CCP110 (CP110) curation notes

Deep research status

just deep-research-falcon human CCP110 was run (first with --fallback perplexity-lite, which is not available in this environment, then with --timeout 2400). See the end of this file for the outcome. The review was written from the cached primary literature in publications/.

Centrosomal CDK substrate required for centrosome duplication PMID:12361598
Required for PLK4-driven procentriole formation; caps growing distal tips PMID:17681131; PMID:16244668
Direct microtubule plus-end capping activity, counteracted by CPAP PMID:39847124
Suppresses ciliogenesis with CEP97 PMID:17719545, partly through CEP290 PMID:18694559
Cap anchoring: KIF24 -> MPHOSPH9 -> CEP97 -> CP110; TTBK2 phosphorylation of MPP9 triggers its degradation and cap removal PMID:30375385; PMID:23141541
Levels controlled by SCF(cyclin F) and USP33 PMID:20596027; PMID:23486064
Cytokinesis role via calmodulin/centrin PMID:16760425
In vivo pro-ciliogenic role in mouse (source of the ISS rows) PMID:26965371; PMID:26965371

34 protein binding IPIs: REMOVE (uninformative), except 3 calmodulin rows -> MODIFY to calmodulin binding (GO:0005516).
Centrosome/centriole, centriole replication, centrosome duplication, negative regulation of cilium assembly, microtubule binding: ACCEPT.
Positive regulation of cilium assembly (ISS from mouse) and regulation of cytokinesis: KEEP_AS_NON_CORE (context-dependent/secondary).
Reactome cytosol rows: KEEP_AS_NON_CORE.
NEW: microtubule plus-end binding (GO:0051010) and regulation of centriole elongation (GO:1903722), both from PMID:39847124. Participation test: CP110 itself caps the plus end (does the work). Comparator: CCP110 orthologs in other species already carry the child term negative regulation of centriole elongation (QuickGO).

Module (modules/primary_cilium_life_cycle.yaml, stage 1_basal_body_licensing): CCP110 is a "distal centriole cap (ciliogenesis suppressor)" component of the CP110-CEP97 cap, with process negative regulation of cilium assembly and location ciliary basal body.
HPA v25 (projects/HUMAN_PROTEIN_ATLAS/cilium_life_cycle/member_evidence.md): only "Centriolar satellite (A)"; main location centriolar satellite. No basal body, centrosome or cilium call. The HPA cilium atlas (Hansen et al. 2025, PMID:41005307) is cached abstract-only, so gene-level details cannot be checked there.
Assessment: the HPA call disagrees with the extensive literature placing CP110 at distal centriole ends (both centrioles in cycling cells, lost from the mother centriole at ciliogenesis). Because the cap is removed from the mother centriole before/at cilium formation, a basal body signal would not be expected in ciliated HPA cells, which may partly explain the absence of a basal-body call; the satellite signal may be a genuine pool or an antibody issue. I keep the module role (negative regulation of cilium assembly at the mother centriole distal end) as a core function; I would quibble with "ciliary basal body" as the module location, since the cap acts on the mother centriole before it becomes a basal body ("centriole" is used in core_functions).

Falcon succeeded on retry (--timeout 2400): CCP110-deep-research-falcon.md. Its synthesis agrees with the review: direct CaM binding (centrin association appears indirect, supporting REMOVE of the centrin protein-binding row), CEP97-CP110 gate, KIF24-MPP9-TTBK2 uncapping, direct plus-end capping with CPAP (Iyer 2025). Additional leads not used for annotations: CCP5/CCP6 and ENKD1 regulation of CP110 retention/removal (2022-2023), and a 2024 report of biallelic CCP110 loss-of-function variants with a ciliopathy-like phenotype (DOI 10.1016/j.ejmg.2024.104955; primary text not retrieved).