA CEP57 record includes cytosol as an additional compartment, with centrosome as the main site. Retain this broad location without equating a cytosolic pool with every function of the centrosome or with nuclear localization.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-2574840; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-2574845; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-3000310; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-3000319; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-380272; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-380283; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-380294; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-380303; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-380311; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-380316; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-380455; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-380508; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-5617816; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-5626220; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-5626223; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-5626227; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-5626228; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-5626681; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-5626699; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-5638009; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-8853405; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: The Reactome event supports broad cytosolic compartment context.

Reason: The current official Q86XR8-to-reactions response includes R-HSA-8853419; the original TAS locates the represented CEP57 protein in cytosol. The event summary describes its named participants rather than a CEP57-specific catalytic step. Preserve the broad compartment assertion, also corroborated by HPA, as non-core. Do not infer that CEP57 performs the reaction named by the event, and do not interpret repeated event-derived locations as independent localization experiments.

Summary: Microtubule-associated CEP57 localization is consistent with its own binding activity.

Reason: PMID:12717444 reports tagged translokin localization overlapping the microtubule network; its Methods include mammalian constructs and the displayed localization is an expression assay. Later endogenous spindle imaging and purified human CEP57 C-terminal co-sedimentation provide independent support for this location and capability. Preserve the original IDA without assigning all five products the same distribution.

Summary: Spindle-microtubule activity agrees with direct mammalian structural evidence.

Reason: The PAINT PTN001456386 assertion is retained as ancestral inference; the current frog donor identity does not alone settle its node placement. Human endogenous spindle-associated CEP57, reduced spindle microtubule organization after depletion, and direct human MT-binding assays support activity at this site. The complete phylogenetic node history was not reconstructed. This is structural participation, not merely the location of a passive spindle substrate.

Summary: CEP57 contributes physical organization to the mitotic spindle.

Reason: Human depletion and rescue experiments connect CEP57 to spindle pole/central-spindle organization, while purified-protein and anchoring experiments establish its own structural capabilities. The source PAINT node PTN001456386 and PomBase SPAC4H3.11c provenance are preserved. The extant fission-yeast donor is not treated as a simple pairwise transfer, and the node history was not independently reconstructed. No kinase activity or generic requirement-only argument is used.

Summary: The cited mouse source demonstrates spermatid-enriched expression rather than a performed developmental step.

Reason: The exact mouse Q8CEE0 donor has GO:0007286 with IEP from PMID:12954732. Actual primary Methods/Results examine developmental and germ-cell expression, including vitamin-A-deficient and RARalpha-null mice, plus localization/binding assays; these are not Tsp57-specific developmental perturbations or a demonstrated structural step in spermatid maturation. Under the participation criterion, that source chain overstates a human spermatid-development role. Preserve the original IEA orthology assertion and donor; this does not claim that CEP57 cannot function during spermatogenesis or that expression data are false.

Summary: The cited mouse source demonstrates spermatid-enriched expression rather than a performed developmental step.

Reason: The exact mouse Q8CEE0 donor has GO:0007286 with IEP from PMID:12954732. Actual primary Methods/Results examine developmental and germ-cell expression, including vitamin-A-deficient and RARalpha-null mice, plus localization/binding assays; these are not Tsp57-specific developmental perturbations or a demonstrated structural step in spermatid maturation. Under the participation criterion, that source chain overstates a human spermatid-development role. Preserve the original ISS assertion and donor; this does not claim that CEP57 cannot function during spermatogenesis or that expression data are false.

Summary: Microtubule binding is an established CEP57 molecular capability.

Reason: Retain the PAINT PTN001456386 ancestral inference. The earlier PMID:18294141 purified biochemistry used mouse fragments and bovine-brain tubulin; independent PMID:26743940 uses human HeLa-derived CEP57 constructs and directly tests its C-terminal microtubule co-sedimentation. PMID:38857398 adds human CEP57 tubulin interaction/reconstitution, chiefly with engineered Cep57S, and separate full-length cellular rescue. These distinct construct scopes support the human activity without treating every assay as purified full-length canonical CEP57.

Summary: Microtubule binding is an established CEP57 molecular capability.

Reason: Retain the combined mouse/Ensembl/InterPro inference. The earlier PMID:18294141 purified biochemistry used mouse fragments and bovine-brain tubulin; independent PMID:26743940 uses human HeLa-derived CEP57 constructs and directly tests its C-terminal microtubule co-sedimentation. PMID:38857398 adds human CEP57 tubulin interaction/reconstitution, chiefly with engineered Cep57S, and separate full-length cellular rescue. These distinct construct scopes support the human activity without treating every assay as purified full-length canonical CEP57.

Summary: CEP57 anchors centrosomal partners to a microtubule-associated scaffold.

Reason: The inherited cytoskeletal-adaptor assertion is consistent with direct human CEP57–PCNT PACT-fragment binding, ectopic recruitment of the PCNT fragment to CEP57-decorated microtubules, and centrosomal PACT-loading/PCM organization assays in PMID:30804344. These assays identify actual anchoring work rather than just necessity. Preserve PAINT PTN001456386/PomBase donor provenance; no complete ancestral-node reconstruction or fixed native bridge stoichiometry is claimed.

Summary: The source supports intracellular FGF2 transport without resolving a strictly nuclear destination.

Reason: PMID:12717444 identifies FGF2-binding translokin and tests a binding-deficient FGF2 chimera. Both ligands enter the cytoplasm, whereas the chimera has reduced nuclear-associated accumulation and mitogenicity despite preserved receptor competition, ERK/p70S6K signaling and differentiation. Translokin RNAi and partial rescue by a ligand nuclear-localization signal support its own binding/transport role. GO:0006886 captures this intracellular movement without equating the predominantly perinuclear signal or nuclear-associated fraction with demonstrated intranuclear delivery. Human-library interaction discovery is distinct from mouse NIH3T3 knockdown and bovine endothelial transport assays; every purified construct species is not unambiguously identified in the Methods. No nuclear-pore motor is established. The tested receptor readouts do not prove universal nonparticipation in receptor signaling; this lateral refinement preserves the original IPI and P09038 partner while representing the directly measured trafficking role.

Proposed replacements: intracellular protein transport

Summary: The inherited physical-attachment claim is unresolved in human CEP57.

Reason: GO:0008608 concerns physical spindle-microtubule association with the kinetochore, not checkpoint signaling alone. The recorded frog donor Q5FWP9 is currently cep57l1 and its PMID:17803911 abstract explicitly reports attachment assays, but this does not by itself invalidate the PAINT PTN001456386 node. Human PMID:26743940 directly establishes Mis12/Mad1 binding and MT-dependent checkpoint behavior while reporting no significant attachment defect after CEP57 depletion. PMID:30804344 also reports different checkpoint results under its conditions. Preserve the IBA and mark the target-specific attachment judgment unresolved rather than converting nonessentiality, paralog nomenclature or incomplete tree knowledge into a removal.

Summary: Direct FGF2 binding supports a contextual cargo-recognition role.

Reason: PMID:12717444 human-library two-hybrid discovery and recombinant binding assays support preferential association with the 18-kDa FGF2 form; FGF1 and the noninteracting FGF2 chimera are controls. Retain fibroblast growth factor binding at non-core scope because its trafficking context is distinct from CEP57's predominant centrosomal structural role. Binding is not an FGF receptor or kinase activity.

Summary: Human domain structures support a homodimerization refinement.

Reason: The original InterPro-based identical-protein binding is consistent with self-association but can be made more informative. PMID:38857398 measures dimers for human N- and C-terminal domains by SAXS/MALS and resolves the C-terminal dimer interface crystallographically. Preserve the original source and propose protein homodimerization activity; do not infer that all native CEP57 assemblies contain exactly two subunits or that every alternative product has the same interface. This replacement deliberately converges on the existing PMID:12717444 homodimerization annotation; it preserves a separate evidence line and is not proposed as additional term coverage.

Proposed replacements: protein homodimerization activity

Summary: Homotypic association is supported, with later domain dimer evidence.

Reason: PMID:12717444 reports translokin self-interaction in its two-hybrid analysis. That assay alone does not determine stoichiometry, while independent PMID:38857398 directly measures human domain dimers and an atomic C-terminal dimer interface. Retain the original Q86XR8 interaction and homodimerization activity at supporting, non-core resolution rather than rewriting its source to the later work.

Summary: Positive human gamma-TuRC coassociation is retained, but the specific gamma-tubulin binding inference remains unresolved.

Reason: The official IPR025913 entry genuinely maps this domain to gamma-tubulin binding, but its sole cited paper, PMID:18294141, uses gamma-tubulin as a centrosomal localization marker rather than testing that specific interaction. Independent PMID:22508265 Fig. 1D and Results positively co-immunoprecipitate endogenous human CEP57 with gamma-tubulin, GCP2 and NEDD1. NEDD1 is the strongest associated partner, and FRET, domain interaction and depletion experiments support CEP57 association with NEDD1 and NEDD1-dependent CEP57 localization/stability. Those experiments do not test whether the gamma-tubulin association depends on NEDD1, so they neither prove an exclusively NEDD1-mediated bridge nor resolve which gamma-TuRC component contacts CEP57. Retain the positive complex association while leaving the original partner-specific electronic inference undecided. This is not a universal purified-binary-binding requirement or evidence that CEP57 cannot bind gamma-tubulin; no gamma-tubulin enzymatic activity is transferred to CEP57.

Summary: CEP57 can form higher-order self-assemblies.

Reason: Retain the mouse orthology inference in light of mouse N-terminal multimerization experiments and human self-assembly evidence. Full-length sfGFP-CEP57 forms condensates, while the detailed multivalent-interaction assays use engineered Cep57S and isolated domains. These support a self-assembly capability without assigning a fixed native oligomer size, equating condensates with a unique physiological oligomer, or claiming that all five products behave identically.