Affinage

CEP55

Centrosomal protein of 55 kDa · UniProt Q53EZ4

Length
464 aa
Mass
54.2 kDa
Annotated
2026-04-28
100 papers in source corpus 33 papers cited in narrative 33 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CEP55 is a coiled-coil centrosomal and midbody protein that serves as the master recruiter of the ESCRT membrane-scission machinery during cytokinetic abscission and additionally functions in PI3K/AKT signaling and cilia disassembly. During interphase CEP55 resides at the mother centriole; sequential phosphorylation by Erk2/Cdk1 (S425/S428) and Plk1 (S436), modulated by Pin1-dependent isomerization and iASPP-PP1-mediated dephosphorylation, controls its timely release from centrosomes and recruitment to the midbody via the centralspindlin complex (MKLP1–MgcRacGAP), where its dimeric EABR domain competitively binds ALIX and TSG101 through GPPX3Y motifs to nucleate ESCRT-III–dependent membrane abscission (PMID:16198290, PMID:18948538, PMID:21079244, PMID:29743530, PMID:16790497). Cep55 knockout mice reveal that most somatic cells complete abscission without CEP55, but neural progenitor cells are uniquely dependent on it—binucleate NPCs activate p53-dependent apoptosis—and Cep55-null mice also display abnormally elongated cilia owing to impaired Aurora A stabilization via the CCT chaperonin complex (PMID:32269212, PMID:33475699). Loss-of-function mutations in CEP55 cause MARCH syndrome (multinucleated neurons, anhydramnios, renal dysplasia, cerebellar hypoplasia, hydranencephaly), attributable to failed midbody localization and abscission (PMID:28264986).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2005 High

    The first mechanistic study established that CEP55 is a centrosomal protein whose sequential phosphorylation by Erk2/Cdk1 and Plk1 drives its mitotic redistribution to the midbody and is essential for cytokinesis, answering how CEP55 dynamics are controlled across the cell cycle.

    Evidence Site-directed mutagenesis of S425/S428/S436, in vitro kinase assays, siRNA knockdown with cytokinesis readout in HeLa cells

    PMID:16198290

    Open questions at the time
    • Upstream signal triggering Erk2/Cdk1 phosphorylation of CEP55 at mitotic entry was not defined
    • No structural basis for how phosphorylation alters CEP55 centrosome association
  2. 2006 High

    Identification of centralspindlin (MKLP1–MgcRacGAP) as the midbody-targeting platform for CEP55 established the epistatic hierarchy: centralspindlin recruits CEP55, which in turn organizes the Flemming body and v-SNARE trafficking for abscission.

    Evidence Direct in vitro binding of CEP55 to MKLP1, siRNA epistasis (centralspindlin KD abolishes CEP55 midbody localization), microtubule-bundling assay

    PMID:16790497

    Open questions at the time
    • Whether CEP55 microtubule-bundling activity is required for abscission was not tested
    • Structural basis of CEP55–MKLP1 interaction unresolved
  3. 2007 Medium

    Discovery that CEP55 forms a complex with PI3K p110α and activates PI3K/AKT signaling revealed a cytokinesis-independent oncogenic function, later validated in multiple cancer types.

    Evidence Co-IP of CEP55 with PI3K, in vitro PI3K kinase assay, nude mouse xenograft in HCC cells

    PMID:17237822 PMID:19337377

    Open questions at the time
    • Direct binding domain on CEP55 for PI3K not mapped
    • Whether PI3K activation requires CEP55 midbody localization or occurs independently was not determined
  4. 2008 High

    The crystal structure of the CEP55 EABR domain revealed the structural basis for ESCRT recruitment: an asymmetric dimeric coiled coil presents a single GPPX3Y-binding groove that competitively accommodates ALIX or TSG101, explaining why multiple CEP55 dimers are needed for abscission.

    Evidence X-ray crystallography at 2.0 Å resolution, biochemical competition assays with ALIX and TSG101 peptides

    PMID:18948538

    Open questions at the time
    • How full-length CEP55 oligomerizes at the midbody ring to provide multiple binding sites was not resolved
    • No structure of the N-terminal or central coiled-coil regions
  5. 2009 High

    Pin1 was identified as a co-factor that promotes Plk1-mediated phosphorylation and post-translational stabilization of CEP55 during mitosis, placing Pin1 in the same cytokinesis pathway as CEP55 through genetic epistasis.

    Evidence Pin1 KO MEFs, double-knockdown epistasis in HeLa, phosphorylation-site mutagenesis

    PMID:19638580 PMID:19855176

    Open questions at the time
    • Specific isomerization event (cis/trans conversion) on CEP55 was not demonstrated biochemically
    • Whether Pin1 acts catalytically or as a scaffold was unclear
  6. 2010 High

    Two studies resolved complementary aspects of CEP55 timing: Plk1 phosphorylation acts as a negative gate preventing premature CEP55 midbody recruitment until Plk1 is degraded at mitotic exit, while in male germ cells TEX14 hijacks the EABR binding site to permanently block ESCRT recruitment and maintain intercellular bridges.

    Evidence Plk1 phosphomutant expression and Plk1 inhibitor live imaging (abscission); TEX14 competitive binding assay and Tex14 KO mice (intercellular bridges)

    PMID:20176808 PMID:21079244

    Open questions at the time
    • How Plk1 degradation kinetics differ between cell types was not explored
    • Whether TEX14 competition is regulated during spermatogenesis was unknown
  7. 2011 Medium

    A p53–Plk1–CEP55 regulatory axis was defined: p53 suppresses both CEP55 transcription and Plk1-dependent CEP55 protein stability, linking tumor suppressor loss to CEP55 overexpression in cancer.

    Evidence p53 overexpression/siRNA, Plk1 inhibitor BI2356, luciferase promoter assay, immunoblotting in HCC cells

    PMID:22184120

    Open questions at the time
    • Whether p53 directly binds the CEP55 promoter or acts indirectly was not resolved
    • Contribution of transcriptional vs. post-translational regulation in vivo not quantified
  8. 2012 High

    BRCA2 was shown to facilitate CEP55–ALIX and CEP55–TSG101 complex formation at the midbody, establishing that cancer-associated BRCA2 mutations disrupt cytokinesis independently of homologous recombination.

    Evidence Reciprocal Co-IP, siRNA knockdown, cancer mutation analysis, immunofluorescence in HeLa cells

    PMID:22771033

    Open questions at the time
    • Mechanism by which BRCA2 promotes CEP55–ESCRT interaction (scaffolding vs. conformational) unresolved
    • Whether BRCA2-dependent abscission defects contribute to tumorigenesis in vivo was not tested
  9. 2015 High

    Zebrafish cep55 mutants demonstrated that CEP55 stabilizes AKT protein against proteasomal degradation in vivo, with constitutively active PI3K/AKT or proteasome inhibition partially rescuing the mutant phenotype.

    Evidence Zebrafish cep55 nonsense mutant, MG132 and constitutively active PIK3CA/AKT1 mRNA rescue

    PMID:25667221

    Open questions at the time
    • Direct physical mechanism by which CEP55 shields AKT from ubiquitin-proteasome degradation not defined
    • Which E3 ligase targets AKT in the absence of CEP55 was unknown
  10. 2017 High

    Identification of a causative CEP55 truncation in MARCH syndrome patients proved that human CEP55 is essential for brain development; the truncated protein fails to reach the midbody and causes multinucleation.

    Evidence Exome sequencing of affected families, patient-derived cell immunofluorescence, zebrafish cep55l morpholino rescue with full-length vs. truncated CEP55

    PMID:28264986

    Open questions at the time
    • Whether partial CEP55 function persists in heterozygous carriers was not assessed
    • Genotype–phenotype correlation across different CEP55 mutations not established
  11. 2018 Medium

    Multiple discoveries in 2018 expanded the regulatory and signaling landscape: iASPP-PP1 dephosphorylates CEP55 S436 to enable midbody recruitment; CEP55 signals through JAK2–STAT3 and interacts with SPAG5 to activate AKT; and CEP55 is a downstream effector of MEK1/2–MYC influencing mitotic cell fate in breast cancer.

    Evidence iASPP–PP1 Co-IP and phospho-specific blotting; JAK2 and SPAG5 Co-IP with inhibitor rescue; CEP55 KD/overexpression in breast cancer syngeneic models with MEK/PLK1 epistasis

    PMID:29743530 PMID:30089483 PMID:30096813 PMID:30108112

    Open questions at the time
    • JAK2 and SPAG5 interactions each rely on single Co-IP studies
    • Whether iASPP-PP1 specificity for CEP55 S436 extends to other Plk1 substrates was untested
    • Relative contribution of PI3K/AKT vs. JAK2/STAT3 arms to CEP55 oncogenic function unclear
  12. 2019 Medium

    Structure–function analysis identified two NEMO-like ubiquitin-binding domains (NOA and ZF) in CEP55 that are essential for abscission, establishing that CEP55 participates in non-degradative ubiquitin signaling at the midbody.

    Evidence In vitro domain characterization, structure-guided mutagenesis, CEP55 KD reconstitution with abscission readout

    PMID:31605944

    Open questions at the time
    • Identity of the ubiquitinated target(s) recognized by CEP55 UBDs at the midbody is unknown
    • Structural model of full-length CEP55 including both UBDs and EABR not available
  13. 2020 High

    Cep55 knockout mice revealed that CEP55 is dispensable for most somatic cell divisions but essential in neural progenitor cells, where abscission failure triggers a cell-type-specific p53-dependent apoptosis that drives microcephaly.

    Evidence Cep55 KO and Cep55/p53 double-KO mice, quantitative live abscission assays in NSCs vs. fibroblasts, ESCRT localization

    PMID:32269212 PMID:33622776

    Open questions at the time
    • Why NPCs but not fibroblasts require CEP55 for abscission is mechanistically unexplained
    • Alternative abscission machinery compensating in fibroblasts not identified
  14. 2021 High

    A cilia-regulatory function was uncovered: CEP55 stabilizes Aurora A kinase by facilitating its association with the CCT chaperonin complex, and Cep55-null mice display elongated cilia and Meckel–Gruber syndrome features, linking CEP55 to ciliopathy.

    Evidence Cep55 KO mice, Co-IP of CEP55 with Aurora A and CCT subunits, cilia length quantification

    PMID:33475699

    Open questions at the time
    • Whether CEP55 directly contacts CCT or acts as an adaptor bringing Aurora A to CCT is not resolved
    • How CEP55 subcellular pool at centrosomes vs. midbody differentially controls cilia vs. abscission is unclear
  15. 2022 Medium

    NEDD4L was identified as an E3 ubiquitin ligase targeting CEP55 for degradation, with the miR-342-3p/NEDD4L axis regulating CEP55 protein levels and downstream PI3K/AKT/mTOR signaling in renal cell carcinoma.

    Evidence Ubiquitination assay, miR-342-3p/NEDD4L luciferase reporter, xenograft rescue

    PMID:37305161

    Open questions at the time
    • Specific lysine residues on CEP55 ubiquitinated by NEDD4L not mapped
    • Whether NEDD4L-mediated degradation is cell-cycle-regulated was not tested
  16. 2025 Medium

    Recent work identified USP8 as a deubiquitinase stabilizing CEP55 and showed CEP55 binds CHMP6 (ESCRT-III) to promote ferroptosis resistance, while ILF3 stabilizes CEP55 mRNA, broadening the regulatory inputs controlling CEP55 abundance.

    Evidence USP8 deubiquitination assay, CEP55–CHMP6 Co-IP, xenograft rescue; ILF3 RIP and mRNA stability assay in breast cancer cells

    PMID:39871389 PMID:40925844

    Open questions at the time
    • CEP55–CHMP6 interaction confirmed by single Co-IP only
    • Whether ferroptosis resistance is a direct consequence of ESCRT function or PI3K/AKT signaling is undetermined
    • ILF3-CEP55 mRNA interaction site not mapped

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key open questions include why neural progenitor cells uniquely depend on CEP55 for abscission while most somatic cells do not, what the ubiquitinated substrates recognized by CEP55's UBDs are, and how CEP55's cytokinetic and PI3K/AKT signaling functions are coordinated in space and time.
  • No structural model of full-length CEP55 exists
  • Alternative abscission machinery in CEP55-independent cells not identified
  • Ubiquitin targets of CEP55 UBDs at the midbody unknown
  • Spatial segregation of cytokinetic vs. signaling pools of CEP55 not resolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 4 GO:0060090 molecular adaptor activity 3 GO:0008092 cytoskeletal protein binding 1
Localization
GO:0005815 microtubule organizing center 2 GO:0005856 cytoskeleton 2 GO:0005829 cytosol 1
Pathway
R-HSA-1640170 Cell Cycle 6 R-HSA-162582 Signal Transduction 5 R-HSA-1852241 Organelle biogenesis and maintenance 1
Partners
ALIXAURKAIASPPMKLP1PIK3CAPLK1TEX14TSG101
Complex memberships
ESCRT-I (via TSG101)ESCRT-III (via CHMP6)centralspindlin (MKLP1–MgcRacGAP)

Evidence

Reading pass · 33 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2005 CEP55 localizes to the mother centriole during interphase. Erk2/Cdk1-dependent phosphorylation at S425 and S428 triggers centrosome dissociation at mitotic entry. S425/428 phosphorylation enables interaction with Plk1, which then phosphorylates CEP55 at S436. This phosphorylation cascade is required for CEP55 recruitment to the midbody and completion of cytokinesis; phosphorylation-deficient mutants cause cytokinesis failure. Site-directed mutagenesis, in vitro kinase assays, Co-IP, siRNA knockdown with cytokinesis readout, immunofluorescence localization Developmental cell High 16198290
2006 CEP55 directly binds MKLP1 in vitro and associates with the MKLP1-MgcRacGAP centralspindlin complex in vivo. CEP55 is a microtubule-bundling protein. Knockdown of centralspindlin abolishes CEP55 localization to the spindle midzone, placing CEP55 downstream of centralspindlin. CEP55 depletion causes absence of the Flemming body and mislocalization of midbody components, and controls endobrevin (v-SNARE) localization for membrane fusion during abscission. In vitro binding assay, Co-IP, siRNA knockdown, immunofluorescence, microtubule-bundling assay Molecular biology of the cell High 16790497
2006 CEP55 homodimerizes (detected by co-immunoprecipitation) and localizes to the centrosome throughout mitosis and to the midbody during cytokinesis via coiled-coil domains. Overexpression does not affect microtubule nucleation. Co-immunoprecipitation, EGFP-fusion live imaging, immunofluorescence, nocodazole/taxol treatment Genomics Medium 16406728
2008 CEP55 recruits both ESCRT-I (via TSG101) and ALIX to the midbody through its EABR (ESCRT and ALIX-binding region). Crystal structure at 2.0 Å shows EABR forms an asymmetric dimeric parallel coiled coil with a single binding site for ALIX or TSG101 GPPX3Y peptides that compete with each other. Both ALIX and ESCRT-I are required for cytokinesis, implying multiple CEP55 dimers are needed. X-ray crystallography (2.0 Å), biochemical competition assays, peptide binding Science High 18948538
2009 Pin1 (peptidyl-prolyl isomerase) binds to CEP55 at the midbody ring and promotes Plk1-mediated phosphorylation of CEP55, which is critical for cytokinesis. Pin1 KO MEFs show cytokinesis delay; Pin1 knockdown does not further worsen cytokinesis in CEP55-depleted cells, indicating they act in the same pathway. Pin1 KO mouse embryonic fibroblasts, HeLa siRNA depletion, epistasis analysis, immunofluorescence, Co-IP Cancer research High 19638580
2009 CEP55 (FLJ10540) forms a complex with the p110-alpha catalytic subunit of PI3K and activates PI3K kinase activity, driving AKT phosphorylation and oncogenic cell transformation. Knockdown of CEP55 destabilizes the PI3K p110/p85 complex. Co-immunoprecipitation, PI3K kinase activity assay, siRNA knockdown, nude mouse tumorigenicity assay PloS one Medium 19337377
2007 CEP55 (FLJ10540) forms a complex with PI3K and activates PI3K activity, mediating oncogenic cell transformation via the PI3K/AKT pathway in hepatocellular carcinoma cells. Co-immunoprecipitation, PI3K kinase activity assay, anchorage-independent growth, nude mouse xenograft Oncogene Medium 17237822
2009 Pin1 promotes post-translational stabilization of CEP55 during mitosis; mutation of Pin1 binding sites or Plk1 phosphorylation site in CEP55 reduces its mitotic stability. Plk1 overexpression increases CEP55 levels, linking Pin1/Plk1 to CEP55 protein stability required for cytokinesis. siRNA knockdown, phosphorylation-site mutagenesis, immunoblotting for protein stability, Pin1 KO MEFs Cell cycle Medium 19855176
2010 Plk1 phosphorylates CEP55 in trans during mitotic exit, preventing premature recruitment of CEP55 to the anaphase spindle. Only after Plk1 degradation can CEP55 target the midbody to promote abscission. A Plk1-site mutant of CEP55 is prematurely recruited to the anaphase spindle and fails to support abscission. Blocking Plk1 degradation prevents CEP55 midbody recruitment. Phosphomutant expression, Plk1 inhibitor treatment (BI2536, GW842862), live-cell imaging, immunofluorescence The Journal of cell biology High 21079244
2010 TEX14 uses a conserved GPPX3Y motif to bind strongly to CEP55 and block the same GPPX3Y motifs of ALIX and TSG101 from binding CEP55, thereby preventing abscission and establishing stable intercellular bridges in male germ cells. CEP55 is a stable component of the intercellular bridge in testes. Biochemical enrichment of intercellular bridges, Co-IP, competitive binding assay, TEX14 KO mice Molecular and cellular biology High 20176808
2011 p53 negatively regulates CEP55 protein stability and promoter activity through suppression of Plk1; Plk1 is a positive regulator of CEP55 post-translational stability. Overexpression of Plk1 or knockdown of p53 enhances CEP55 stability; the Plk1 inhibitor BI2356 prevents CEP55 accumulation in p53-depleted cells, defining a p53–Plk1–CEP55 regulatory axis. p53 overexpression/siRNA knockdown, Plk1 inhibitor, luciferase promoter assay, immunoblotting The Journal of biological chemistry Medium 22184120
2012 BRCA2 localizes to the midbody through interaction with Filamin A, where it facilitates formation of CEP55-ALIX and CEP55-TSG101 complexes and proper recruitment of ESCRT-associated proteins during abscission. Cancer-associated BRCA2 mutations disrupt these interactions and increase cytokinetic defects without affecting homologous recombination. Co-IP, siRNA knockdown, immunofluorescence, cancer mutation analysis Developmental cell High 22771033
2015 In zebrafish, cep55 loss-of-function causes destabilization of Akt protein; constitutively active PIK3CA or AKT1 partially rescues cep55 mutant phenotype. Proteasome inhibitor MG132 also partially rescues, indicating CEP55 promotes Akt stability by protecting it from proteasomal degradation. Zebrafish cep55 nonsense mutant, morpholino knockdown, mRNA rescue, pharmacological rescue (MG132), constitutively active PI3K/AKT expression FASEB journal High 25667221
2017 A truncating mutation in CEP55 causes MARCH syndrome. The truncated protein fails to localize to the midbody, leading to abscission failure and multinucleated daughter cells. Full-length but not truncated CEP55 rescues zebrafish cep55l knockdown phenotypes. Exome sequencing, patient-derived cell immunofluorescence, zebrafish morpholino knockdown, mRNA rescue with full-length vs. truncated CEP55 Journal of medical genetics High 28264986
2018 iASPP acts as a PP1-targeting subunit that facilitates PP1-CEP55 interaction to remove Plk1-mediated Ser436 phosphorylation from CEP55 during late mitosis, enabling timely CEP55 recruitment to the midbody. iASPP depletion results in abnormal midbody structure and failed cytokinesis. Protein affinity purification, Co-IP, phospho-specific immunoblotting, siRNA knockdown with cytokinesis readout Cell death & disease Medium 29743530
2018 CEP55 overexpression dictates cell fate during perturbed mitosis; it is a downstream effector of the MEK1/2-MYC axis. Loss of CEP55 sensitizes breast cancer cells to anti-mitotic agents through premature CDK1/cyclin B activation and caspase-dependent mitotic death. Blocking MEK1/2-PLK1 signaling reduces breast tumor outgrowth in vivo. CEP55 KD/overexpression in breast cancer cells and syngeneic mouse models, CDK1 activity assays, epistasis (MEK inhibitors, PLK1 inhibition) EMBO molecular medicine Medium 30108112
2018 SPAG5 interacts with CEP55 (detected by Co-IP) to trigger phosphorylation of AKT at Ser473 and activate PI3K/AKT signaling in hepatocellular carcinoma. Inhibition of PI3K/AKT markedly attenuates SPAG5-mediated cell growth. Co-immunoprecipitation, AKT phosphorylation assay, in vitro/in vivo tumor models, PI3K/AKT inhibitor treatment Molecular cancer Medium 30089483
2018 CEP55 overexpression in mice causes hyperactivation of PI3K/Akt signaling in testis, increased phosphorylation of FoxO1 suppressing its nuclear retention, enrichment of PLZF-positive undifferentiated spermatogonia, and progressive germ cell loss causing male sterility. Ubiquitous Cep55 transgenic mice, phospho-Akt/FoxO1 immunoblotting, immunofluorescence, gene expression analysis FASEB journal Medium 29683733
2018 CEP55 physically interacts with JAK2 and promotes its phosphorylation, activating downstream STAT3 signaling and target genes MMP2/9, thereby promoting HCC cell migration and invasion. Blocking JAK2 or STAT3 blunts the migration/invasion stimulated by CEP55 overexpression. Co-immunoprecipitation, phospho-JAK2/STAT3 immunoblotting, JAK2/STAT3 inhibitor rescue, transwell migration assay Cells Medium 30096813
2019 CEP55 contains two NEMO-like ubiquitin-binding domains (NOA, a dimeric coiled coil; ZF, a UBZ scaffold). Structure-guided mutations in either domain cause severe abscission defects in reconstituted CEP55-KD cells. The ZF domain's ubiquitin-receptor function can be replaced by other UBZ-family domains, indicating CEP55 participates in non-degradative ubiquitin signaling during cytokinetic abscission. In vitro domain characterization, structure-guided mutagenesis, CEP55 KD reconstitution assays, abscission phenotype readout iScience Medium 31605944
2019 CEP55 depletion during meiotic anaphase I in mouse oocytes causes persistent Cdk1 activity due to inadequate inhibitory Cdk1 phosphorylation consequent on failure to suppress Cdc25 phosphatase, identifying a proteolysis-independent step required for anaphase I exit. siRNA injection in mouse oocytes, Cdk1 kinase activity assay, Cdc25 analysis, live imaging Journal of cell science Medium 31427428
2020 Cep55 knockout mice show that Cep55 is dispensable for most somatic cell divisions but required specifically for neural progenitor cell (NPC) abscission and survival. Cep55 facilitates ESCRT recruitment and timely microtubule disassembly during abscission in NPCs. Binucleate NPCs (but not fibroblasts) elevate p53 and undergo apoptosis; double KO of p53 and Cep55 blocks apoptosis but only partially rescues brain size. Cep55 and p53/Cep55 double-KO mice, quantitative abscission assays in fixed and live NSCs, ESCRT localization, p53/apoptosis analysis Nature communications High 32269212
2020 Cep55 overexpression in MEFs compromises the Chk1-dependent S-phase checkpoint, causing increased replication speed and DNA damage, and a prolonged aberrant mitosis. PI3K/Akt inhibition or expression of Akt-insensitive Chk1 (S280A) rescues this phenotype, placing Cep55→Pi3k/Akt→Chk1 in a pathway regulating genomic stability. Cep55 overexpression also causes microtubule stabilization. Cep55 transgenic MEFs, Chk1 phosphorylation assay, DNA fiber assay, pharmacological PI3K/Akt inhibition, Chk1 S280A mutant rescue Communications biology Medium 33087841
2021 CEP55 promotes cilia disassembly by interacting with and stabilizing Aurora A kinase through facilitation of the chaperonin CCT complex to Aurora A. Cep55-/- mice exhibit abnormally elongated cilia and Meckel-Gruber syndrome features. CEP55 mutations in MKS cause failure of cilia disassembly. Cep55 KO mice, Co-IP of CEP55 with Aurora A and CCT complex, cilia length measurement, immunofluorescence The Journal of cell biology High 33475699
2021 Loss of Cep55 in mouse cortical NSCs causes abscission defects (increased failure rate and slowed abscission), and binucleate NSCs activate p53-dependent apoptosis. Most NSCs complete abscission without Cep55, but failures trigger a cell-type-specific p53 response not seen in fibroblasts. Cep55 KO and p53/Cep55 double-KO mice, quantitative live and fixed abscission assays, p53/apoptosis immunostaining The Journal of neuroscience High 33622776
2016 Integrin-mediated FAK-Src signaling decelerates PLK1 degradation at the midbody, thereby controlling the timing of CEP55 accumulation and subsequent ALIX/TSG101/CHMP4B (ESCRT-III) recruitment. In non-adherent cells, PLK1 disappears more rapidly and CEP55 cannot efficiently recruit ESCRT components, causing abscission failure. FAK/Src inhibitor treatment, PLK1 inhibition, immunofluorescence of midbody proteins, adherent vs. non-adherent cell comparison Oncotarget Medium 27127172
2022 NEDD4L ubiquitinates CEP55 and promotes its degradation; M2-macrophage-derived exosomal miR-342-3p suppresses NEDD4L, thereby elevating CEP55 protein via reduced ubiquitination and activating the PI3K/AKT/mTOR pathway in renal cell carcinoma. Ubiquitination assay, miR-342-3p/NEDD4L luciferase reporter, Co-IP, in vivo xenograft Oncology research Medium 37305161
2021 CEP55 loading into exosomes does not occur via canonical early-to-late endosome trafficking but instead through Alix-mediated recruitment to secretory CD63-positive late endosomes. Mutation of the CEP55-Alix interaction site strongly reduces CEP55 dot formation and CEP55 presence in extracellular vesicles. High-resolution microscopy, EGFP-CEP55 trafficking analysis, Rab5/Rab7/CD63 marker co-localization, CEP55-Alix interaction-site mutagenesis Journal of extracellular vesicles Medium 39976236
2021 UXT is a novel TSG101-interacting protein; CEP55 is recruited to TSG101-containing cytoplasmic vesicles and degraded via the lysosome pathway. UXT depletion promotes TSG101 vesicle-lysosome association and enhances CEP55 degradation upon TSG101 overexpression. Co-IP, lysosome inhibitor treatment, immunofluorescence, siRNA depletion Biochemical and biophysical research communications Low 33486193
2023 α-catenin physically interacts with CEP55 in the cytoplasm of HCC cells (identified by BioID mass spectrometry and confirmed by Co-IP and proximity ligation), stabilizing CEP55 protein. CEP55 is also transcriptionally induced by a FoxM1/TEAD/YAP complex. CEP55 supports HCC cell migration in conjunction with α-catenin but does not affect proliferation. BioID proximity labeling + mass spectrometry, Co-IP, proximity ligation assay, chromatin immunoprecipitation, siRNA knockdown Cell communication and signaling Medium 37381005
2025 USP8 deubiquitinates CEP55 to maintain its protein stability; CEP55 binds to CHMP6 (confirmed by Co-IP) and promotes its expression, thereby facilitating ferroptosis resistance and macrophage M2 polarization in TNBC. USP8 knockdown effects on tumor growth are reversed by CEP55 overexpression. Ubiquitination/deubiquitination assay, Co-IP, siRNA knockdown, flow cytometry (ferroptosis markers, macrophage polarization), xenograft model Clinical breast cancer Medium 40925844
2025 ILF3 stabilizes CEP55 mRNA (confirmed by RIP and mRNA stability assay), maintaining CEP55 protein levels in breast cancer cells. ILF3 depletion reduces CEP55 expression, impairs cell growth and invasion, and promotes ferroptosis; CEP55 restoration rescues these effects. RNA immunoprecipitation (RIP), CEP55 mRNA stability assay, siRNA knockdown, xenograft model Hereditas Medium 39871389
2025 CEP55 promotes resistance to cisplatin in prostate cancer by regulating CDK1 phosphorylation at Tyr15, driving neuroendocrine differentiation. CEP55 overexpression enhances NEPC biomarker expression; knockdown reduces proliferation and invasiveness. scRNA-seq analysis, in vitro/in vivo CEP55 KD/overexpression, CDK1 Tyr15 phosphorylation immunoblot, clinical sample validation Cancer pathogenesis and therapy Low 41403895

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 Cdk1/Erk2- and Plk1-dependent phosphorylation of a centrosome protein, Cep55, is required for its recruitment to midbody and cytokinesis. Developmental cell 271 16198290
2008 Midbody targeting of the ESCRT machinery by a noncanonical coiled coil in CEP55. Science (New York, N.Y.) 219 18948538
2006 Cep55, a microtubule-bundling protein, associates with centralspindlin to control the midbody integrity and cell abscission during cytokinesis. Molecular biology of the cell 196 16790497
2010 Plk1 negatively regulates Cep55 recruitment to the midbody to ensure orderly abscission. The Journal of cell biology 126 21079244
2009 VEGFA upregulates FLJ10540 and modulates migration and invasion of lung cancer via PI3K/AKT pathway. PloS one 114 19337377
2015 Beyond cytokinesis: the emerging roles of CEP55 in tumorigenesis. Oncogene 112 25915844
2010 Downstream targets of FOXM1: CEP55 and HELLS are cancer progression markers of head and neck squamous cell carcinoma. Oral oncology 79 20400365
2007 FLJ10540-elicited cell transformation is through the activation of PI3-kinase/AKT pathway. Oncogene 79 17237822
2009 Cep55/c10orf3, a tumor antigen derived from a centrosome residing protein in breast carcinoma. Journal of immunotherapy (Hagerstown, Md. : 1997) 78 19609239
2009 Expression of FLJ10540 is correlated with aggressiveness of oral cavity squamous cell carcinoma by stimulating cell migration and invasion through increased FOXM1 and MMP-2 activity. Oncogene 72 19525975
2006 The novel centrosomal associated protein CEP55 is present in the spindle midzone and the midbody. Genomics 72 16406728
2018 SPAG5 interacts with CEP55 and exerts oncogenic activities via PI3K/AKT pathway in hepatocellular carcinoma. Molecular cancer 71 30089483
2012 BRCA2 localization to the midbody by filamin A regulates cep55 signaling and completion of cytokinesis. Developmental cell 71 22771033
2018 CEP55 is a determinant of cell fate during perturbed mitosis in breast cancer. EMBO molecular medicine 69 30108112
2010 TEX14 interacts with CEP55 to block cell abscission. Molecular and cellular biology 68 20176808
2014 CEP55 contributes to human gastric carcinoma by regulating cell proliferation. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 62 24390615
2019 MiR-195-5p Inhibits Proliferation and Induces Apoptosis of Non-Small Cell Lung Cancer Cells by Targeting CEP55. OncoTargets and therapy 60 31920335
2019 CEP55 promotes epithelial-mesenchymal transition in renal cell carcinoma through PI3K/AKT/mTOR pathway. Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico 55 30607788
2017 A truncating mutation in CEP55 is the likely cause of MARCH, a novel syndrome affecting neuronal mitosis. Journal of medical genetics 51 28264986
2016 Lentivirus-mediated knockdown of CEP55 suppresses cell proliferation of breast cancer cells. Bioscience trends 47 26902787
2018 MiR-144 suppresses proliferation, invasion, and migration of breast cancer cells through inhibiting CEP55. Cancer biology & therapy 46 29561704
2018 Cep55 overexpression causes male-specific sterility in mice by suppressing Foxo1 nuclear retention through sustained activation of PI3K/Akt signaling. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 45 29683733
2018 Circ-8073 regulates CEP55 by sponging miR-449a to promote caprine endometrial epithelial cells proliferation via the PI3K/AKT/mTOR pathway. Biochimica et biophysica acta. Molecular cell research 45 29800603
2006 Elevated expression of C10orf3 (chromosome 10 open reading frame 3) is involved in the growth of human colon tumor. Oncogene 45 16170351
2018 CEP55 Promotes Cell Motility via JAK2⁻STAT3⁻MMPs Cascade in Hepatocellular Carcinoma. Cells 44 30096813
2020 Cep55 promotes cytokinesis of neural progenitors but is dispensable for most mammalian cell divisions. Nature communications 42 32269212
2019 Genes CEP55, FOXD3, FOXF2, GNAO1, GRIA4, and KCNA5 as potential diagnostic biomarkers in colorectal cancer. BMC medical genomics 38 30987631
2009 The peptidyl-prolyl isomerase Pin1 regulates cytokinesis through Cep55. Cancer research 38 19638580
2010 The feasibility of Cep55/c10orf3 derived peptide vaccine therapy for colorectal carcinoma. Experimental and molecular pathology 37 20950610
2017 A nonsense mutation in CEP55 defines a new locus for a Meckel-like syndrome, an autosomal recessive lethal fetal ciliopathy. Clinical genetics 33 28295209
2009 Cep55 stabilization is required for normal execution of cytokinesis. Cell cycle (Georgetown, Tex.) 33 19855176
2020 Cep55 overexpression promotes genomic instability and tumorigenesis in mice. Communications biology 29 33087841
2018 CEP55 promotes cell proliferation and inhibits apoptosis via the PI3K/Akt/p21 signaling pathway in human glioma U251 cells. Oncology letters 28 29552118
2015 Cep55 regulates spindle organization and cell cycle progression in meiotic oocyte. Scientific reports 28 26582107
2012 FLJ10540 is associated with tumor progression in nasopharyngeal carcinomas and contributes to nasopharyngeal cell proliferation, and metastasis via osteopontin/CD44 pathway. Journal of translational medicine 28 22591637
2021 Human bone marrow mesenchymal stem cell-derived extracellular vesicles impede the progression of cervical cancer via the miR-144-3p/CEP55 pathway. Journal of cellular and molecular medicine 27 33417281
2020 miR-34a/c induce caprine endometrial epithelial cell apoptosis by regulating circ-8073/CEP55 via the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR pathways. Journal of cellular physiology 27 32474960
2018 CEP55 promotes the proliferation and invasion of tumour cells via the AKT signalling pathway in osteosarcoma. Carcinogenesis 26 29579156
2016 Integrin signaling via FAK-Src controls cytokinetic abscission by decelerating PLK1 degradation and subsequent recruitment of CEP55 at the midbody. Oncotarget 26 27127172
2014 Expression and clinical significance of Centrosomal protein 55 (CEP55) in human urinary bladder transitional cell carcinoma. Immunobiology 26 25178936
2011 Centrosomal protein 55 (Cep55) stability is negatively regulated by p53 protein through Polo-like kinase 1 (Plk1). The Journal of biological chemistry 25 22184120
2022 Macrophage-derived exosomal miR-342-3p promotes the progression of renal cell carcinoma through the NEDD4L/CEP55 axis. Oncology research 24 37305161
2021 Loss of Coiled-Coil Protein Cep55 Impairs Neural Stem Cell Abscission and Results in p53-Dependent Apoptosis in Developing Cortex. The Journal of neuroscience : the official journal of the Society for Neuroscience 24 33622776
2018 MicroRNA-144-3p inhibits cell proliferation and induces cell apoptosis in prostate cancer by targeting CEP55. American journal of translational research 23 30210684
2015 Cep55 regulates embryonic growth and development by promoting Akt stability in zebrafish. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 23 25667221
2021 The RNA-helicase DDX21 upregulates CEP55 expression and promotes neuroblastoma. Molecular oncology 22 33497018
2020 SP1-induced upregulation of lncRNA CTBP1-AS2 accelerates the hepatocellular carcinoma tumorigenesis through targeting CEP55 via sponging miR-195-5p. Biochemical and biophysical research communications 22 32988587
2019 An Amish founder variant consolidates disruption of CEP55 as a cause of hydranencephaly and renal dysplasia. European journal of human genetics : EJHG 22 30622327
2011 Linking expression of FOXM1, CEP55 and HELLS to tumorigenesis in oropharyngeal squamous cell carcinoma. The Laryngoscope 22 22109759
2021 CEP55 promotes cilia disassembly through stabilizing Aurora A kinase. The Journal of cell biology 21 33475699
2016 Suppression of CEP55 reduces cell viability and induces apoptosis in human lung cancer. Oncology reports 21 27633074
2018 CEP55 promotes the proliferation, migration and invasion of esophageal squamous cell carcinoma via the PI3K/Akt pathway. OncoTargets and therapy 20 30050313
2020 Tumor promoting effects of circRNA_001287 on renal cell carcinoma through miR-144-targeted CEP55. Journal of experimental & clinical cancer research : CR 19 33256799
2015 Suppression of Aurora-A-FLJ10540 signaling axis prohibits the malignant state of head and neck cancer. Molecular cancer 18 25889801
2021 Cep55: abscission boss or assistant? Trends in cell biology 17 34400044
2021 Inhibition of miR-144-3p exacerbates non-small cell lung cancer progression by targeting CEP55. Acta biochimica et biophysica Sinica 17 34435195
2019 CEP55 promoted the migration, invasion and neuroshpere formation of the glioma cell line U251. Neuroscience letters 17 31005653
2018 iASPP-PP1 complex is required for cytokinetic abscission by controlling CEP55 dephosphorylation. Cell death & disease 16 29743530
2023 Hsa-miR-195-5p Inhibits Autophagy and Gemcitabine Resistance of Lung Adenocarcinoma Cells via E2F7/CEP55. Biochemical genetics 15 36658310
2010 Characterization of centrosomal proteins Cep55 and pericentrin in intercellular bridges of mouse testes. Journal of cellular biochemistry 15 20186884
2023 CEP55 as a Promising Immune Intervention Marker to Regulate Tumor Progression: A Pan-Cancer Analysis with Experimental Verification. Cells 13 37887301
2019 First meiotic anaphase requires Cep55-dependent inhibitory cyclin-dependent kinase 1 phosphorylation. Journal of cell science 13 31427428
2018 Assessment of CEP55, PLK1 and FOXM1 expression in patients with bladder cancer in comparison with healthy individuals. Cancer investigation 13 30277841
2018 MicroRNA-144-3p inhibits cell proliferation and promotes apoptosis in castration-resistant prostate cancer by targeting CEP55. European review for medical and pharmacological sciences 13 30536308
2024 Centrosomal Protein 55 (CEP55) Drives Immune Exclusion and Resistance to Immune Checkpoint Inhibitors in Colorectal Cancer. Vaccines 11 38250876
2023 α-catenin interaction with YAP/FoxM1/TEAD-induced CEP55 supports liver cancer cell migration. Cell communication and signaling : CCS 11 37381005
2014 Upregulation of FLJ10540, a PI3K-association protein, in rostral ventrolateral medulla impairs brain stem cardiovascular regulation during mevinphos intoxication. Biochemical pharmacology 11 25449601
2023 CEP55 as a promising biomarker and therapeutic target on gallbladder cancer. Frontiers in oncology 10 37274251
2022 CEP55 3'-UTR promotes epithelial-mesenchymal transition and enhances tumorigenicity of bladder cancer cells by acting as a ceRNA regulating miR-497-5p. Cellular oncology (Dordrecht, Netherlands) 10 36374443
2019 Two NEMO-like Ubiquitin-Binding Domains in CEP55 Differently Regulate Cytokinesis. iScience 10 31605944
2024 ALKBH5 activates CEP55 transcription through m6A demethylation in FOXP2 mRNA and expedites cell cycle entry and EMT in ovarian cancer. Biology direct 9 39511642
2021 CEP55 Inhibitor: Extensive Computational Approach Defining a New Target of Cell Cycle Machinery Agent. Advanced pharmaceutical bulletin 9 35517890
2019 Furosine Posed Toxic Effects on Primary Sertoli Cells through Regulating Cep55/NF-κB/PI3K/Akt/FOX01/TNF-α Pathway. International journal of molecular sciences 9 31366014
2018 PTEN/FLJ10540/PI3K/Akt cascade in experimental brain stem death: A newfound role for a classical tumorigenic signaling pathway. Biochemical pharmacology 9 30008438
2024 Pan-cancer analysis of oncogenic role of CEP55 and experiment validation in clear cell renal cell carcinoma. Scientific reports 8 39550427
2022 KMT2B promotes the growth of renal cell carcinoma via upregulation of SNHG12 expression and promotion of CEP55 transcription. Cancer cell international 8 35597996
2020 Expanding the spectrum of CEP55-associated disease to viable phenotypes. American journal of medical genetics. Part A 8 32100459
2020 The function and molecular mechanism of CEP55 in anaplastic thyroid cancer. European review for medical and pharmacological sciences 8 33015797
2018 Correlations Between mRNA Levels of Centrosomal Protein 55 (CEP55) and Clinical Features of Patients with Lung Cancer. Medical science monitor : international medical journal of experimental and clinical research 8 29750778
2022 Circ_0136666 aggravates osteosarcoma development through mediating miR-1244/CEP55 axis. Journal of orthopaedic surgery and research 7 36109749
2024 SPI1-mediated transcriptional activation of CEP55 promotes the malignant growth of triple-negative breast cancer and M2 macrophage polarization. Pathology, research and practice 6 39197215
2025 RNA binding protein ILF3 increases CEP55 mRNA stability to enhance malignant potential of breast cancer cells and suppress ferroptosis. Hereditas 5 39871389
2024 miR-378a-5p exerts tumor-suppressive effects on esophageal squamous cell carcinoma after neoadjuvant immunotherapy by downregulating APOC1/CEP55. Scientific reports 5 38172247
2023 A Comprehensive Pan-Cancer Analysis Identifies CEP55 as a Potential Oncogene and Novel Therapeutic Target. Diagnostics (Basel, Switzerland) 5 37175004
2022 Construction of lncRNA TYMSOS/hsa-miR-101-3p/CEP55 and TYMSOS/hsa-miR-195-5p/CHEK1 Axis in Non-small Cell Lung Cancer. Biochemical genetics 5 36352081
2021 MicroRNA-148a-3p suppresses cell proliferation and migration of esophageal carcinoma by targeting CEP55. Cellular & molecular biology letters 5 34952571
2020 MicroRNA-449a Suppresses Mouse Spermatogonia Proliferation via Inhibition of CEP55. Reproductive sciences (Thousand Oaks, Calif.) 5 33095425
2019 Involvement of the centrosomal protein 55 (cep55) gene in zebrafish head formation. Genes to cells : devoted to molecular & cellular mechanisms 4 31365163
2025 Mechanism of Centrosomal Protein 55 (CEP55) Loading Into Exosomes. Journal of extracellular vesicles 3 39976236
2025 Cuproptosis-related gene CEP55 as a biomarker of pancreatic adenocarcinoma via multi-omics techniques and experimental validation. Radiology and oncology 3 40677006
2019 [CEP55 may be a potential therapeutic target for non-obstructive azoospermia with maturation arrest]. Nan fang yi ke da xue xue bao = Journal of Southern Medical University 3 31640955
2025 CEP55: Implications for Immunotherapy and Survival in Hepatocellular Carcinoma. Combinatorial chemistry & high throughput screening 2 38847172
2023 CEP55, serving as a diagnostic marker gene for osteosarcoma, triggers the JAK2-STAT3-MMPs axis. Annals of medicine and surgery (2012) 2 38222763
2025 CEP55 Promotes Acral Melanoma Progression via MAPK Pathway and Predicts Survival Following Immunotherapy. Oncology research 1 40918457
2025 The USP8/CEP55/CHMP6 Axis Orchestrates Triple-Negative Breast Cancer Progression by Regulating Ferroptosis and Macrophage M2 Polarization. Clinical breast cancer 1 40925844
2024 Biallelic missense CEP55 variants cause prenatal MARCH syndrome. Journal of human genetics 1 39414989
2021 Depletion of UXT, a novel TSG101 interaction protein, leads to enhanced CEP55 attenuation through lysosome degradation. Biochemical and biophysical research communications 1 33486193
2025 Cancer/testis antigens FBXO39 and CEP55 expression correlates with survival in GBM patients. PloS one 0 40504854
2025 Neuroendocrine prostate cancer (NEPC)-associated CEP55 promotes cisplatin resistance in prostate cancer by regulating CDK1 phosphorylation. Cancer pathogenesis and therapy 0 41403895
2025 CBX2 promoted oral squamous cell carcinoma via increasing CEP55/NF-κB/METTL3/SHP2 signaling induced metastasis/proliferation and angiogenesis. Scientific reports 0 41423460