Affinage

CCP110

Centriolar coiled-coil protein of 110 kDa · UniProt O43303

Length
1012 aa
Mass
113.4 kDa
Annotated
2026-04-28
40 papers in source corpus 31 papers cited in narrative 30 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CCP110 (CP110) is a centriolar distal-end capping protein that integrates cell-cycle cues with centriole biogenesis, centriole length control, and ciliogenesis. Phosphorylation by CDK2 (Ser170, Thr194) and PLK4 (Ser98) licenses centrosome duplication and centriole assembly, while precisely timed ubiquitin-dependent degradation—executed by SCF(Cyclin F) in G2, counterbalanced by the deubiquitinase USP33, and augmented by EDD1, HERC2, MIB1, and LUBAC-generated linear ubiquitin chains recognized by PRPF8—removes CP110 from the mother centriole to permit ciliogenesis (PMID:12361598, PMID:20596027, PMID:23486064, PMID:34813648, PMID:37074924). CP110 forms distinct complexes with Cep97, CEP290, Talpid3, Kif24, MPP9, calmodulin, and centrin at the centriole distal end; these complexes restrain centriolar microtubule elongation, suppress premature cilia formation in cycling cells, and, at appropriate levels in multiciliated cells, promote basal body docking and ciliary vesicle recruitment via Rab8a (PMID:17719545, PMID:18694559, PMID:19481458, PMID:24421332, PMID:27623009). Removal of CP110 from the mother centriole at ciliogenesis onset requires the coordinated action of TTBK2-triggered MPP9 degradation, ENKD1-mediated displacement of CEP97, centrin-2, NudCL2-directed selective autophagy, BICD2, EHD1-mediated satellite trafficking, and p97/VCP-dependent extraction of polyubiquitinated CP110, while miR-34/449 and miR-129-3p post-transcriptionally repress CP110 mRNA to lower overall protein levels (PMID:30375385, PMID:35301795, PMID:34480124, PMID:39785673, PMID:24899310, PMID:25753040). Cp110 knockout mice die perinatally with ciliopathy-like organogenesis defects including impaired Hedgehog signaling, demonstrating that CP110 is essential not only as a ciliogenesis suppressor but also as a positive regulator of basal body maturation and subdistal appendage assembly in vivo (PMID:26965371).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2002 High

    Identification of CP110 as a CDK2 substrate at centrosomes resolved how centrosome duplication is coupled to S-phase entry, establishing that CP110 phosphorylation is required for duplication licensing and that its disruption causes unscheduled centrosome separation and polyploidy.

    Evidence CDK substrate screen, in vitro kinase assay, RNAi depletion, and cell-cycle analysis in human cells

    PMID:12361598

    Open questions at the time
    • Specific phosphorylation sites were not mapped in this study
    • Downstream effectors of CP110 phosphorylation were unknown
  2. 2006 High

    Demonstration that CP110 directly binds calmodulin and centrin and exists in large native complexes established CP110 as a multivalent scaffold at centrosomes, and its requirement for cytokinesis completion expanded its functional repertoire beyond duplication.

    Evidence Yeast two-hybrid, co-IP, in vitro binding, RNAi, and dominant-negative expression in human cells

    PMID:16760425

    Open questions at the time
    • The stoichiometry and composition of the large native complexes were not resolved
    • The mechanism by which calmodulin binding supports cytokinesis was not determined
  3. 2007 High

    Discovery that Cep97 recruits CP110 to centrosomes and that loss of either protein triggers ectopic cilia formation in cycling cells reframed CP110 as a ciliogenesis suppressor, providing the first molecular mechanism for how cilia assembly is blocked during proliferation.

    Evidence Biochemical purification of CP110 complexes, RNAi, gain-of-function rescue, immunofluorescence

    PMID:17719545

    Open questions at the time
    • How CP110 removal is triggered at ciliogenesis onset was unknown
    • Mechanism by which CP110 prevents axoneme extension was not defined
  4. 2008 High

    Identification of a discrete CP110–CEP290 complex that is essential for CP110's cilia-suppressive function, and the link to Rab8a-mediated vesicle trafficking, connected CP110 removal to the downstream ciliary membrane delivery pathway.

    Evidence Reciprocal co-IP, RNAi, dominant-negative analysis, immunofluorescence

    PMID:18694559

    Open questions at the time
    • Whether CP110 directly blocks Rab8a recruitment or acts through CEP290 was unresolved
    • Structural basis of CP110–CEP290 interaction was unknown
  5. 2009 High

    Ultrastructural evidence that CP110 depletion causes centriole over-elongation established CP110 as a physical distal-end cap that restrains tubulin addition, placing it antagonistic to CPAP in centriole length control.

    Evidence Overexpression and siRNA depletion with electron microscopy in human cells

    PMID:19481458

    Open questions at the time
    • Whether the capping is direct or involves intermediary proteins was not resolved
    • Precise binding site on centriolar microtubules was unknown
  6. 2010 High

    Identification of SCF(Cyclin F) as the E3 ligase that ubiquitinates and degrades CP110 in G2 explained how CP110 levels are restrained during mitotic entry, preventing multipolar spindles and genome instability from excess CP110.

    Evidence Unbiased interaction screen, co-IP, ubiquitination assay, siRNA epistasis, stable mutant expression

    PMID:20596027

    Open questions at the time
    • Whether additional E3 ligases contribute to CP110 turnover at different cell-cycle stages was not addressed
    • The ubiquitin chain type was not specified
  7. 2011 High

    Discovery that the kinesin-13 motor Kif24 interacts with CP110–Cep97, depolymerizes centriolar microtubules, and maintains CP110 at mother centrioles in cycling cells revealed a microtubule-remodeling mechanism that keeps the cilia-suppressive cap in place.

    Evidence Co-IP, in vitro microtubule depolymerization assay, RNAi, immunofluorescence

    PMID:21620453

    Open questions at the time
    • How Kif24 activity is switched off at ciliogenesis onset was unknown
    • Whether Kif24 directly stabilizes the CP110 cap or acts only on microtubules was unclear
  8. 2012 High

    Demonstration that miR-129-3p and, subsequently, miR-34/449 directly repress CP110 mRNA to promote ciliogenesis established post-transcriptional downregulation as a parallel pathway to protein degradation for lowering CP110 levels during cilia formation.

    Evidence miRNA overexpression/inhibition, luciferase reporter, zebrafish morpholinos; miR-34/449 knockout mice with CP110 epistasis in Xenopus

    PMID:22684256 PMID:24899310

    Open questions at the time
    • Relative contributions of transcriptional vs. post-transcriptional CP110 regulation were not quantified
    • Whether additional miRNAs target CP110 was not comprehensively addressed
  9. 2013 High

    Identification of USP33 as the deubiquitinase that specifically counteracts SCF(Cyclin F)-mediated CP110 ubiquitination completed the ubiquitin-balance model for CP110 abundance, showing that tipping this balance toward stabilization drives centrosome amplification.

    Evidence Reciprocal co-IP, in vitro deubiquitination assay, siRNA, immunofluorescence

    PMID:23486064

    Open questions at the time
    • What signals regulate USP33 activity or localization at specific cell-cycle stages was not determined
    • Whether USP33 acts on all ubiquitin chain types on CP110 was untested
  10. 2014 High

    Incorporation of Talpid3 into the CP110 distal-end complex, upstream of Rab8a, established a centriolar satellite-organizing module required for ciliary vesicle docking, explaining a key step between CP110 cap removal and axoneme extension.

    Evidence Reciprocal co-IP, RNAi, activated Rab8a rescue epistasis, super-resolution microscopy

    PMID:24421332

    Open questions at the time
    • Whether Talpid3 directly contacts CP110 or only CEP290 within the complex was not resolved
    • Mechanism of satellite redistribution upon Talpid3 loss was unclear
  11. 2015 High

    Mapping CDK2 phosphorylation to Ser170 and Thr194 and showing that phospho-resistant mutants cause anaphase catastrophe linked CP110 phospho-regulation to mitotic fidelity in cancer cells, and demonstration that centrin-2 is required for CP110 removal during ciliogenesis identified another component of the removal machinery.

    Evidence Site-directed mutagenesis, live-cell imaging, CDK2 inhibitor epistasis; CETN2 knockout with CP110 knockdown rescue

    PMID:25753040 PMID:25808870 PMID:26304236

    Open questions at the time
    • How centrin-2 mechanistically promotes CP110 removal was not defined
    • Whether CDK2 phosphorylation of CP110 directly regulates its centriolar binding affinity was not tested
  12. 2016 High

    Cp110 knockout mice dying perinatally with ciliopathy-like defects, combined with Xenopus data showing CP110 is required at optimal levels for basal body docking, overturned the simple view that CP110 is purely a cilia suppressor and established it as a dose-sensitive positive regulator of centriole maturation and cilia formation in vivo.

    Evidence Cp110 knockout mouse with EM and Shh signaling analysis; Xenopus multiciliated cell imaging with CP110 mutant expression

    PMID:26965371 PMID:27623009

    Open questions at the time
    • Molecular basis of subdistal appendage assembly defects in CP110-null centrioles was not defined
    • Precise CP110 concentration thresholds for positive vs. negative ciliogenesis roles were not quantified
  13. 2017 High

    Identification of PLK4 as a second kinase phosphorylating CP110 (Ser98) that is required for centriole assembly and SAS6 recruitment connected CP110 to the earliest cartwheel-formation step, adding a new layer of kinase control beyond CDK2.

    Evidence In vitro kinase assay, phospho-mimetic/resistant mutagenesis, centrosome duplication assay

    PMID:28562169

    Open questions at the time
    • Whether PLK4 phosphorylation of CP110 alters its binding partners was not examined
    • Whether this site is conserved in invertebrate orthologs was not tested
  14. 2018 High

    Discovery that MPP9 acts as an intermediary bridge—recruited by KIF24 and binding CEP97 to anchor CP110, then degraded upon TTBK2 phosphorylation—provided the first ordered kinase-triggered cascade for CP110 removal at ciliogenesis onset.

    Evidence Co-IP, super-resolution microscopy, RNAi, TTBK2 kinase assay, mouse kidney model

    PMID:30375385

    Open questions at the time
    • Whether TTBK2 phosphorylation of MPP9 is sufficient or requires additional signals was not resolved
    • Identity of the E3 ligase ubiquitinating phospho-MPP9 was not determined
  15. 2021 High

    Three parallel mechanisms for CP110 ubiquitination and removal were established: NudCL2-mediated selective autophagy via an LIR motif, EDD1-DYRK2-DDB1(VPRBP) recruitment through CEP78-CEP350, and LUBAC-generated linear ubiquitin chains recognized by PRPF8, revealing an unexpectedly complex, multi-pathway degradation network.

    Evidence NudCL2 KO MEFs/zebrafish with LIR mutagenesis; CEP78 interactome with siRNA epistasis; LUBAC ubiquitination assay with PRPF8 receptor identification

    PMID:34259627 PMID:34480124 PMID:34813648

    Open questions at the time
    • Hierarchy and temporal ordering of these three pathways during ciliogenesis was not established
    • Whether linear and K48/K63 ubiquitin chains coexist on the same CP110 molecule was not tested
  16. 2022 High

    Discovery that CP110–CEP97–CEP290 and centriolar satellites are required for aggresome assembly extended CP110 function beyond centrosome biology to proteostasis, while ENKD1 was identified as a competitor that displaces CEP97 from CP110 to trigger its removal, adding a non-enzymatic mechanism to the removal repertoire.

    Evidence Quantitative imaging with siRNA for aggresome phenotype; ENKD1 competition binding assay, knockout mouse, siRNA epistasis

    PMID:35301795 PMID:35411088

    Open questions at the time
    • Physiological contexts in which the aggresome function of CP110 is critical remain unexplored
    • Whether ENKD1 competes with CEP97 directly at the same binding surface was not structurally resolved
  17. 2023 High

    EHD1-mediated satellite trafficking was shown to deliver HERC2 and MIB1 E3 ligases to the mother centriole for CP110 ubiquitination, and CCP5/CCP6 were identified as factors that retain CP110 at the mother centriole, further expanding the network of CP110-regulating proteins.

    Evidence Ubiquitination assays identifying HERC2 and MIB1, satellite trafficking analysis, siRNA; CCP5 CoIP-MS with siRNA phenotype

    PMID:37074924 PMID:37226238

    Open questions at the time
    • The ubiquitin chain types generated by HERC2 and MIB1 on CP110 were not specified
    • Mechanism by which CCP5/CCP6 retain CP110 is not defined beyond physical interaction
  18. 2025 Medium

    Identification of p97/VCP as the AAA-ATPase that unfolds and extracts polyubiquitinated CP110 from the mother centriole, and BICD2 as a dynein adaptor that binds CP110 and facilitates its removal, added the final known extraction steps linking ubiquitination to physical removal.

    Evidence p97 inhibitor and siRNA with CP110 epistasis; BICD2 co-IP, siRNA, zebrafish morpholino epistasis

    PMID:39785673 PMID:41102520

    Open questions at the time
    • Whether p97 and BICD2 operate sequentially or in parallel has not been tested
    • Structural basis of BICD2–CP110 interaction is unknown
    • Both findings are from single labs and await independent confirmation

Open questions

Synthesis pass · forward-looking unresolved questions
  • The temporal hierarchy and epistatic relationships among the numerous CP110 removal pathways (LUBAC, HERC2, MIB1, NudCL2-autophagy, ENKD1 competition, MPP9 degradation, p97 extraction, BICD2 transport) remain unintegrated into a unified, ordered model, and no high-resolution structure of CP110 or its centriolar complexes exists.
  • No structural model of CP110 or its centriolar cap complex exists
  • Temporal ordering of multiple E3-ligase and removal pathways during ciliogenesis has not been resolved
  • Dose-dependent switch between cilia-suppressive and cilia-promoting roles is not mechanistically explained

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 2 GO:0008092 cytoskeletal protein binding 2
Localization
GO:0005815 microtubule organizing center 7 GO:0005929 cilium 4
Pathway
R-HSA-1852241 Organelle biogenesis and maintenance 7 R-HSA-1640170 Cell Cycle 6 R-HSA-392499 Metabolism of proteins 4 R-HSA-9612973 Autophagy 1
Partners
CALM1CCNFCEP290CEP97KIF24MPP9TALPID3USP33
Complex memberships
CP110-CEP290 complexCP110-CEP97 complexCP110-CEP97-MPP9-KIF24 complex

Evidence

Reading pass · 30 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 CP110 is phosphorylated by CDKs (CDK2) in vitro and in vivo, localizes to centrosomes, is induced at the G1-to-S transition coincident with centrosome duplication initiation, and is required for centrosome duplication; disruption of CP110 phosphorylation leads to unscheduled centrosome separation and polyploidy. CDK substrate screen, in vitro kinase assay, RNAi-mediated depletion, cell cycle analysis Developmental cell High 12361598
2006 CP110 directly interacts with calmodulin (CaM) and centrin in vivo; yeast two-hybrid and biochemical analyses identify multiple high-affinity CaM-binding domains in CP110. Native CP110 exists in large complexes (~300 kDa to 3 MDa) containing both centrin and CaM. Depletion of CP110 or expression of a CaM-binding-deficient CP110 mutant causes failure at a late stage of cytokinesis and binucleate cell formation. Yeast two-hybrid, co-immunoprecipitation, in vitro binding assay, RNAi, dominant-negative mutant expression Molecular biology of the cell High 16760425
2007 Cep97 recruits CP110 to centrosomes and forms a complex with CP110. Depletion of Cep97 causes CP110 disappearance from centrosomes, spindle defects, and polyploidy. Loss of either Cep97 or CP110 promotes primary cilia formation in growing cells; enforced CP110 expression in quiescent cells suppresses cilia assembly, establishing that CP110 and Cep97 together suppress a ciliogenesis program. Biochemical purification of CP110 complexes, RNAi, dominant-negative mutant expression, immunofluorescence Cell High 17719545
2008 CP110 interacts with CEP290 in a discrete complex separable from other CP110 complexes. This interaction is absolutely required for CP110 to suppress primary cilia formation. CEP290 and CP110 also interact with Rab8a; depletion of CEP290 prevents ciliogenesis and mislocalization of Rab8a to centrosomes/cilia, indicating CEP290 cooperates with Rab8a to promote ciliogenesis, a process antagonized by CP110. Co-immunoprecipitation, RNAi, dominant-negative mutant analysis, immunofluorescence Developmental cell High 18694559
2009 CP110 functions as a distal end-capping protein of centrioles that restrains tubulin addition; depletion of CP110 leads to elongated centriolar microtubule structures, and CPAP and CP110 play antagonistic roles in controlling centriole length. Overexpression, siRNA depletion, immunofluorescence, ultrastructural analysis Current biology : CB High 19481458
2010 Cyclin F (F-box protein) is the substrate recognition subunit of the SCF(Cyclin F) ubiquitin ligase that ubiquitinates and degrades CP110 during G2 phase. CP110 and Cyclin F physically associate at centrioles during G2; siRNA depletion of Cyclin F induces centrosomal and mitotic abnormalities (multipolar spindles, lagging chromosomes) that are reverted by co-silencing CP110. Expression of a stable CP110 mutant that cannot bind Cyclin F recapitulates these mitotic defects and promotes micronuclei formation. Unbiased protein interaction screen, co-immunoprecipitation, ubiquitination assay, siRNA epistasis, stable mutant expression Nature High 20596027
2011 Kif24, a kinesin-13 subfamily motor protein, specifically interacts with CP110 and Cep97 at the mother centriole. Loss of Kif24 causes CP110 disappearance from mother centrioles specifically in cycling cells capable of forming cilia. Kif24 can bind and depolymerize microtubules in vitro and specifically remodels centriolar microtubules in cells, thereby regulating cilia assembly. Co-immunoprecipitation, RNAi, in vitro microtubule depolymerization assay, immunofluorescence Cell High 21620453
2012 miR-129-3p controls cilia biogenesis by post-transcriptionally downregulating CP110 (and actin regulators). Blocking miR-129-3p inhibits serum-starvation-induced ciliogenesis; overexpression induces ciliation in proliferating cells, demonstrating that CP110 is a direct target of miR-129-3p. miRNA overexpression/inhibition, RNAi, luciferase reporter assay, zebrafish morpholino knockdown Nature cell biology High 22684256
2012 In Drosophila, the kinesin-13 Klp10A cooperates with CP110 to control centriole length; Klp10A depolymerizes centriolar microtubules, and unlike in mammals, depletion of Drosophila CP110 results in centriole length diminution (not elongation), which is overcome by co-depletion of Klp10A. RNAi in cultured cells and testes, ultrastructural analysis Current biology : CB Medium 22365849
2013 USP33, a deubiquitinating enzyme, interacts with CP110 and localizes to centrioles primarily during S and G2/M phases. USP33 specifically deubiquitinates CP110 (not other cyclin-F substrates), antagonizing SCF(Cyclin F)-mediated ubiquitination. USP33 overactivity promotes supernumerary centrioles; USP33 ablation destabilizes CP110 and inhibits centrosome amplification. Co-immunoprecipitation, in vitro deubiquitination assay, siRNA, immunofluorescence Nature High 23486064
2013 In Drosophila, CP110 subtly influences centriole length by counteracting centriole-elongating activities of centriole duplication proteins; CP110 ensures centriolar microtubules do not extend beyond the distal centriole end; and CP110 suppresses centriole overduplication induced by overexpression of duplication proteins. CP110 null mutant flies, overexpression, electron microscopy, in vivo genetic analysis The Journal of cell biology Medium 24297749
2014 Talpid3/KIAA0586 is a component of a CP110-containing protein complex at the distal end of centrioles. Talpid3 depletion causes aberrant centriolar satellite distribution, mislocalization of Rab8a, and cilia assembly defects. Expression of activated Rab8a suppresses cilia assembly defects caused by Talpid3 depletion, placing Talpid3 upstream of Rab8a in the CP110 complex pathway for ciliary vesicle formation. Co-immunoprecipitation, RNAi, epistasis with activated Rab8a rescue, immunofluorescence, super-resolution microscopy The Journal of cell biology High 24421332
2014 miR-34/449 miRNAs promote motile ciliogenesis by post-transcriptionally repressing Cp110; miR-34/449-deficient mice exhibit defective basal body maturation and apical docking. Cp110 knockdown in miR-34/449-deficient multiciliated cells restores ciliogenesis, demonstrating that Cp110 repression is a key effector mechanism of miR-34/449 in ciliogenesis. miR-34/449 knockout mice, Xenopus model, Cp110 knockdown epistasis, basal body imaging Nature High 24899310
2015 Centrin2 (CETN2) is required for CP110 removal from the mother centriole during ciliogenesis; CETN2-deficient human RPE-1 cells fail to remove CP110 and cannot form cilia despite intact centrioles; knockdown of CP110 in CETN2-deficient cells rescues ciliation. CETN2 knockout (DT40), siRNA knockdown in RPE-1 cells, epistasis by CP110 knockdown rescue, immunofluorescence The Journal of cell biology High 25753040
2015 CDK2 phosphorylates CP110 at Ser170 and Thr194; phospho-resistant CP110 mutants alter centrosome clustering and cause anaphase catastrophe in lung cancer cells. CP110 siRNA depletion induces anaphase catastrophe, while CP110 overexpression antagonizes CDK2 inhibitor-mediated anaphase catastrophe. Site-directed mutagenesis, siRNA, live-cell imaging, CDK2 inhibitor treatment Cancer research / Molecular cancer therapeutics High 25808870 26304236
2016 CP110 localizes to cilia-forming basal bodies and rootlets in Xenopus multiciliated cells. At high levels, CP110 inhibits cilia formation; at optimal levels, it promotes ciliogenesis by being required for ciliary adhesion complexes that facilitate actin interactions. Coiled-coil domains mediate preferential binding to centrioles over rootlets. Both transcriptional (via ciliary transcription factors) and post-transcriptional (via miRNAs including miR-34/449) mechanisms precisely control Cp110 levels. Xenopus in vivo imaging, CP110 mutant expression, RNAi, miRNA manipulation eLife Medium 27623009
2016 CP110 is required for anchoring basal bodies to the plasma membrane during cilia formation in vivo. Cp110-/- mice die shortly after birth with ciliopathy-like organogenesis defects. Loss of CP110 results in abnormal distribution of subdistal appendage components and recycling endosomes, and premature extension of axonemal microtubules, implicating CP110 in SDA assembly and ciliary vesicle docking. Cp110 knockout mouse, immunofluorescence, electron microscopy, Shh signaling assay Development (Cambridge, England) High 26965371
2017 PLK4 directly phosphorylates CP110 at Ser98. A phospho-resistant CP110 mutant inhibits centriole assembly, while a phospho-mimetic mutant drives centriole assembly even under PLK4-limiting conditions and enhances centrosomal SAS6 levels, indicating PLK4 phosphorylation of CP110 is required for efficient centriole assembly. In vitro kinase assay, site-directed mutagenesis, immunofluorescence, centrosome duplication assay Cell cycle (Georgetown, Tex.) High 28562169
2018 MPP9 is recruited by KIF24 to the distal end of the mother centriole where it forms a ring-like structure and recruits the CP110-CEP97 complex by directly binding CEP97. Upon phosphorylation by TTBK2 at the onset of ciliogenesis, MPP9 is ubiquitinated and degraded by the proteasome, which facilitates CP110 and CEP97 removal from the mother centriole to allow ciliogenesis. Co-immunoprecipitation, super-resolution microscopy, RNAi, TTBK2 kinase assay, mouse kidney model Nature communications High 30375385
2021 CEP78 interacts with CEP350 and the EDD1-DYRK2-DDB1VPRBP E3 ubiquitin ligase complex involved in CP110 ubiquitination/degradation. CEP350 promotes CEP78 centrosomal recruitment, which in turn recruits EDD1. Cells lacking CEP78 have increased centrosomal CP110 levels; CP110 depletion in CEP78-deficient cells restores normal ciliation frequency. Interactome analysis (CEP78 disease-causing mutant), co-immunoprecipitation, siRNA epistasis, immunofluorescence eLife High 34259627
2021 NudCL2 functions as a selective autophagy receptor at mother centrioles; it contains an LIR motif that mediates association with CP110 and the autophagosome marker LC3, thereby directing autophagic degradation of CP110. Knockout of NudCL2 impairs CP110 removal and ciliogenesis; this is rescued by wild-type NudCL2 but not LIR-motif mutant. CP110 depletion reverses ciliogenesis defects in NudCL2-deficient cells and zebrafish morphants. Knockout MEF cells and zebrafish morpholinos, LIR motif mutagenesis, co-immunoprecipitation, autophagy inhibition, epistasis Cell research High 34480124
2021 LUBAC (linear ubiquitin chain assembly complex) generates linear ubiquitin chains specifically on CP110, which are required for CP110 removal from the mother centriole. PRPF8, located at the distal end of the mother centriole, acts as the receptor for these linear ubiquitin chains to facilitate CP110 removal at the initial stage of ciliogenesis. Co-immunoprecipitation, ubiquitination assay, siRNA, immunofluorescence The Journal of cell biology High 34813648
2022 CP110-CEP97-CEP290 and centriolar satellites are required for aggresome assembly at the centrosome; depletion of these proteins impairs formation of the initial phosphorylated HSP27 ring that seeds aggresome growth. Senescent cells with low CP110 levels are defective in aggresome formation. CP110-CEP97-CEP290 and satellites are also required for aggregation of mutant huntingtin. High-resolution quantitative imaging, siRNA depletion, immunofluorescence Nature cell biology Medium 35411088
2022 In Drosophila embryos, CP110 and Cep97 form a complex at the distal end of centrioles whose levels oscillate during the cell cycle entrained by the CDK-Cyclin oscillator. Changing levels of CP110 and Cep97 alters the Plk4 oscillation and cartwheel growth at the proximal end, revealing crosstalk between distal- and proximal-end factors coordinating centriole growth. Live imaging in Drosophila embryos, quantitative fluorescence microscopy, genetic manipulation Journal of cell science Medium 35707992
2022 ENKD1 is a centrosomal protein that mediates CP110 removal from the mother centriole by competing with CEP97 for binding to CP110. ENKD1 depletion enhances the CP110-CEP97 interaction and detains CP110 at the mother centriole. Enkd1 knockout mice exhibit ciliogenesis defects in multiple organs; co-knockdown of CP110 reverses ciliogenesis defects in ENKD1-depleted cells. Co-immunoprecipitation, protein competition assay, super-resolution microscopy, Enkd1 knockout mouse, siRNA epistasis EMBO reports High 35301795
2023 EHD1 regulates CP110 ubiquitination during ciliogenesis by transporting centriolar satellites and the E3 ubiquitin ligase HERC2 to the mother centriole. HERC2 and MIB1 directly interact with and ubiquitinate CP110; HERC2 is required for ciliogenesis. Co-immunoprecipitation, ubiquitination assay, siRNA, immunofluorescence, centriolar satellite trafficking analysis EMBO reports High 37074924
2023 CCP5 and CCP6 retain CP110 at the mother centriole and suppress ciliogenesis. CCP5 directly interacts with CP110 through its N-terminus (identified by CoIP-MS). Loss of CCP5 or CCP6 causes CP110 disappearance from the mother centriole and abnormally increased ciliation in cycling RPE-1 cells; co-depletion of CCP5 and CCP6 synergistically increases this phenotype. Co-immunoprecipitation mass spectrometry, siRNA, immunofluorescence, overexpression BMC biology Medium 37226238
2023 ODF2 negatively regulates CP110 levels at centrioles; ODF2 knockdown reduces CP110 levels. ODF2 likely acts as a scaffold for NEURL4 or HYLS1, proteins involved in ubiquitin-dependent proteasomal degradation of CP110. Co-expression of ODF2 and HYLS1 promotes formation of tube-like centriolar structures. siRNA knockdown, rapamycin-mediated targeted recruitment, overexpression, immunofluorescence Cells Low 37681926
2025 p97/VCP (an AAA ATPase) is responsible for unfolding and extracting polyubiquitinated CP110 from the mother centriole. p97 knockdown or inhibition impairs ciliogenesis in a CP110-dependent manner, establishing p97-mediated unfolding as a prerequisite for CP110 degradation and ciliogenesis progression. siRNA knockdown, p97 inhibitor treatment, CP110 epistasis, immunofluorescence Molecular biology of the cell Medium 39785673
2025 BICD2 localizes to the mother centriole during ciliogenesis, directly binds CP110, and facilitates its removal to promote ciliogenesis. BICD2 depletion inhibits ciliogenesis and CP110 removal; CP110 knockdown rescues ciliogenesis defects in BICD2-deficient cells. zebrafish bicd2 morphants exhibit developmental abnormalities reversed by bicd2 mRNA or Cp110 depletion. Co-immunoprecipitation, siRNA, immunofluorescence, zebrafish morpholino epistasis EMBO reports Medium 41102520

Source papers

Stage 0 corpus · 40 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2007 Cep97 and CP110 suppress a cilia assembly program. Cell 385 17719545
2009 Control of centriole length by CPAP and CP110. Current biology : CB 281 19481458
2002 CP110, a cell cycle-dependent CDK substrate, regulates centrosome duplication in human cells. Developmental cell 256 12361598
2010 SCF(Cyclin F) controls centrosome homeostasis and mitotic fidelity through CP110 degradation. Nature 228 20596027
2008 CP110 suppresses primary cilia formation through its interaction with CEP290, a protein deficient in human ciliary disease. Developmental cell 220 18694559
2014 miR-34/449 miRNAs are required for motile ciliogenesis by repressing cp110. Nature 180 24899310
2011 Centriolar kinesin Kif24 interacts with CP110 to remodel microtubules and regulate ciliogenesis. Cell 165 21620453
2012 miR-129-3p controls cilia assembly by regulating CP110 and actin dynamics. Nature cell biology 132 22684256
2013 USP33 regulates centrosome biogenesis via deubiquitination of the centriolar protein CP110. Nature 111 23486064
2014 The CP110-interacting proteins Talpid3 and Cep290 play overlapping and distinct roles in cilia assembly. The Journal of cell biology 97 24421332
2006 CP110 cooperates with two calcium-binding proteins to regulate cytokinesis and genome stability. Molecular biology of the cell 80 16760425
2013 CP110 and its network of partners coordinately regulate cilia assembly. Cilia 70 24053599
2016 Centrosomal protein CP110 controls maturation of the mother centriole during cilia biogenesis. Development (Cambridge, England) 68 26965371
2018 M-Phase Phosphoprotein 9 regulates ciliogenesis by modulating CP110-CEP97 complex localization at the mother centriole. Nature communications 67 30375385
2016 Ciliary transcription factors and miRNAs precisely regulate Cp110 levels required for ciliary adhesions and ciliogenesis. eLife 61 27623009
2015 Centrin2 regulates CP110 removal in primary cilium formation. The Journal of cell biology 61 25753040
2012 Klp10A, a microtubule-depolymerizing kinesin-13, cooperates with CP110 to control Drosophila centriole length. Current biology : CB 51 22365849
2013 CP110 exhibits novel regulatory activities during centriole assembly in Drosophila. The Journal of cell biology 47 24297749
2015 CDK2 Inhibition Causes Anaphase Catastrophe in Lung Cancer through the Centrosomal Protein CP110. Cancer research 42 25808870
2015 MiR-129-3p promotes docetaxel resistance of breast cancer cells via CP110 inhibition. Scientific reports 40 26487539
2022 Aggresome assembly at the centrosome is driven by CP110-CEP97-CEP290 and centriolar satellites. Nature cell biology 33 35411088
2021 CEP78 functions downstream of CEP350 to control biogenesis of primary cilia by negatively regulating CP110 levels. eLife 31 34259627
2022 ENKD1 promotes CP110 removal through competing with CEP97 to initiate ciliogenesis. EMBO reports 26 35301795
2021 NudCL2 is an autophagy receptor that mediates selective autophagic degradation of CP110 at mother centrioles to promote ciliogenesis. Cell research 22 34480124
2021 LUBAC regulates ciliogenesis by promoting CP110 removal from the mother centriole. The Journal of cell biology 21 34813648
2016 miR-129-3p controls centrosome number in metastatic prostate cancer cells by repressing CP110. Oncotarget 21 26918338
2017 PLK4 phosphorylation of CP110 is required for efficient centriole assembly. Cell cycle (Georgetown, Tex.) 20 28562169
2015 Specific CP110 Phosphorylation Sites Mediate Anaphase Catastrophe after CDK2 Inhibition: Evidence for Cooperation with USP33 Knockdown. Molecular cancer therapeutics 20 26304236
2023 EHD1 promotes CP110 ubiquitination by centriolar satellite delivery of HERC2 to the mother centriole. EMBO reports 16 37074924
2024 Emerging insights into CP110 removal during early steps of ciliogenesis. Journal of cell science 13 38415788
2022 Centriole distal-end proteins CP110 and Cep97 influence centriole cartwheel growth at the proximal end. Journal of cell science 11 35707992
2023 lncRNA XIST/miR‑129‑2‑3p axis targets CCP110 to regulate the proliferation, invasion and migration of endometrial cancer cells. Experimental and therapeutic medicine 9 36911384
2023 ODF2 Negatively Regulates CP110 Levels at the Centrioles/Basal Bodies to Control the Biogenesis of Primary Cilia. Cells 7 37681926
2023 CCP5 and CCP6 retain CP110 and negatively regulate ciliogenesis. BMC biology 6 37226238
2023 CP110 and CEP135 localize near the proximal and distal centrioles of cattle and human spermatozoa. microPublication biology 5 37822686
2013 Cell biology: DUBing CP110 controls centrosome numbers. Current biology : CB 4 23701692
2024 CP110 and CEP135 Localize Near the Proximal Centriolar Remnants of Mice Spermatozoa. microPublication biology 3 38351906
2025 Valosin-containing protein p97 extracts capping protein CP110 from the mother centriole to promote ciliogenesis. Molecular biology of the cell 2 39785673
2024 Biallelic loss-of-function variants in the centriolar protein CCP110 leads to a ciliopathy-like phenotype. European journal of medical genetics 1 38857829
2025 BICD2 promotes ciliogenesis by facilitating CP110 removal from the mother centriole. EMBO reports 0 41102520