CEP85L

Summary: CEP85L localizes to pericentriolar material.

Reason: PMID:32097630 Figure 3A–C maps tagged human CEP85L in U2OS cells relative to centrin, SAS6 and pericentrin, placing it around the centriole rather than in its lumen. The Methods identify human NM_001042475 for the HA construct. Figure 3D separately shows tagged mouse Cep85l at the centrosome of migrating cortical neurons. These experiments support the original human localization assertion without assigning every alternative product the tested construct.

Summary: CEP85L contributes to cortical neuronal migration.

Reason: PMID:32097630 Figure 2 tests Cep85l knockdown in embryonic mouse cortex, with partial cDNA rescue and a persistent migration defect at P7; neuronal maturation assessed by NeuN appeared unaffected. Retain the conserved neuronal-migration role under the original IMP rather than describe a human-neuron perturbation. Independent PMID:32097629 connects CEP85L association with centrosomal CDK5 to kinase localization and organization of migration-associated proteins, supporting performed organizational work in this process.

Summary: Centrosomal activity is consistent with CEP85L-dependent CDK5 recruitment.

Reason: Retain the PAINT active-in inference: human CEP85L associates with CDK5 and its depletion displaces CDK5 from the centrosome, providing target-specific functional support beyond localization alone. The ancestral PTN001257853 node and alignment history were not reconstructed. Q6P2H3 is human CEP85, while Q5SZL2 is CEP85L itself; target self-evidence is legitimate grounding for a phylogenetic inference, not circularity. No loss or misplaced-node claim is made.

Summary: The electronic centrosome localization agrees with direct human evidence.

Reason: The original SL-0048 mapping is consistent with the selected UniProt record and with human CEP85L imaging in both 2020 studies. Retain this general localization assertion alongside the separately supported pericentriolar-material term; the original qualifier and evidence source remain unchanged.

Summary: The original centrosome screen identifies CEP85L as C6orf204.

Reason: PMID:21399614 Table 1 and the selected full primary Results explicitly include C6orf204. Its PCP-SILAC score is 1.9 and HPA staining is positive, whereas the GFP fusion was too weak to confirm centrosome association. Retain the TAS at the resolution of that screen, independently corroborated by the 2020 tagged and endogenous localization experiments. The unchanged repository cache is partial despite its full-text flag; the target table was inspected through indexed primary PMC text, not inferred from the title.

Summary: CEP85L associates with CDK5 in a centrosomal recruitment mechanism.

Reason: PMID:32097629 Figure 4E and the HeLa immunoprecipitation Methods establish CEP85L–CDK5 association. Depletion displaces centrosomal CDK5 without reducing total CDK5, connecting the association to its biological role. Add the experimentally supported serine/threonine-kinase-binding MF because the assayed partner is human CDK5 (Q00535), a serine/threonine kinase, and the five source annotations contain only location and migration terms. Co-immunoprecipitation does not resolve a purified binary interface. The pCDK5 changes support an activation model but do not by themselves establish an autonomous kinase-activator mechanism or substrate-turnover activity of CEP85L.

Summary: CEP85L helps maintain CDK5 at the centrosome.

Reason: Human endogenous CEP85L associates with CDK5 by HeLa co-immunoprecipitation, and CEP85L depletion removes centrosomal CDK5 in U2OS cells while total CDK5 remains unchanged. CEP85L remains centrosomal in CDK5-deficient patient fibroblasts. Together, this physical association and directional localization dependency support organizational work in maintaining another protein at the centrosome, rather than CEP85L merely being cargo or a necessary migration factor. The molecular tethering interface and whether retention or delivery is affected remain unresolved. Current same-role comparator annotations include CEP192, PCM1 and CEP83; negative exact-term results for CEP164 and CEP63 are retained in the source record. The term's localization/maintenance meaning and both typed hierarchy directions were checked against all existing and proposed terms, with no redundancy. The exact-head GO-CAM index has no target entry.