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CEP192

Centrosomal protein of 192 kDa · UniProt Q8TEP8

Length
2537 aa
Mass
279.1 kDa
Annotated
2026-06-09
27 papers in source corpus 23 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CEP192 (the mammalian ortholog of C. elegans SPD-2) is an essential centrosomal scaffold that drives pericentriolar material (PCM) assembly and centrosome maturation during mitosis, with its acute loss causing collapse of functional mitotic centrosomes and loss of γ-tubulin, pericentrin, and downstream PCM proteins (PMID:17980596, PMID:18207742). Its conserved Spd-2 (SP2D) domain, built from two closely spaced ASH domains forming an 'extended cradle', does not itself target CEP192 to centrosomes but promotes higher-order oligomerization of the PCM scaffold in a PLK1-phosphorylation-dependent manner (PMID:40106572). CEP192 functions as a master organizer of two centrosomal kinases: it directly binds and activates Aurora A by wrapping around the kinase through a conserved Helix-1 interface that overlaps the TPX2 site, supplying the pool of phosphorylated Aurora A required for centrosomal accumulation and for subsequent TPX2-dependent spindle function (PMID:21097701, PMID:37083534, PMID:39327527), and it recruits Plk4 and Plk1 to centrioles—cooperating hierarchically and competitively with CEP152 to load Plk4 onto the centriole for duplication (PMID:23641073, PMID:24277814), and engaging Plk1 through two phosphorylated motifs (p-T44 and p-S995) to recruit Plk1 and γ-tubulin for bipolar spindle formation (PMID:26012549). CEP192 itself is recruited to spindle poles by combined input from the centriole wall and the PCM scaffolds pericentrin and CDK5RAP2 in a PLK1-dependent manner (PMID:33443571), and its abundance is tuned by multiple degradation pathways including PHD1 prolyl-hydroxylation of Pro1717 licensing SCF(Skp2) ubiquitination (PMID:23932902) and FBXL13-mediated ubiquitination and degradation (PMID:29348145). In vivo, acute CEP192 degradation in mice impairs γ-tubulin recruitment and spindle assembly and causes division failure in proliferative tissues without blocking centriole duplication, establishing PCM/spindle assembly as its core organismal requirement (PMID:40020058).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2007 High

    Established that CEP192 is required to build a functional mitotic centrosome, defining it as a core PCM scaffolding factor rather than a passive structural component.

    Evidence siRNA depletion in human cells with immunofluorescence readout of γ-tubulin and pericentrin

    PMID:17980596

    Open questions at the time
    • Did not define the molecular interactions through which CEP192 recruits PCM
    • Interphase role not addressed
  2. 2008 High

    Placed CEP192 in a recruitment hierarchy by showing mutual dependence with pericentrin and a shared requirement for NEDD1/γ-TuRC assembly, framing CEP192 as part of an interdependent maturation network.

    Evidence siRNA knockdown and reciprocal co-immunoprecipitation in mammalian cells

    PMID:18207742

    Open questions at the time
    • Direct vs. indirect nature of the pericentrin dependency not resolved
    • No structural basis for the interactions
  3. 2010 High

    Identified the first kinase-activation function of CEP192 by showing it directly binds Aurora A, promotes its dimerization/activation, and targets it to centrosomes independently of TPX2.

    Evidence Co-IP, in vitro kinase assays, antibody-induced dimerization, and dominant-negative interference

    PMID:21097701

    Open questions at the time
    • Structural interface of the CEP192–Aurora A interaction unknown
    • Relationship to TPX2 pool of Aurora A not defined
  4. 2013 High

    Defined CEP192 as a Plk4-recruiting scaffold acting in parallel with CEP152, mapping a negatively charged N-terminal region that engages the Plk4 polo-box domain and showing both scaffolds are required for centriole duplication.

    Evidence Single/double siRNA depletion, domain mapping, and competitive Co-IP across two independent studies

    PMID:23641073 PMID:24277814

    Open questions at the time
    • Stoichiometry and temporal order of CEP192 vs CEP152 handoff not fully resolved
    • Regulation of the competition in cells unclear
  5. 2013 High

    Connected centrosome biogenesis to metabolic/oxygen sensing by showing PHD1 hydroxylates CEP192 at Pro1717 to license SCF(Skp2)-mediated degradation.

    Evidence MS site identification, P1717 mutagenesis, Co-IP with SCF(Skp2), ubiquitination and proteasome-inhibitor assays

    PMID:23932902

    Open questions at the time
    • Physiological conditions controlling PHD1 activity on CEP192 not defined
    • Whether this regulates a specific cell-cycle window unclear
  6. 2015 High

    Resolved how CEP192 recruits Plk1 by identifying two distinct phospho-motifs (p-T44 and p-S995) with Aurora-A-dependent preference, linking the two kinase-recruitment functions of CEP192.

    Evidence Phospho-specific Co-IP, mutagenesis, and additive loss-of-function phenotype analysis

    PMID:26012549

    Open questions at the time
    • Kinase generating p-T44/p-S995 not fully established
    • Quantitative contribution of each motif in vivo unclear
  7. 2017 Medium

    Extended CEP192 regulation to phosphatase recruitment, identifying a conserved KHVTF PP1-docking motif whose threonine is PLK1-phosphorylated in mitosis.

    Evidence Peptide pull-down, Co-IP, phospho-site identification, kinase-inhibitor studies

    PMID:28188792

    Open questions at the time
    • Single method/lab; functional consequence of CEP192–PP1 docking not demonstrated
    • No reciprocal validation
  8. 2017 Medium

    Showed in oocyte meiosis that CIP2A scaffolds CEP192-mediated MTOC assembly by helping recruit Aurora A and Plk1, broadening CEP192's role to acentriolar spindle-pole organization.

    Evidence Reciprocal Co-IP, microinjection depletion, and S904 phospho-mutagenesis in mouse oocytes

    PMID:28935709

    Open questions at the time
    • Directness of CIP2A–CEP192 association not structurally defined
    • Single lab
  9. 2018 Medium

    Identified FBXL13 as a second E3-pathway controlling CEP192 abundance, linking its degradation to centrosomal γ-tubulin levels and cell motility.

    Evidence Co-IP, ubiquitination assay, and reciprocal overexpression/depletion phenotypes

    PMID:29348145

    Open questions at the time
    • Relationship between FBXL13 and PHD1/Skp2 degradation pathways unclear
    • Single lab
  10. 2018 Medium

    Demonstrated in centriole-free oocytes that CEP192 is required for MTOC integrity and that CDK1 differentially regulates CEP152 (but not CEP192) exclusion, distinguishing the regulation of the two scaffolds.

    Evidence Morpholino depletion, CDK1-inhibitor treatment, and live imaging in mouse oocytes

    PMID:28970258

    Open questions at the time
    • Mechanism of CEP192 retention at acentriolar MTOCs unresolved
    • Single lab
  11. 2021 High

    Defined how CEP192 itself is recruited to spindle poles, showing cooperative input from the centriole wall and the PCM scaffolds pericentrin and CDK5RAP2 in a PLK1-dependent manner.

    Evidence Systematic double/triple siRNA depletions and centriole removal across HeLa, RPE1, and A549 cells

    PMID:33443571

    Open questions at the time
    • Direct binding partners at the centriole wall not identified
    • PLK1 substrate(s) enabling PCM-based recruitment unknown
  12. 2023 High

    Provided structural basis for CEP192's Aurora A activation, showing a Helix-1 interface distinct from the TPX2 site that is required for centrosomal AURKA accumulation and activation-loop phosphorylation.

    Evidence X-ray crystallography of the CEP192 Helix-1–AURKA complex with cell-based interface deletion

    PMID:37083534

    Open questions at the time
    • Did not resolve how CEP192-activated AURKA is handed to spindle effectors
    • Full-length CEP192–AURKA architecture not determined
  13. 2024 High

    Unified the Aurora A and TPX2 axes by showing CEP192 wraps around Aurora A, competes with spindle partners, and supplies the phospho-Aurora A pool needed for TPX2 binding on spindles.

    Evidence Structural comparison plus interface mutagenesis with cell-based spindle phenotype analysis

    PMID:39327527

    Open questions at the time
    • Spatial choreography of Aurora A transfer from CEP192 to TPX2 in cells not directly visualized
  14. 2025 High

    Solved the CEP192 Spd-2 (SP2D) domain structure, revealing a two-ASH 'extended cradle' that drives PLK1-dependent oligomerization to assemble the PCM scaffold rather than to target CEP192 to centrosomes.

    Evidence X-ray crystallography (human and honeybee SP2D), in vitro PLK1 phosphorylation, SEC-MALS, and Drosophila in vivo rescue with interface mutants

    PMID:40106572

    Open questions at the time
    • How oligomerized SP2D scaffolds specific PCM clients not defined
    • Human in vivo requirement of the oligomerization interface not tested
  15. 2025 High

    Established the organismal requirement for CEP192 in mammals, showing acute degradation impairs γ-tubulin recruitment and spindle assembly causing lethal division failure in proliferative tissues but sparing centriole duplication.

    Evidence AID2 auxin-inducible degron in live mice with γ-tubulin/spindle immunofluorescence and tissue histology

    PMID:40020058

    Open questions at the time
    • Tissue-specific differences in CEP192 dependence not detailed
    • Decoupling of PCM vs centriole roles mechanistically unexplained

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how the multiple CEP192 degradation pathways (PHD1/Skp2, FBXL13, APC/C(FZR-1)) and kinase/phosphatase docking events are integrated to time PCM assembly, kinase activation, and centriole disengagement within a single cell cycle.
  • No unified model linking the distinct E3 pathways to specific cell-cycle stages
  • Functional output of CEP192–PP1 docking undefined
  • Disease relevance of CEP192 dysregulation in human tissue not directly established

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0005198 structural molecule activity 3 GO:0098772 molecular function regulator activity 3
Localization
GO:0005815 microtubule organizing center 4
Pathway
R-HSA-1640170 Cell Cycle 4 R-HSA-1852241 Organelle biogenesis and maintenance 3
Partners
AURKACDK5RAP2CEP152FBXL13NEDD1PCNTPLK1PLK4
Complex memberships
centrosome/pericentriolar material (PCM)

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 siRNA depletion of Cep192 in human cells causes complete loss of functional centrosomes in mitotic (but not interphase) cells, with loss of γ-tubulin, pericentrin, and other PCM proteins from centrosomes, establishing Cep192 as an essential component of centrosome maturation machinery and PCM scaffold assembly during mitosis. siRNA knockdown with immunofluorescence readout of γ-tubulin, pericentrin, and spindle assembly; overexpression studies showing ectopic γ-tubulin/pericentrin foci Current biology : CB High 17980596
2008 Cep192 (human homolog of C. elegans SPD-2) is a major regulator of PCM recruitment, centrosome maturation, and centriole duplication in mammalian cells; Cep192 and Pericentrin are mutually dependent for localization to mitotic centrosomes, and both are required for NEDD-1 (GCP-WD) recruitment and subsequent γ-TuRC assembly. siRNA knockdown, reciprocal co-immunoprecipitation, immunofluorescence Current biology : CB High 18207742
2010 Cep192 directly interacts with Aurora A (AurA), targets AurA to mitotic centrosomes, and promotes AurA dimerization/oligomerization that triggers potent kinase activation driving microtubule assembly. This Cep192-mediated activation mechanism is distinct from TPX2-mediated AurA activation on microtubules. Depletion of Cep192 or interference with AurA–Cep192 binding abolishes centrosomal AurA activity and microtubule assembly. Co-immunoprecipitation, in vitro kinase assay, siRNA depletion, antibody-induced dimerization, dominant-negative interference Proceedings of the National Academy of Sciences of the United States of America High 21097701
2012 CEP192 interacts with the K63-deubiquitinase CYLD (identified by mass spectrometry) and NEDD1; co-depletion of CYLD alleviates the bipolar spindle assembly defects caused by CEP192 depletion, placing CYLD downstream of CEP192 in regulating the spindle microtubule landscape. Mass spectrometry interactome, co-immunoprecipitation, double siRNA knockdown with spindle assembly phenotype readout Cell cycle (Georgetown, Tex.) Medium 22895009
2013 Cep192 plays a key role in centrosome recruitment of both Cep152 and Plk4; Cep192 directly binds Plk4 through an N-terminal extension specific to its largest isoform (binding region rich in negatively charged residues interacting with the positively charged polo-box domain of Plk4); double-depletion of Cep192 and Cep152 completely abolishes Plk4 binding to centrioles and centriole duplication. siRNA depletion (single and double), co-immunoprecipitation, domain mapping, immunofluorescence Journal of cell science High 23641073
2013 Cep192 and Cep152 serve as two distinct, hierarchically ordered scaffolds that recruit Plk4 to centrosomes; both proteins competitively interact with the cryptic polo box of Plk4 through homologous N-terminal sequences containing acidic-α-helix and N/Q-rich motifs; loss of either Cep192- or Cep152-dependent Plk4 interaction impairs centriole duplication. Co-immunoprecipitation, domain competition assays, siRNA depletion, immunofluorescence, proximity ligation Proceedings of the National Academy of Sciences of the United States of America High 24277814
2013 PHD1 prolyl-4-hydroxylase hydroxylates Cep192 on proline residue 1717; this hydroxylation is required for binding of the SCF(Skp2) E3 ubiquitin ligase, which ubiquitinates Cep192 and targets it for proteasomal degradation. By modulating Cep192 protein levels, PHD1 connects oxygen/metabolic sensing to centriole duplication and centrosome maturation. Mass spectrometry to identify hydroxylation site, site-directed mutagenesis (P1717), co-immunoprecipitation with SCF(Skp2), ubiquitination assay, siRNA depletion, proteasomal inhibitor treatment Developmental cell High 23932902
2014 In interphase cells, Cep192 promotes centrosomal microtubule nucleation by recruiting γ-tubulin; however, Cep192 maintains an antagonistic relationship with Pericentrin at interphase centrosomes (depletion of Cep192 increases centrosomal Pericentrin, and vice versa). Depletion of Cep192 impairs cell motility and alters cell polarization. siRNA knockdown, overexpression, immunofluorescence quantification of γ-tubulin and Pericentrin, microtubule regrowth assay, cell motility assay PloS one Medium 24971877
2015 Plk1 interacts with Cep192 through two distinct phosphorylated motifs: p-T44 (analogous to Xenopus p-T46) via its polo-box domain, which is preferred when AurA is bound to Cep192, and a newly identified p-S995 motif preferred in the absence of AurA. Loss of both Cep192–Plk1 interactions additively impairs Plk1 and γ-tubulin recruitment to centrosomes and bipolar spindle formation. Co-immunoprecipitation with phospho-specific motif analysis, site-directed mutagenesis, siRNA depletion, immunofluorescence, in vitro binding assay Molecular and cellular biology High 26012549
2015 SPD-2/CEP192 and CDK activity from mitotic cells are rate-limiting for MTOC function at the centrosome; cell fusion experiments in live C. elegans embryos show that the centrosome MTOC state is dominant and reactivated by SPD-2/CEP192 and CDK from a mitotic partner cell. Cell fusion experiments in live C. elegans embryos, fluorescence live imaging, genetic analysis Current biology : CB Medium 26119750
2017 CEP192 recruits protein phosphatase 1 (PP1) via a highly conserved KHVTF docking motif; the threonine in this motif is phosphorylated during mitosis in a PLK1-dependent manner. Peptide pull-down, co-immunoprecipitation, phospho-site identification, kinase inhibitor studies Biochemical and biophysical research communications Medium 28188792
2017 CIP2A is reciprocally associated with CEP192 and acts as a scaffold promoting CEP192-mediated MTOC assembly by recruiting Aurora A and Plk1 at spindle poles during mouse oocyte meiotic maturation; CIP2A is phosphorylated by Plk1 at S904, which targets CIP2A to MTOCs. Co-immunoprecipitation, microinjection-based depletion (morpholino/antibody), immunofluorescence, site-directed mutagenesis Development (Cambridge, England) Medium 28935709
2018 FBXL13 (SCF-family F-box protein) interacts with CEP192 at centrosomes and specifically targets CEP192 for proteasomal degradation; FBXL13-induced CEP192 degradation downregulates centrosomal γ-tubulin and disrupts centrosomal microtubule arrays, while FBXL13 depletion causes CEP192 and γ-tubulin accumulation with cell motility defects. Co-immunoprecipitation, ubiquitination assay, inducible overexpression, siRNA depletion, immunofluorescence EMBO reports Medium 29348145
2018 In mouse oocytes lacking centrioles, Cep192 is required for MTOC integrity; Cep192 depletion ablates MTOCs, delays spindle formation, and causes abnormal chromosomal alignment. CDK1 activity regulates Cep152 exclusion from MTOCs (but not Cep192 removal), establishing distinct regulatory mechanisms for the two proteins. Microinjection-based depletion (morpholino), immunofluorescence, CDK1 inhibitor treatment, live imaging FASEB journal Medium 28970258
2020 Cep215 (CDK5RAP2) contains a mitosis-specific centrosome-targeting domain (215N) that directly interacts with Cep192 and phosphorylated Aurora A; Cep192 is essential for targeting 215N to centrosomes, and centrosomal localization of 215N and phospho-AurA is mutually dependent. Co-immunoprecipitation, domain deletion/truncation analysis, siRNA depletion, immunofluorescence, rescue experiments Journal of cell science Medium 33376154
2021 CEP192 recruitment to spindle poles during mitosis requires cooperative input from the centriole wall and PCM scaffold proteins pericentrin and CDK5RAP2; CEP192 remaining at centriole walls is sufficient for bipolar spindle formation when PCM scaffolds are absent, but pericentrin and CDK5RAP2 can recruit CEP192 at acentriolar spindle poles, with PLK1 activity required for this PCM-based pathway. Systematic siRNA double and triple depletions, centriole removal by Plk4 inhibition, immunofluorescence, multiple cell line validation (HeLa, RPE1, A549) The Journal of cell biology High 33443571
2023 Crystal structure of a conserved helix (Helix-1) of CEP192 bound to Aurora A (AURKA) revealed a distinct binding site different from the TPX2 binding site; disrupting the Helix-1–AURKA interaction in cells prevented centrosomal accumulation of AURKA, reduced activation-loop phosphorylation of AURKA, and caused mitotic defects. Crystal structure (X-ray crystallography), quantitative binding studies, cell-based interference (Helix-1 domain deletion), immunofluorescence for AURKA localization Science advances High 37083534
2024 CEP192 wraps around Aurora A and occupies binding sites used by spindle-associated partners, competing with them. CEP192 interaction with Aurora A modifies kinase activity through the same site used for TPX2-mediated activation. Deleting the Aurora A-binding interface in CEP192 prevents centrosomal Aurora A accumulation, reduces activation-loop phosphorylation, and decreases spindle-bound TPX2:Aurora A complexes, resulting in error-prone mitosis. CEP192 thereby supplies the pool of phosphorylated Aurora A required for TPX2 binding on spindles. Crystal structure/cryo-EM structural comparison, mutagenesis of CEP192 Aurora A-binding interface, immunofluorescence, cell-based spindle phenotype analysis The EMBO journal High 39327527
2025 Crystal structures of the human and honeybee Spd-2 domain (SP2D) of CEP192 revealed an unusual 'extended cradle' structure formed by two closely spaced ASH domains with a conserved interaction interface. The SP2D does not target CEP192 to centrosomes but promotes PCM scaffold assembly; PLK1-dependent phosphorylation of Drosophila SP2D drives higher-order oligomerization, and mutations at the oligomerization interface perturb PCM scaffold assembly in vivo. X-ray crystallography (human and honeybee SP2D), in vitro phosphorylation by PLK1, SEC-MALS oligomerization assay, Drosophila in vivo functional rescue with interface mutants, AlphaFold predictions Science advances High 40106572
2025 CEP192 loss by auxin-inducible degron in live mice decreased γ-tubulin recruitment to centrosomes, impaired mitotic spindle assembly, and caused cell division failure and cell death in proliferative tissues, but did not affect centriole duplication. AID2 auxin-inducible degron system in vivo, immunofluorescence for γ-tubulin and spindle markers, histological analysis of proliferative tissues Science advances High 40020058
2025 In C. elegans, SPD-2 (CEP192 ortholog) is a substrate of APC/C(FZR-1); SPD-2 physically associates with FZR-1 in vivo, and canonical D-box motifs (D-box1, D-box2, D-box3) each contribute to SPD-2 degradation with distinct functional consequences for centrosomal localization and centriole duplication. In vivo co-immunoprecipitation (SPD-2 with FZR-1), D-box mutagenesis, genetic epistasis with zyg-1 mutants, fluorescence quantification of centrosomal SPD-2 levels bioRxivpreprint Medium bio_10.1101_2025.10.14.682142
2025 CEP192 (through its centrosomal localization) is a key activator of Plk1 specifically for the centriole disengagement step of the centrosome cycle; Bora drives Plk1 activation for mitotic entry and centrosome maturation whereas CEP192 and Cenexin control a distinct Plk1 pool governing centriole disengagement. Additionally, Plk1 and CEP192 promote replication origin firing during S-phase. Selective depletion of Plk1 coactivators (Bora, Cep192, Cenexin) with cell-cycle stage-specific phenotype readouts, DNA replication assays bioRxivpreprint Medium bio_10.1101_2025.09.30.679461
2026 Nur77 phosphorylated at Thr143 by Cdk1 accumulates at the centrosome during mitosis and directly binds CEP192; this interaction maintains centrosome integrity in tumor cells and facilitates PLK1 recruitment to centrosomes. Disruption of the Nur77–CEP192 interaction (by siRNA or the small molecule NMA39) causes mitotic arrest. Co-immunoprecipitation, site-directed mutagenesis (T143), immunofluorescence, small-molecule inhibitor (NMA39), siRNA depletion Cell death & disease Medium 42236697

Source papers

Stage 0 corpus · 27 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 Human Cep192 and Cep152 cooperate in Plk4 recruitment and centriole duplication. Journal of cell science 196 23641073
2007 Human Cep192 is required for mitotic centrosome and spindle assembly. Current biology : CB 180 17980596
2013 Hierarchical recruitment of Plk4 and regulation of centriole biogenesis by two centrosomal scaffolds, Cep192 and Cep152. Proceedings of the National Academy of Sciences of the United States of America 178 24277814
2008 The mammalian SPD-2 ortholog Cep192 regulates centrosome biogenesis. Current biology : CB 158 18207742
2010 Centrosomal protein of 192 kDa (Cep192) promotes centrosome-driven spindle assembly by engaging in organelle-specific Aurora A activation. Proceedings of the National Academy of Sciences of the United States of America 94 21097701
2013 PHD1 links cell-cycle progression to oxygen sensing through hydroxylation of the centrosomal protein Cep192. Developmental cell 74 23932902
2015 SPD-2/CEP192 and CDK Are Limiting for Microtubule-Organizing Center Function at the Centrosome. Current biology : CB 43 26119750
2015 Bimodal Interaction of Mammalian Polo-Like Kinase 1 and a Centrosomal Scaffold, Cep192, in the Regulation of Bipolar Spindle Formation. Molecular and cellular biology 42 26012549
2021 Centriole and PCM cooperatively recruit CEP192 to spindle poles to promote bipolar spindle assembly. The Journal of cell biology 39 33443571
2014 Cep192 controls the balance of centrosome and non-centrosomal microtubules during interphase. PloS one 37 24971877
2012 CEP192 interacts physically and functionally with the K63-deubiquitinase CYLD to promote mitotic spindle assembly. Cell cycle (Georgetown, Tex.) 29 22895009
2018 FBXL13 directs the proteolysis of CEP192 to regulate centrosome homeostasis and cell migration. EMBO reports 26 29348145
2018 Distinct roles of Cep192 and Cep152 in acentriolar MTOCs and spindle formation during mouse oocyte maturation. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 23 28970258
2017 CIP2A acts as a scaffold for CEP192-mediated microtubule organizing center assembly by recruiting Plk1 and aurora A during meiotic maturation. Development (Cambridge, England) 19 28935709
2023 Structural basis for CEP192-mediated regulation of centrosomal AURKA. Science advances 17 37083534
2008 Cep192 and the generation of the mitotic spindle. Cell cycle (Georgetown, Tex.) 11 18469523
2017 Recruitment of PP1 to the centrosomal scaffold protein CEP192. Biochemical and biophysical research communications 10 28188792
2021 Cep192, a Novel Missing Link between the Centrosomal Core and Corona in Dictyostelium Amoebae. Cells 8 34572033
2024 CEP192 localises mitotic Aurora-A activity by priming its interaction with TPX2. The EMBO journal 6 39327527
2023 Mosaic variegated aneuploidy syndrome with tetraploid, and predisposition to male infertility triggered by mutant CEP192. HGG advances 6 37981762
2020 A novel mitosis-specific Cep215 domain interacts with Cep192 and phosphorylated Aurora A for organization of spindle poles. Journal of cell science 6 33376154
2025 Rapid and sustained degradation of the essential centrosome protein CEP192 in live mice using the AID2 system. Science advances 5 40020058
2023 Centrosomal protein of 192 kDa (Cep192) fragment possesses bactericidal and parasiticidal activities in Larimichthys crocea. International journal of biological macromolecules 4 38287570
2025 Synthesis of an RBM39 Degrader That Downregulates CEP192 and Induces Disorganized Spindle Structures. Journal of medicinal chemistry 2 40107850
2025 The conserved Spd-2/CEP192 domain adopts a unique protein fold to promote centrosome scaffold assembly. Science advances 1 40106572
2026 The Kifc3 Motor Protein Controls Centrosomal Factor Cep192 in Ontogenic Coordination of Megakaryocyte Development. bioRxiv : the preprint server for biology 0 41929089
2026 Cdk1-phosphorylated Nur77 accumulates at the centrosome during mitosis to regulate the Cep192-PLK1 signaling axis. Cell death & disease 0 42236697

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