just fetch-gene human CEP152 produced a 61-row GOA snapshot and UniProt record for O94986.just fetch-gene-pmids human CEP152 cached every PMID used by the GOA snapshot.CEP152-deep-research-manual.md.PTN000818649 carries IBD assertions for centrosome and centriole replication and seeds the human O94986 and mouse Cep152 annotations. The node is CEP152-specific even though the broader PTHR10337 family also contains SHC-family proteins. The IBA calls are therefore biologically coherent and independently supported, but are not independent experimental evidence because human CEP152 is one of the source genes.mitotic spindle assembly but does not justify assigning catalytic ubiquitin-ligase or microtubule-nucleator activity to CEP152.protein-macromolecule adaptor activity and protein kinase binding. Replace PLK4-supported generic protein binding records with protein kinase binding; replace the CENPJ/CPAP generic binding record with adaptor activity because the experiment establishes a two-ended scaffold.mitotic spindle assembly from the direct APC/C-CEP152-CEP57-pericentrin study.This dated audit supersedes the earlier action explanations where they conflict. The historical notes above and the existing manual-research file are preserved exactly; their earlier quotations and conclusions are not newly authored evidence. All 61 original GOA source objects, four UniProt products, and original reference identifiers/titles remain intact. The inherited reviewer-authored NEW proposal is corrected to the regulatory term described below; its full original object is preserved in the audit provenance. There are still 62 entries and no additional proposed process row. The refreshed normal seed had 61 rows; its newer source-chain fields were archived separately and were not substituted into the published original assertions.
The binding decisions apply the explicit project/user instruction at the frozen main revision. Supported generic associations remain non-core when a more informative function is not established. The instruction does not itself verify an interaction. Four prior informational OVER decisions are changed only after source-specific checks: CEP131, MOV10, CCDC66 and CINP.
CEP152 is an integral complex scaffold. The current official GO:0030674 record directs protein-complex scaffolds to GO:0140378, whose definition concerns a component that holds a protein-containing complex together. Human PLK4/CPAP recruitment and binding experiments in PMID:20852615 and PMID:21059844, coupled with the CEP63–CEP152 structural/reconstitution and human mutant-rescue studies in PMID:30858376 and PMID:37433832, establish this role. The adaptor row and CPAP generic-binding refinement now use GO:0140378. PLK4 partner-specific rows retain protein kinase binding. No intrinsic kinase activity is assigned to CEP152. Purified fragment stoichiometry, ectopic engineered cylinders and native centrosomal architecture remain distinguishable experiments.
PMID:20852615 was read in the genuine full publisher Main/Figure 4 and human U2OS Methods, despite the unchanged abstract-only repository cache. The human clone is BC117182, and the experiment separately assays human PLK4 and CPAP. The fly Asl microtubule-organizing phenotype is not automatically a human CEP152 activity. PMID:21059844 uses endogenous/tagged human associations and an in-vitro-translated partner in its biochemical assay; it is not described as a purified-both-partners assay.
For the prior spindle-assembly proposal (row 61), the original reviewer-authored GO:0090307/IMP/PMID:34878135 proposal is revised to GO:1901673, regulation of mitotic spindle assembly, retaining action NEW and its IMP/PMID:34878135 evidence. The prior object is preserved in the audit provenance. The exact-GOA validator correctly rejects MODIFY for a term never present in the machine source, so the authored proposal itself is corrected; neither GOA nor validator is altered. The actual human study provides regulatory work beyond substrate necessity: CEP152 recruits centrosomal APC/C while centrioles remain present; its DBK substrate-recognition mutant retains APC/C co-IP; and depletion of CEP152 or CEP63 increases CEP57–pericentrin association and centrosomal pericentrin (Figures 3 and 5). The persistent DBK mutant delays microtubule regrowth and bipolar spindle formation. CEP152 therefore organizes an inhibitory complex and its remodeling, rather than being credited with its partners' nucleation or ligase catalysis. The study could not test purified direct APC/C–CEP152 binding because recombinant CEP152 was unstable. Its Discussion explicitly allows ubiquitylation-dependent relocation without obligatory degradation; the old definite turnover/degradation language is superseded.
The prior NEW bar was revisited rather than used to manufacture another row. Official term ancestry distinguishes spindle assembly from its regulation, and no ancestor/descendant redundancy with the original centriole-duplication process terms was identified. Exact-current target GOA and a same-role scaffold comparison were inspected: CEP192 carries experimental GO:0090307, whereas the queried CEP63 and NUMA1 records gave no exact-term hit. This mixed result is not evidence of a systematic annotation gap or proof of the target claim. The claim instead rests on CEP152's own complex/recruitment work. The frozen-main GO-CAM index has no literal O94986 or CEP152 match. No additional NEW process is introduced. Independent ROOT source/ontology review concurs with the regulatory refinement.
The companion source-evidence JSON retains literal interaction accessions, methods, partners, taxa/hosts, features, negative flags and raw-response hashes/URLs. It omits curator free-text comments. Absence of other papers from this particular IntAct query is not negative evidence; their primary texts provide the relevant support.
The core location is the proximal pericentriolar scaffold, not the centriole lumen. PMID:26337392 uses CEP152 as the PCM-ring comparator to MDM1; PMID:32060285 Figure 2e/f measures CEP152 recruitment in control and CEP44-depleted human cells. PMID:22020124 Figure 1C directly detects CEP152 in STIL-induced procentriole rosettes; its separate negative STIL–CEP152 co-IP does not negate localization. The original procentriole row is assessed with the distinction between the peripheral assembly-site scaffold and intrinsic cartwheel structure retained. The exact supplementary target row in the broad PMID:21399614 proteomics study was not separately re-extracted; its source remains preserved, with localization independently supported by human target-specific studies.
Current HPA antibody HPA039408 supports centrosome and ciliary basal-body locations, including ciliated human ASC52telo, RPTEC/TERT1 and serum-starved hTERT-RPE1 contexts. Basal-body localization is therefore not inferred merely by equating centrioles with basal bodies. The 22 original Reactome cytosol assertions are preserved as curated compartment contexts. Their event narratives concern other factors and do not assign those factors' activities to CEP152. Official human entity R-HSA-380277 explicitly maps O94986, residues 1–1710, to cytosol; it is not 22 independent localization experiments.
PAINT IBD PTN000818649 for centrosome/centriole replication is present in the exact-main PTHR10337 record. Its human O94986 evidence is a legitimate descendant source, not circularity. The whole ancestral reconstruction was not independently repeated. No new family ID or node was invented.
The two transfer chains for multiciliogenesis differ. A2AUM9 is mouse Cep152, with experimental donor annotations from PMID:24240477. Selected full publisher Figure 7/Results shows that mouse Cep152 RNAi blocks centriole biogenesis while Deup1-positive deuterosome structures persist: CEP152's centriole-scaffold role must not become an autonomous requirement for constructing the deuterosome. Q498G2 is Xenopus laevis, not mouse or rat. Its exact donor source is PMID:24075808, now fetched through the normal cache workflow. Full Results/Figures 3–4 and Methods identify frog Cep152 at deuterosomes/nascent centrioles, overexpression, a first-306-residue dominant-negative construct and PLK4 coexpression rescue. These experiments support the conserved specialized role while preserving the human rows as ortholog inferences. PMID:33627667 contributes mouse multiciliated localization; PMID:33658185's engineered HeLa Deup1 condensates are not native human deuterosomes.
Selected primary text and assay descriptions were read, not every figure pixel or every supplementary experiment. Abstract-only cache status is recorded separately from successful external full-text access; no unavailable flag is imposed on externally read papers merely because the normal cache is short. Reference assessments state their access scope. Existing publications, Reactome files, UniProt, GOA and PANTHER bytes remain unchanged. The only additional publication cache is the genuinely fetched PMID:24075808; PMID:24240477 reuses exact existing-main bytes.
Normal intake and publication caching succeeded. The first provider attempt raced the not-yet-complete UniProt intake and failed its template context; the authentic Perplexity fallback failed for quota. A bounded Falcon retry after intake timed out at 90 seconds. No provider report was fabricated. This dated manual audit and its source records are the research output.
All newly authored YAML/append quotations combined remain within 25 words per primary source. The YAML retains one 19-word source anchor from PMID:21059844; long or repeated inherited YAML excerpts were replaced by precise source citations and assay explanations. The untouched historical notes prefix and immutable old manual-research file retain their original quotations as historical records, not newly authored evidence.
The following are genuine retrieved publisher resources, manually read at the specified sections. SHA256 values describe the downloaded files, not fabricated normal publication caches.
PMID:20852615: Main/Figure 4; human U2OS and construct Methods; SHA256 82f6c8d2c61eb4f6273472c418ffd2367fd4ca19e1f41433c947788f147d5001.
PMID:21131973: Main target Results/Figure 2; SHA256 d021a37463a8d892a56253d7ac696ffc9f2facc57ca817dc08e8a71c2c15710b.
PMID:21131973: Supplementary Figure 8; expression constructs and Y2H Methods; SHA256 6b819bfbad692871a17eabe2b51f415347318ac57e3b7dd31585f8a199e9f840.
PMID:22020124: Figure 1C/Results; human construct and antibody Methods; SHA256 7672df15a16f80e258f0fbe5bc4e8cccb71c7a0d27ccee88b3fa654e8dd2959f.
PMID:24240477: Figure 7 and associated Results; SHA256 6baa7eca464746684b71459e73208da252520d3ca7cdf1f359db36ce8caee1ed.
This section supersedes the earlier audit's CCDC66 assay locator: PMID:35849559 Figure 2E, not Figure 2A, is the FLAG co-immunoprecipitation of FLAG-miniTurbo–CCDC66 with myc-BirA*–CEP152 in HEK293T cells. The full Results and Figure 2 legend were read again; Figure 2A/B describes centrosomal immunofluorescence. The supported generic association and the independent centrosomal-localization decisions are unchanged. Primary paper, Figure 2.
The authored GO:1901673 proposal and the mitotic scaffold core now have separate short exact anchors from PMID:34878135: the recruitment result and the CEP152–CEP63 inhibitory-complex result. These anchors support CEP152's own regulatory contribution; they do not turn substrate necessity into participation or assert obligatory degradation. The centriole-replication core retains a concise target-specific recruitment anchor from PMID:21059844. Detailed experimental context remains in the reasons and prior source-access locators. All new/retained YAML excerpts combined stay below 25 quoted words per primary source, counting repeated excerpts; this is authoring discipline, not a repository validator rule. The historical notes prefix is preserved user-provided repository material and contains longer inherited quotations; its whole-file totals are reported separately and are not asserted to meet that new-authoring limit. No historical quotation is copied again into this append.
The 22 broad cytosol-event Reactome references are now labelled LOW relevance because their narratives concern other factors and provide contextual compartment evidence. Their identities, annotations and non-core decisions are unchanged. DRAFT is the normal status tool's computed assessment, independent of campaign completion or merge state; all 62 decisions are adjudicated, and the status is not promoted merely by merging this PR.
CEP152-source-evidence.json is an unchanged deterministic extract of authenticated source database fields, with query/source identifiers and raw-response hashes. It is not a new manually curated proposal table; this follow-up does not rename it or reinterpret it as independent biological replication. Previously inspected external primary text remains distinguished from the abstract-only normal caches. No source cache is hand-edited or refreshed for these presentation fixes. The molecular-function and biological-process choices, all 61 machine source objects, the pre-existing authored NEW term, four products and 53 reference identities remain unchanged.