Affinage

Showing CPAP — CENPJ is a alias.

CPAP

Centrosomal P4.1-associated protein · UniProt Q9HC77

Length
1338 aa
Mass
153.0 kDa
Annotated
2026-06-09
100 papers in source corpus 41 papers cited in narrative 41 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CPAP (CENPJ/SAS-4/MCPH6) is a cell-cycle-regulated centrosomal scaffold protein that governs centriole biogenesis, elongation, and length through its intrinsic tubulin-binding activity (PMID:19503075, PMID:27219064). Its PN2-3/MDD module binds GTP-tubulin heterodimers and caps microtubule plus ends at a site engaged in longitudinal tubulin-tubulin contacts, dampening growth and limiting the length of centriolar microtubules; mutations that alter this affinity produce either short centrioles with incomplete microtubule triplets or over-elongated centriolar and ciliary microtubules via a clutch-like dynamic release of tubulin (PMID:15047868, PMID:27219064, PMID:27306797). CPAP is recruited to nascent procentrioles through direct interactions with STIL (via its TCP/G-box proline-recognition domain), CEP135, CEP120, CEP152, and centrobin, which together build a recruitment and stability hierarchy at the procentriole base (PMID:21059844, PMID:22020124, PMID:23511974, PMID:24700465, PMID:23857771); structural work establishes the G-box as a β-sheet platform that tethers the SAS-4–PCM scaffold to centrioles (PMID:24052813, PMID:24076405, PMID:24385583). Its activity is tuned by phosphorylation (PLK2 at S589/S595 for procentriole formation, Aurora-A at S467 to switch from microtubule to PCM binding, and Cdk1/Polo in flies for centriole conversion and PCM expansion) and by tankyrase-1 PARsylation and centrobin-dependent control of its turnover, which restrict productive CPAP to the appropriate cell-cycle window (PMID:20531387, PMID:22699936, PMID:24700465, PMID:25616662, PMID:26997271, PMID:27326932, PMID:30590037). CPAP scaffolds cytoplasmic PCM complexes and tethers them to centrioles to maintain centrosome integrity, and it homodimerizes via its fifth coiled-coil domain to preserve centrosome cohesion until mitotic phosphorylation permits splitting (PMID:19889632, PMID:21694707, PMID:35404385). Beyond duplication, CPAP negatively regulates ciliary length and promotes timely cilium disassembly by recruiting the Nde1–Aurora A–OFD1 disassembly complex to the ciliary base (PMID:23213448, PMID:26929011, PMID:30626697). Loss or microcephaly-associated mutation of CPAP causes spindle defects, p53-dependent progenitor apoptosis, randomized cleavage-plane orientation, defective ciliogenesis, and primary microcephaly/Seckel syndrome (PMID:15793586, PMID:23166506, PMID:26929011, PMID:32501282, PMID:35309908). In non-centrosomal contexts, CPAP acts as a transcriptional coactivator of STAT5 and STAT3 and, when SUMOylated, augments NF-κB activity (PMID:12198240, PMID:23369793, PMID:31511651).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2000 Medium

    Established CPAP as a centrosomal protein physically associated with the γ-tubulin complex and functionally required for microtubule aster formation, framing it as a microtubule-nucleation-related centrosomal factor.

    Evidence Yeast two-hybrid, co-sedimentation and Co-IP with γ-tubulin, antibody inhibition of asters

    PMID:11003675

    Open questions at the time
    • No domain responsible for tubulin/γ-tubulin association mapped
    • Role in centriole biology not yet recognized
  2. 2002 Medium

    Revealed an unexpected non-centrosomal role of CPAP as a nuclear transcriptional coactivator, showing the protein has functions beyond the centrosome.

    Evidence Yeast two-hybrid, reporter assay, fractionation showing Stat5-specific coactivation upon PRL signaling

    PMID:12198240

    Open questions at the time
    • Mechanism of nuclear shuttling unresolved
    • Relationship to centrosomal pool unclear
  3. 2004 High

    Identified the microtubule-destabilizing domain that binds tubulin heterodimers, providing the first biochemical mechanism for CPAP's action on microtubules.

    Evidence Deletion mapping with in vitro depolymerization and tubulin-binding assays

    PMID:15047868

    Open questions at the time
    • How destabilizing activity reconciles with centriole growth not yet known
    • Structural basis of tubulin binding undefined
  4. 2005 Medium

    Connected CPAP to human disease and to centrosome integrity, showing loss-of-function causes primary microcephaly and depletion causes multipolar spindles via Eg5-dependent mechanisms.

    Evidence Genetic mapping/mutation analysis (MCPH6) and siRNA with Eg5-inhibition epistasis

    PMID:15793586 PMID:16316625

    Open questions at the time
    • Molecular basis of microcephaly mutations undefined
    • Cell-biological cause of microcephaly not yet linked to centriole biogenesis
  5. 2008 High

    Refined the structural determinants of tubulin binding and destabilization through mutagenesis, confirming the MDD as the active module and its conservation across species.

    Evidence Site-specific mutagenesis with in vitro MT binding/destabilization assays

    PMID:18586240

    Open questions at the time
    • Atomic structure of the domain–tubulin complex still absent
    • In vivo consequence of mutations not assessed here
  6. 2009 High

    Reframed CPAP as a positive regulator of centriole elongation whose tubulin-binding activity drives procentriole assembly, and established cell-cycle control of its levels and a coiled-coil-mediated homodimer required for centrosome cohesion.

    Evidence Cell-cycle analysis, overexpression/knockdown, EM, tubulin-binding-defective mutants, and Co-IP/domain mapping across multiple labs

    PMID:19481458 PMID:19481460 PMID:19503075 PMID:19889632

    Open questions at the time
    • Recruitment partners targeting CPAP to procentrioles not yet identified
    • Kinase responsible for cohesion-disrupting phosphorylation unknown
  7. 2010 High

    Identified CEP152 as the centrosomal receptor for CPAP and PLK2 phosphorylation at S589/S595 as a positive signal for procentriole formation, defining recruitment and regulatory inputs.

    Evidence Co-IP/knockdown for CEP152 and in vitro/in vivo kinase assays with phospho-mutant rescue for PLK2

    PMID:20531387 PMID:21059844

    Open questions at the time
    • Spatial relationship between CEP152 and other recruiters undefined
    • Direct phosphatase counteracting PLK2 unknown
  8. 2011 High

    Established CPAP as a scaffold that tethers pre-assembled PCM complexes to centrioles and identified STIL as a direct partner whose binding is disrupted by a microcephaly mutation, linking molecular interactions to disease.

    Evidence Drosophila genetics, in vitro binding with purified S-CAP complexes, Co-IP/direct binding, MCPH mutation (E1235V) analysis, domain mapping with spindle-orientation assays

    PMID:21694707 PMID:22020124 PMID:22100914

    Open questions at the time
    • Structural basis of STIL recognition not yet solved at this stage
    • Stoichiometry of CPAP–PCM scaffold undefined
  9. 2012 Medium

    Defined post-translational and developmental control of CPAP — tankyrase-1 PARsylation/degradation restricting CPAP to the proper window, and ciliogenesis and disease-model phenotypes — broadening its functional repertoire.

    Evidence In vitro PARsylation and reciprocal tankyrase perturbation; ciliogenesis assays with 377EE mutant; Cenpj hypomorphic Seckel mouse

    PMID:22699936 PMID:23166506 PMID:23213448

    Open questions at the time
    • How tankyrase activity is timed to G1 unresolved
    • Distinction between cilium and centriole functions of CPAP not yet separated
  10. 2013 High

    Provided atomic structures of the CPAP TCP/G-box–STIL complex defining a novel proline-recognition fold and identified CEP135 and CEP120 as direct partners linking CPAP to SAS-6 and microtubules during elongation.

    Evidence X-ray crystallography/NMR with ITC/SPR and in vivo duplication assays; Co-IP/direct binding/knockdown/dominant-negative for CEP135 and CEP120

    PMID:23511974 PMID:23857771 PMID:24052813 PMID:24076405

    Open questions at the time
    • How multiple recruiters are spatially coordinated at the procentriole unclear
    • Order of assembly among STIL/CEP135/CEP120 not fully resolved
  11. 2014 High

    Resolved how the G-box β-sheet platform tethers the SAS-4–PCM scaffold to centrioles and identified centrobin as a stabilizer protecting CPAP from proteasomal degradation, separating scaffolding from tethering functions.

    Evidence Crystallography with mutagenesis across fly/human/iPSC-NPC systems; Co-IP, knockdown, dominant-negative, proteasome inhibition for centrobin

    PMID:24385583 PMID:24700465

    Open questions at the time
    • Identity of the ubiquitin ligase targeting CPAP unknown
    • How centrobin physically shields CPAP undefined
  12. 2015 Medium

    Integrated CPAP into a developmental transcriptional program (Ascl1 target) controlling radial glia centrosome biogenesis and showed centrobin sets CPAP abundance to control centriole length.

    Evidence In utero electroporation knockdown/rescue with ChIP for Ascl1; gain/loss-of-function with mutagenesis and proteasome inhibition for centrobin

    PMID:25616662 PMID:25753651

    Open questions at the time
    • Transcriptional control of CPAP in non-neural tissues not assessed
    • Mechanism by which centrobin overexpression accumulates ubiquitinated CPAP unresolved
  13. 2016 High

    Delivered the mechanistic core: structural and reconstitution evidence that CPAP caps microtubule plus ends to limit growth, that PN2-3 engages GTP-tubulin via a clutch-like mechanism setting centriole length, and that Aurora-A and Cdk1/Polo phosphorylation switch CPAP between microtubule and PCM functions; also defined a dedicated role in cilium disassembly.

    Evidence Crystallography + TIRF single-molecule reconstitution + in-cell assays; kinase assays with phospho-mutant rescue; iPSC-NPC/organoid and patient-cell ciliary studies

    PMID:26929011 PMID:26997271 PMID:27219064 PMID:27306797 PMID:27326932

    Open questions at the time
    • How capping, elongation, and PCM functions are partitioned within one cell cycle still being clarified
    • Direct disassembly-complex contact surfaces on CPAP undefined
  14. 2018 Medium

    Showed tubulin negatively regulates CPAP-dependent PCM recruitment and nucleation and exploited the CPAP–tubulin interface pharmacologically to selectively kill centrosome-amplified cancer cells.

    Evidence Compound screen (CCB02), Co-IP, genetic perturbation, organotypic invasion assay

    PMID:30530478

    Open questions at the time
    • Therapeutic window and selectivity in vivo unresolved
    • How tubulin occupancy is dynamically regulated at centrosomes unclear
  15. 2019 Medium

    Extended CPAP's transcriptional moonlighting to STAT3-driven tumor angiogenesis and SUMO-dependent NF-κB/HBx interactions, and identified Kif2a as a mediator of CPAP-dependent cilia disassembly in vivo.

    Evidence Co-IP/reporter/xenograft for STAT3; ChIP/Co-IP/PLA for HBx; conditional KO with Kif2a epistasis

    PMID:30626697 PMID:31170980 PMID:31511651

    Open questions at the time
    • Whether transcriptional and centrosomal pools are functionally separable not established
    • Mechanism linking CPAP to Kif2a at the cilium undefined
  16. 2020 Medium

    Defined the disease-relevant recruitment hierarchies and downstream cell-death pathway: WDR62 recruits CPAP for ciliogenesis, CPAP loss triggers p53-dependent progenitor apoptosis, and the E1235V mutation disrupts recruitment of multiple centriolar proteins causing short centrioles but long cilia.

    Evidence CRISPR knock-in/conditional KO mice with p53 epistasis; isogenic hiPSC brain organoids with spindle-orientation and p53 analyses

    PMID:31816041 PMID:32501282 PMID:35309908

    Open questions at the time
    • How a single mutation simultaneously shortens centrioles and lengthens cilia mechanistically unclear
    • Cell-type specificity of p53-dependent death not fully explained
  17. 2022 High

    Used acute degradation and superresolution/EM to dissect CPAP's essential function, showing it is required for assembling centriole microtubule triplets and cohesion between blades, but not for PCM recruitment onto pre-formed centrioles, refining its role to centriole construction.

    Evidence Auxin-inducible degron, STORM/STED, live imaging, electron microscopy

    PMID:35404385

    Open questions at the time
    • Molecular basis of inter-blade cohesion provided by CPAP undefined
    • How three distinct CPAP populations are differentially regulated unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CPAP's centrosomal, ciliary, and nuclear transcriptional activities are partitioned and coordinated within the same cell, and the structural basis of its contacts with the cilium-disassembly complex and inter-microtubule-blade cohesion, remain unresolved.
  • No structure of CPAP bound to Nde1/Aurora A/OFD1 disassembly complex
  • Functional separability of transcriptional vs centrosomal pools not demonstrated
  • Mechanism coupling CPAP populations to cell-cycle stage unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 4 GO:0060090 molecular adaptor activity 3 GO:0140110 transcription regulator activity 3 GO:0005198 structural molecule activity 2
Localization
GO:0005815 microtubule organizing center 4 GO:0005929 cilium 3 GO:0005634 nucleus 2 GO:0005856 cytoskeleton 2
Pathway
R-HSA-1852241 Organelle biogenesis and maintenance 4 R-HSA-1266738 Developmental Biology 3 R-HSA-1640170 Cell Cycle 3 R-HSA-74160 Gene expression (Transcription) 3
Partners
CENTROBINCEP120CEP135CEP152STAT5STILTUBULINWDR62
Complex memberships
S-CAP (SAS-4–PCM scaffold)centrosome/centriolecilium disassembly complex (Nde1–Aurora A–OFD1)γ-tubulin complex

Evidence

Reading pass · 41 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 CPAP (centrosomal P4.1-associated protein) was identified as a novel centrosomal protein that interacts with the head domain of 4.1R-135 via yeast two-hybrid, co-sediments with gamma-tubulin in sucrose gradients, and co-immunoprecipitates with gamma-tubulin, indicating it is part of the gamma-tubulin complex. Anti-CPAP antibody significantly inhibited formation of microtubule asters, demonstrating a role in microtubule nucleation. Yeast two-hybrid, sucrose gradient co-sedimentation, co-immunoprecipitation, immunofluorescence, antibody inhibition assay Molecular and cellular biology Medium 11003675
2002 CPAP interacts specifically with Stat5a and Stat5b (but not Stat1 or Stat3) via yeast two-hybrid screening. CPAP augments Stat5-mediated transcription and translocates to the nucleus upon PRL pathway activation, acting as a transcriptional coactivator of Stat5. Yeast two-hybrid, co-immunoprecipitation, reporter transcription assay, immunofluorescence, cellular fractionation Molecular endocrinology Medium 12198240
2004 CPAP contains a novel 112-residue microtubule-destabilizing motif (MDD, residues 311–422) that binds tubulin heterodimers, inhibits microtubule nucleation from the centrosome, depolymerizes taxol-stabilized microtubules, and when overexpressed induces G2/M arrest and apoptosis. Deletion mapping, in vitro microtubule depolymerization assay, tubulin-binding assay, tetracycline-controlled overexpression, cell cycle analysis Molecular biology of the cell High 15047868
2005 CPAP (CENPJ) localizes to spindle poles of mitotic cells during neuroepithelial neurogenesis; homozygous loss-of-function mutations in CENPJ cause primary microcephaly (MCPH6), implicating a centrosomal mechanism in controlling neuron number. Genetic mapping, mutation analysis, immunofluorescence localization in human tissue Nature genetics Medium 15793586
2005 RNAi-mediated depletion of CPAP in human cells arrests cells in mitosis, induces apoptosis, and causes multipolar spindle formation in >40% of mitotic cells. Inhibition of kinesin Eg5 in CPAP-depleted cells results in monopolar spindles, indicating Eg5 is required downstream of CPAP for multipolar spindle formation, revealing a structural role for CPAP in centrosome integrity. siRNA knockdown, immunofluorescence, Eg5 inhibition epistasis Biochemical and biophysical research communications Medium 16316625
2008 The microtubule-binding domain (MBD, residues 423–607) of CPAP is located adjacent to its microtubule-destabilizing domain (MDD, residues 311–422). Point mutations disrupting alpha-helical structure (Y341P, I346P, L348P, triple-P) or charge (KR377EE) in the MDD abolish MT-destabilizing activity and significantly reduce tubulin heterodimer binding. The conserved ~20-aa sequence in Drosophila d-SAS-4 functions similarly. Site-specific mutagenesis, in vitro microtubule binding and destabilization assays, truncation analysis Experimental cell research High 18586240
2009 CPAP protein levels are cell-cycle regulated, being degraded in late mitosis. Excess CPAP induces formation of elongated procentriole-like structures (PLSs) containing stable microtubules and centriolar proteins. A tubulin-binding-defective mutant (CPAP-377EE) fails to induce PLSs, demonstrating that CPAP's intrinsic tubulin-dimer binding activity is required for procentriole elongation. Cell cycle analysis, siRNA knockdown, overexpression, immunofluorescence, ultrastructural EM analysis, mutagenesis Nature cell biology High 19503075
2009 Overexpression of CPAP in human cells leads to abnormally long centrioles and formation of supernumerary procentrioles, resulting in multipolar spindle assembly and cytokinesis defects. CPAP is required for centrosome duplication in cycling human cells. Overexpression, siRNA knockdown, immunofluorescence, time-lapse microscopy Current biology : CB High 19481460
2009 CPAP and CP110 play antagonistic roles in controlling centriole length: CPAP overexpression enhances centriolar tubulin accumulation leading to elongated centrioles, while CP110 depletion produces elongated MT structures that are distinct from primary cilia. Overexpression, siRNA depletion, immunofluorescence, electron microscopy Current biology : CB High 19481458
2009 CPAP forms homodimers via its fifth coiled-coil domain during interphase. This self-interaction is required for maintaining centrosome cohesion and preventing premature centrosome splitting before G2/M. CPAP is phosphorylated during mitosis, and this phosphorylation disrupts the homodimer interaction to allow centrosome splitting. Co-immunoprecipitation, domain deletion analysis, immunofluorescence, cell cycle analysis The Journal of biological chemistry Medium 19889632
2010 PLK2 phosphorylates CPAP at S589 and S595 in vitro and in vivo. This phosphorylation is critical for procentriole formation during the centrosome cycle; phosphorylated CPAP preferentially localizes to procentrioles. PLK4 also phosphorylates S595 but this is not critical for PLK4-driven procentriole assembly. Overexpression of phospho-resistant CPAP mutant inhibits elongated centriole formation. In vitro kinase assay, in vivo phosphorylation (mass spectrometry/western), site-directed mutagenesis, immunofluorescence, overexpression The EMBO journal High 20531387
2010 Cep152 directly interacts with CPAP and is required for recruitment of CPAP to the centrosome. Reduction of Cep152 causes loss of CPAP from centrosomes, failure of centriole duplication, and monopolar spindle formation. Co-immunoprecipitation, siRNA knockdown, immunofluorescence The Journal of cell biology Medium 21059844
2011 Drosophila Sas-4 provides a scaffold for cytoplasmic complexes (S-CAP) including CNN, Asl, and D-PLP. In the absence of Sas-4, nascent procentrioles are unstable and lack PCM. When Sas-4 cannot form S-CAP complexes, centrosomes have dramatically reduced PCM. Purified S-CAP complexes or recombinant Sas-4 can bind centrosomes stripped of PCM, demonstrating that Sas-4 tethers pre-assembled PCM complexes to centrioles. Genetic null and point mutant analysis, mass spectrometry, in vitro binding with purified proteins, immunofluorescence Nature communications High 21694707
2011 Human STIL directly interacts with CPAP and forms a complex with hSAS6. A microcephaly-causing CPAP mutation (E1235V) significantly reduces binding to STIL. STIL depletion inhibits centriole duplication, Plk4-induced centriole amplification, and CPAP-induced centriole elongation, and blocks localization of hSAS6 and CPAP to the nascent procentriole base. Co-immunoprecipitation, direct interaction assay, siRNA knockdown, immunofluorescence, MCPH mutation analysis The EMBO journal High 22020124
2011 CPAP protein domains required for centriolar localization, centriole elongation, and centriole formation were identified. Conditions mimicking CPAP MCPH patient mutations impair centriole formation in tissue culture cells and correlate with randomization of spindle position on adhesive micropatterns. STIL is also essential for centriole formation and proper spindle positioning. Domain deletion mutagenesis, siRNA knockdown, immunofluorescence, adhesive micropattern spindle orientation assay Journal of cell science Medium 22100914
2012 Tankyrase 1 PARsylates CPAP in vitro and in vivo, targeting it for proteasomal degradation. Overexpression of tankyrase 1 leads to CPAP degradation and prevents centriole duplication; depletion of tankyrase 1 stabilizes CPAP in G1, generating elongated procentrioles and multipolarity. Tankyrase 1 localizes to centrosomes exclusively in G1, coinciding with CPAP degradation. In vitro PARsylation assay, co-immunoprecipitation, siRNA knockdown, overexpression, immunofluorescence, proteasome inhibitor treatment EMBO reports High 22699936
2012 CPAP is required for cilia biogenesis in neuronal CAD cells and hippocampal neurons. Overexpression of wild-type CPAP promotes cilia formation and longer cilia. The tubulin-binding-defective mutant CPAP-377EE inhibits cilia formation and causes cilia shortening. Depletion of CPAP inhibits ciliogenesis, rescued by wild-type but not CPAP-377EE. siRNA knockdown, overexpression, mutagenesis (CPAP-377EE), immunofluorescence in neuronal cell lines and primary neurons Biology open Medium 23213448
2012 Mouse Cenpj hypomorphic allele recapitulates Seckel syndrome features. Cenpj-deficient embryonic fibroblasts exhibit irregular centriole and centrosome numbers, mono- and multipolar spindles, and near-tetraploidy. Genomic instability arises from mitotic failure rather than defective ATR-dependent DNA damage signaling. Hypomorphic mouse model, immunohistochemistry, centrosome counting, karyotyping, ATR pathway analysis PLoS genetics Medium 23166506
2013 Crystal structures of the CPAP TCP domain in complex with a conserved STIL fragment reveal that the TCP domain is a novel proline recognition domain forming a 1:1 complex with STIL. The TCP domain adopts an all-β structure. A microcephaly mutation in CPAP (E1235V) maps to the STIL-binding interface and compromises complex formation. Point mutations abolishing complex formation block centriole duplication in vivo. X-ray crystallography, ITC binding assay, site-directed mutagenesis, in vivo centriole duplication assay eLife High 24052813
2013 CEP135 directly interacts with hSAS-6 via its C-terminus and with CPAP via its N-terminal domain. CEP135 depletion perturbs CPAP centriolar localization and blocks CPAP-induced centriole elongation. Overexpression of a CEP135 mutant lacking hSAS-6 binding has a dominant-negative effect on centriole assembly. CEP135 acts as a linker connecting hSAS-6 to outer centriolar microtubules and is required for CPAP-mediated centriole elongation. Co-immunoprecipitation, direct binding assays, siRNA knockdown, overexpression, dominant-negative mutant, immunofluorescence, EM The EMBO journal High 23511974
2013 The G-box (TCP) domain of CPAP adopts a single elongated β-sheet capable of forming supramolecular assemblies. The G-box structure was determined alone and in complex with a STIL fragment. The conserved CPAP-STIL complex is confirmed by structural and biophysical studies. A microcephaly missense mutation in the G-box reduces affinity for STIL. CPAP is proposed to act as a horizontal strut joining the centriolar scaffold with microtubules. X-ray crystallography, NMR, biophysical binding assays (ITC/SPR), mutagenesis Structure High 24076405
2013 CPAP is SUMOylated by SUMO-1 upon TNF-α stimulus, and this SUMOylation is essential for its NF-κB co-activator activity. CPAP siRNA abolishes the interaction between IKKβ and NF-κB, while CPAP overexpression enhances IKKβ–NF-κB interaction and augments NF-κB activation. SUMO-deficient CPAP mutant loses co-activator activity and fails to enter the nucleus. SUMOylated CPAP synergistically increases HBx-induced NF-κB activity. In situ PLA assay, reporter assay, RT-PCR, siRNA knockdown, overexpression, western blot, in vivo SUMO modification assay Journal of hepatology Medium 23369793
2014 The crystal structure of the Sas-4/CPAP TCP domain reveals a solvent-exposed single-layer β-sheet fold that provides an extended surface platform for tethering the Sas-4-PCM scaffold to centrioles. Point mutations in β-strands 9–10 (including an MCPH-associated mutation) perturb PCM tethering while allowing Sas-4/CPAP to scaffold cytoplasmic PCM complexes. The β9-10 surface mediates interactions with Ana2 and Bld-10 for efficient centriole tethering. X-ray crystallography, site-directed mutagenesis, Drosophila genetics, human cell functional assays, iPSC-derived neural progenitor cell assays Proceedings of the National Academy of Sciences of the United States of America High 24385583
2014 Centrobin interacts with CPAP and is required for CPAP localization to centrioles during centriole duplication. Centrobin depletion causes disappearance of CPAP from centrioles and its proteasome-mediated degradation; centrobin protects ubiquitinated CPAP from degradation. Restoration of centrobin expression restores centriolar CPAP. The CPAP-binding fragment of centrobin acts as a dominant negative to displace centriolar CPAP. Co-immunoprecipitation, siRNA knockdown, overexpression, dominant-negative fragment, proteasome inhibitor treatment, immunofluorescence The Journal of biological chemistry Medium 24700465
2015 Centrobin controls CPAP levels and centriole elongation: centrobin overexpression causes massive CPAP accumulation and abnormal centriole elongation; centrobin depletion causes CPAP undetectability via ubiquitin-proteasome degradation. Only full-length centrobin (not CPAP-binding-defective mutant) restores CPAP levels. Centrobin-overexpressing cells show proteasome-independent accumulation of ubiquitinated CPAP. siRNA knockdown, overexpression, mutagenesis, proteasome inhibitor treatment, immunofluorescence The Journal of biological chemistry Medium 25616662
2015 CPAP (Cenpj) is a transcriptional target of proneural factor Ascl1 in the embryonic cerebral cortex. Knockdown of Cenpj by in utero electroporation disrupts centrosome biogenesis and randomizes cleavage plane orientation of radial glia progenitors. In post-mitotic neurons, Cenpj downregulation increases stable microtubules, slows neuronal migration, and causes aberrant centrosome position and morphology. Rescue experiments show Cenpj mediates Ascl1's role in centrosome biogenesis and microtubule dynamics. In utero electroporation knockdown, rescue experiments, immunofluorescence, chromatin immunoprecipitation (Ascl1 binding to Cenpj promoter) Nature communications Medium 25753651
2016 CPAP (SAS-4) binds and caps microtubule plus ends by associating with a site on β-tubulin engaged in longitudinal tubulin-tubulin interactions. This capping dampens microtubule growth and stabilizes microtubules by inhibiting catastrophes and promoting rescues. Crystallographic, biophysical (TIRF reconstitution), and in-cell assays demonstrate that CPAP's capping function limits growth of centriolar microtubules. X-ray crystallography, TIRF-based single-molecule reconstitution assay, biophysical binding assays, in-cell functional assays Developmental cell High 27219064
2016 CPAP PN2-3 domain forms a high-affinity complex with GTP-tubulin: a C-terminal loop-helix targets β-tubulin at the MT outer surface while an N-terminal helical motif caps the α-β surface of β-tubulin. CPAP(F375A) with strongly reduced tubulin interaction causes shorter centrioles with doublet- instead of triplet-microtubules. CPAP(EE343RR) with slightly reduced affinity but unmasked β-tubulin polymerization surface causes over-elongation of centriolar/ciliary microtubules via enhanced dynamic release of bound tubulin ('clutch-like' mechanism). X-ray crystallography, ITC binding assays, site-directed mutagenesis, centriole length measurements, electron microscopy Nature communications High 27306797
2016 CPAP is phosphorylated by Aurora-A at serine 467 during mitosis. This phosphorylation is required for maintaining spindle pole integrity; non-phosphorylatable CPAP-S467A fails to rescue PCM dispersion upon CPAP depletion, while phospho-mimic CPAP-S467D rescues it. CPAP-S467D has low affinity for microtubule binding but high affinity for PCM proteins, linking Aurora-A phosphorylation to PCM organization. In vitro kinase assay, co-immunoprecipitation, site-directed mutagenesis (S467A/S467D), siRNA knockdown, immunofluorescence Cell reports High 26997271
2016 In Drosophila, Cdk1 phosphorylates Sas-4 during mitosis, creating a Polo-docking site that recruits Polo to daughter centrioles. This is required for subsequent recruitment of Asterless (Asl) and for centriole conversion (allowing daughter centrioles to duplicate and organize centrosomes). Point mutations preventing Cdk1 phosphorylation or Polo docking block centriole conversion and lead to embryonic lethality. In vitro kinase assay, site-directed mutagenesis, Drosophila genetics, immunofluorescence, time-lapse imaging Developmental cell High 27326932
2016 CPAP acts as a negative regulator of ciliary length independent of its role in centrosome biogenesis. At the onset of cilium disassembly, CPAP provides a scaffold for the cilium disassembly complex (CDC) comprising Nde1, Aurora A, and OFD1, recruiting them to the ciliary base for timely cilium disassembly. A Seckel syndrome CPAP mutation fails to localize at the ciliary base, causing inefficient CDC recruitment, long cilia, retarded cilium disassembly, and delayed cell cycle re-entry leading to premature NPC differentiation. iPSC-derived neural progenitor cells, patient-derived cells, immunofluorescence, co-immunoprecipitation, brain organoids The EMBO journal High 26929011
2013 CEP120 directly interacts with CPAP and positively regulates centriole elongation. CEP120 is a cell-cycle-regulated protein peaking at S to G2/M. Forced overexpression of either CEP120 or CPAP induces overly long centrioles and atypical supernumerary centrioles. Depletion of CEP120 inhibits CPAP-induced centriole elongation and vice versa. A microtubule-binding-defective CEP120-K76A mutant suppresses elongated centriole formation. Co-immunoprecipitation, siRNA knockdown, overexpression, mutagenesis (K76A), immunofluorescence The Journal of cell biology Medium 23857771
2018 Tubulin interacts with CPAP to negatively regulate CPAP-dependent PCM recruitment and microtubule nucleation. A small molecule CCB02 selectively binds at the CPAP-binding site of tubulin, perturbing CPAP-tubulin interaction. Perturbation of CPAP-tubulin interaction activates extra centrosomes to nucleate enhanced microtubules, causing centrosome de-clustering, multipolar mitosis, and cell death in centrosome-amplified cancer cells. Compound screening, co-immunoprecipitation, genetic perturbation, 3D-organotypic invasion assay, immunofluorescence, in vitro binding assay The EMBO journal Medium 30530478
2018 In Drosophila, Plk1/Polo kinase phosphorylates Sas-4 in vitro at the onset of mitosis, enabling Sas-4's localization to expand outward from centrosomes. This phosphorylation is required for efficient recruitment of Cnn and γ-tubulin (PCM proteins essential for PCM expansion). Point mutations at Plk1/Polo sites reduce affinity for Cnn and γ-tubulin without affecting centrosome structure or centriole duplication. In vitro kinase assay, site-directed mutagenesis, Drosophila genetics, immunofluorescence Cell reports High 30590037
2019 CPAP acts as a transcriptional coactivator of STAT3 by directly binding to STAT3. CPAP overexpression upregulates STAT3 target genes IL-8 and CD44 involved in angiogenesis. Knockdown of CPAP impairs IL-6-mediated STAT3 activation, target gene expression, cell migration, and invasion. Interrupting the CPAP-STAT3 interaction attenuates STAT3-mediated tumor growth and angiogenesis. Co-immunoprecipitation, reporter assay, siRNA knockdown, overexpression, in vivo xenograft, migration/invasion assay Cell death and differentiation Medium 31511651
2019 HBx transcriptionally upregulates CPAP via interacting with CREB at the CPAP promoter (ChIP). Overexpressed CPAP directly interacts with HBx (Co-IP and PLA). SUMO modification of CPAP is required for CPAP-HBx interaction. Overexpressed CPAP maintains HBx protein stability in an NF-κB-dependent manner. Chromatin immunoprecipitation, co-immunoprecipitation, in situ PLA, reporter assay, siRNA knockdown, overexpression Journal of biomedical science Medium 31170980
2019 Cenpj regulates cilia disassembly in mouse neural progenitor cells through Kif2a (a plus-end-directed motor protein). Conditional Cenpj depletion leads to long cilia and abnormal cilia disassembly. Reduced cell proliferation, uncompleted cell division, and apoptosis result in microcephaly. Cenpj also regulates cilium structure of adult neural stem cells. Conditional knockout mice, in vivo immunofluorescence, epistasis with Kif2a, BrdU proliferation assay The Journal of neuroscience Medium 30626697
2020 Conditional knockout of Cpap in mouse CNS preferentially induces monopolar spindles in radial glia progenitors (RGPs) at ~E14.5, causing robust apoptosis. Loss of one p53 allele reduces RGP death, and complete p53 removal rescues RGP death, placing CPAP-loss-induced apoptosis downstream of p53. Cpap deletion also causes cilia loss, RGP mislocalization, junctional integrity disruption, and severe cerebellar hypoplasia. Conditional knockout mouse (CNS-specific), genetic epistasis with p53, immunofluorescence, histological analysis Journal of cell science Medium 32501282
2020 WDR62 mutant proteins (V66M and R439H) localize to the basal body but fail to recruit CPAP. As a consequence, IFT88 recruitment is deficient, leading to failure of cilia formation. This underpins premature differentiation of radial glia and microcephaly in WDR62 mutant mice. CRISPR/Cas9 knock-in mice, immunofluorescence, co-localization studies Human molecular genetics Medium 31816041
2022 Using auxin-inducible degron-mediated fast CPAP degradation combined with superresolution microscopy, three independent centrosomal CPAP populations were identified with distinct cell-cycle regulation. CPAP is critical for assembly of human centrioles but not for PCM recruitment onto already-assembled centrioles. CPAP insufficiency leads to centrioles with incomplete microtubule triplets that can still convert to centrosomes, duplicate, and form spindle poles, but ultimately fragment due to loss of cohesion between microtubule blades. Auxin-inducible degron fast protein degradation, superresolution microscopy (STORM/STED), live imaging, electron microscopy The Journal of cell biology High 35404385
2022 The CPAP-E1235V microcephaly mutant perturbs recruitment of centriolar proteins CEP120, CEP295, CENTROBIN, POC5, and POC1B to nascent centrioles, resulting in short centrioles but long cilia in hiPSC-derived brain organoids. CPAP-E1235V induces p53-dependent neuronal cell death, produces smaller brain organoids, and alters spindle orientation of neuronal progenitor cells causing premature neuronal differentiation. CRISPR-Cas9 isogenic hiPSC generation, brain organoids, immunofluorescence, spindle orientation assay, p53 pathway analysis Frontiers in cell and developmental biology Medium 35309908

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 A centrosomal mechanism involving CDK5RAP2 and CENPJ controls brain size. Nature genetics 447 15793586
2014 CPAP, weight loss, or both for obstructive sleep apnea. The New England journal of medicine 370 24918371
2009 Control of centriole length by CPAP and CP110. Current biology : CB 282 19481458
2003 SAS-4 is a C. elegans centriolar protein that controls centrosome size. Cell 263 12600319
2010 Cep152 acts as a scaffold for recruitment of Plk4 and CPAP to the centrosome. The Journal of cell biology 233 21059844
2009 CPAP is a cell-cycle regulated protein that controls centriole length. Nature cell biology 233 19503075
2009 Overly long centrioles and defective cell division upon excess of the SAS-4-related protein CPAP. Current biology : CB 205 19481460
2011 The human microcephaly protein STIL interacts with CPAP and is required for procentriole formation. The EMBO journal 204 22020124
2016 CPAP promotes timely cilium disassembly to maintain neural progenitor pool. The EMBO journal 194 26929011
2003 SAS-4 is essential for centrosome duplication in C elegans and is recruited to daughter centrioles once per cell cycle. Developmental cell 190 12636923
2013 Human microcephaly protein CEP135 binds to hSAS-6 and CPAP, and is required for centriole assembly. The EMBO journal 166 23511974
2000 Protein 4.1 R-135 interacts with a novel centrosomal protein (CPAP) which is associated with the gamma-tubulin complex. Molecular and cellular biology 143 11003675
2010 Novel CENPJ mutation causes Seckel syndrome. Journal of medical genetics 126 20522431
2011 Sas-4 provides a scaffold for cytoplasmic complexes and tethers them in a centrosome. Nature communications 106 21694707
2008 SAS-4 is recruited to a dynamic structure in newly forming centrioles that is stabilized by the gamma-tubulin-mediated addition of centriolar microtubules. The Journal of cell biology 104 18299348
2013 CEP120 interacts with CPAP and positively regulates centriole elongation. The Journal of cell biology 101 23857771
2011 Spindle positioning in human cells relies on proper centriole formation and on the microcephaly proteins CPAP and STIL. Journal of cell science 95 22100914
2008 Selective effects of CPAP on sleep apnoea-associated manifestations. European journal of clinical investigation 93 18627419
2008 CPAP decreases plasma levels of soluble tumour necrosis factor-alpha receptor 1 in obstructive sleep apnoea. The European respiratory journal 88 18508832
2013 Crystal structures of the CPAP/STIL complex reveal its role in centriole assembly and human microcephaly. eLife 87 24052813
2004 Identification of a novel microtubule-destabilizing motif in CPAP that binds to tubulin heterodimers and inhibits microtubule assembly. Molecular biology of the cell 85 15047868
2013 Integrating psychology and medicine in CPAP adherence--new concepts? Sleep medicine reviews 84 23725820
2012 Disruption of mouse Cenpj, a regulator of centriole biogenesis, phenocopies Seckel syndrome. PLoS genetics 78 23166506
2016 Centriolar CPAP/SAS-4 Imparts Slow Processive Microtubule Growth. Developmental cell 75 27219064
2012 Influence of CPAP treatment on airway and systemic inflammation in OSAS patients. Sleep & breathing = Schlaf & Atmung 70 22945540
2021 Helmet CPAP to treat hypoxic pneumonia outside the ICU: an observational study during the COVID-19 outbreak. Critical care (London, England) 67 33627169
2013 Structural analysis of the G-box domain of the microcephaly protein CPAP suggests a role in centriole architecture. Structure (London, England : 1993) 67 24076405
2006 Molecular evolution of the brain size regulator genes CDK5RAP2 and CENPJ. Gene 64 16631324
2016 Molecular basis for CPAP-tubulin interaction in controlling centriolar and ciliary length. Nature communications 63 27306797
2008 Functional characterization of the microtubule-binding and -destabilizing domains of CPAP and d-SAS-4. Experimental cell research 61 18586240
2020 Pitolisant for Residual Excessive Daytime Sleepiness in OSA Patients Adhering to CPAP: A Randomized Trial. Chest 58 33121980
2014 Conserved TCP domain of Sas-4/CPAP is essential for pericentriolar material tethering during centrosome biogenesis. Proceedings of the National Academy of Sciences of the United States of America 57 24385583
2010 PLK2 phosphorylation is critical for CPAP function in procentriole formation during the centrosome cycle. The EMBO journal 57 20531387
2012 Tankyrase 1 regulates centrosome function by controlling CPAP stability. EMBO reports 52 22699936
2010 Nasal inflammation in sleep apnoea patients using CPAP and effect of heated humidification. The European respiratory journal 51 20595158
1996 Effect of nasal CPAP treatment on plasma volume, aldosterone and 24-h blood pressure in obstructive sleep apnoea. Journal of sleep research 50 8956208
2005 Depletion of CPAP by RNAi disrupts centrosome integrity and induces multipolar spindles. Biochemical and biophysical research communications 49 16316625
2017 Blood pressure response to CPAP treatment in subjects with obstructive sleep apnoea: the predictive value of 24-h ambulatory blood pressure monitoring. The European respiratory journal 48 28982776
2016 Cdk1 Phosphorylates Drosophila Sas-4 to Recruit Polo to Daughter Centrioles and Convert Them to Centrosomes. Developmental cell 47 27326932
2015 Cenpj/CPAP regulates progenitor divisions and neuronal migration in the cerebral cortex downstream of Ascl1. Nature communications 47 25753651
2012 In silico prediction of a disease-associated STIL mutant and its affect on the recruitment of centromere protein J (CENPJ). FEBS open bio 47 23772360
2019 CPAP promotes angiogenesis and metastasis by enhancing STAT3 activity. Cell death and differentiation 46 31511651
2017 CPAP Does Not Reduce Inflammatory Biomarkers in Patients With Coronary Artery Disease and Nonsleepy Obstructive Sleep Apnea: A Randomized Controlled Trial. Sleep 46 29029237
2019 Cenpj Regulates Cilia Disassembly and Neurogenesis in the Developing Mouse Cortex. The Journal of neuroscience : the official journal of the Society for Neuroscience 44 30626697
2014 Markers of inflammation: data from the MOSAIC randomised trial of CPAP for minimally symptomatic OSA. Thorax 44 25182045
2007 Cardiovascular outcomes of CPAP therapy in obstructive sleep apnea syndrome. American journal of physiology. Regulatory, integrative and comparative physiology 44 17634199
2006 A novel deletion mutation in CENPJ gene in a Pakistani family with autosomal recessive primary microcephaly. Journal of human genetics 44 16900296
2002 CPAP is a novel stat5-interacting cofactor that augments stat5-mediated transcriptional activity. Molecular endocrinology (Baltimore, Md.) 44 12198240
2010 Effects of CPAP therapy on the sympathovagal balance and arterial stiffness in obstructive sleep apnea. Respiratory medicine 43 20138492
2018 The CXCL12-CXCR4 axis promotes migration, invasiveness, and EMT in human papillary thyroid carcinoma B-CPAP cells via NF-κB signaling. Biochemistry and cell biology = Biochimie et biologie cellulaire 42 29316404
1979 The value of a sensitive assay of carcino-placental alkaline phosphatase (CPAP) in the follow-up of gynecological cancers. International journal of cancer 42 385513
2016 Quercetin-Induced Cell Death in Human Papillary Thyroid Cancer (B-CPAP) Cells. Journal of thyroid research 38 27057371
2012 Tubulin nucleotide status controls Sas-4-dependent pericentriolar material recruitment. Nature cell biology 38 22729084
2013 Inflammatory processes and effects of continuous positive airway pressure (CPAP) in overlap syndrome. Inflammation 36 22886310
2020 The association of microcephaly protein WDR62 with CPAP/IFT88 is required for cilia formation and neocortical development. Human molecular genetics 35 31816041
2007 Chronic inflation of ferret lungs with CPAP reduces airway smooth muscle contractility in vivo and in vitro. Journal of applied physiology (Bethesda, Md. : 1985) 35 18096756
1990 Overnight decrease in hematocrit after nasal CPAP treatment in patients with OSA. Chest 35 2407456
2024 CPAP may promote an endothelial inflammatory milieu in sleep apnoea after coronary revascularization. EBioMedicine 34 38403558
2015 SAS-4 Protein in Trypanosoma brucei Controls Life Cycle Transitions by Modulating the Length of the Flagellum Attachment Zone Filament. The Journal of biological chemistry 34 26504079
2015 Re-examining the role of Drosophila Sas-4 in centrosome assembly using two-colour-3D-SIM FRAP. eLife 34 26530814
2010 C-reactive protein evolution in obstructive sleep apnoea patients under CPAP therapy. European journal of clinical investigation 34 20629709
2009 Impact of CPAP treatment on cardiac biomarkers and pro-BNP in obstructive sleep apnea syndrome. Sleep & breathing = Schlaf & Atmung 34 19813037
2013 SUMOylated CPAP is required for IKK-mediated NF-κB activation and enhances HBx-induced NF-κB signaling in HCC. Journal of hepatology 33 23369793
2012 Effect of CPAP treatment on endothelial function and plasma CRP levels in patients with sleep apnea. Medical science monitor : international medical journal of experimental and clinical research 33 23197238
2020 An update of pathogenic variants in ASPM, WDR62, CDK5RAP2, STIL, CENPJ, and CEP135 underlying autosomal recessive primary microcephaly in 32 consanguineous families from Pakistan. Molecular genetics & genomic medicine 32 32677750
2014 Impact of CPAP on activity patterns and diet in patients with obstructive sleep apnea (OSA). Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine 32 24910546
2020 Randomised, cOntrolled Multicentre trial of 26 weeks subcutaneous liraglutide (a glucagon-like peptide-1 receptor Agonist), with or without contiNuous positive airway pressure (CPAP), in patients with type 2 diabetes mellitus (T2DM) and obstructive sleep apnoEa (OSA) (ROMANCE): study protocol assessing the effects of weight loss on the apnea-hypnoea index (AHI). BMJ open 30 32699168
2019 Hepatitis B virus X protein (HBx) enhances centrosomal P4.1-associated protein (CPAP) expression to promote hepatocarcinogenesis. Journal of biomedical science 30 31170980
2011 CRP evolution pattern in CPAP-treated obstructive sleep apnea patients. Does gender play a role? Sleep & breathing = Schlaf & Atmung 30 21881894
2020 Obstructive sleep apnea and CPAP therapy alter distinct transcriptional programs in subcutaneous fat tissue. Sleep 29 31872261
2020 Loss of CPAP in developing mouse brain and its functional implication for human primary microcephaly. Journal of cell science 28 32501282
2019 Oxidative stress and inflammatory profiles in obstructive sleep apnea: are short-term CPAP or aerobic exercise therapies effective? Sleep & breathing = Schlaf & Atmung 28 31313021
2020 Effectiveness of an intensive weight-loss program for severe OSA in patients undergoing CPAP treatment: a randomized controlled trial. Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine 27 32003737
2015 CPAP therapy induces favorable short-term changes in epicardial fat thickness and vascular and metabolic markers in apparently healthy subjects with obstructive sleep apnea-hypopnea syndrome (OSAHS). Sleep & breathing = Schlaf & Atmung 27 26223484
2015 Effect of Nasal CPAP on SIRT1 and Endothelial Function in Obstructive Sleep Apnea Syndrome. Lung 26 26345325
2008 Continuous positive airway pressure (CPAP) induces early nasal inflammation. Sleep 26 18220086
2022 CPAP insufficiency leads to incomplete centrioles that duplicate but fragment. The Journal of cell biology 25 35404385
2019 Compliance after switching from CPAP to bilevel for patients with non-compliant OSA: big data analysis. BMJ open respiratory research 25 31178999
2016 Effects of CPAP therapy on visceral fat thickness, carotid intima-media thickness and adipokines in patients with obstructive sleep apnoea. Respirology (Carlton, Vic.) 25 27933703
2015 Centrobin-mediated regulation of the centrosomal protein 4.1-associated protein (CPAP) level limits centriole length during elongation stage. The Journal of biological chemistry 25 25616662
2018 Inhibition of CPAP-tubulin interaction prevents proliferation of centrosome-amplified cancer cells. The EMBO journal 24 30530478
2015 Obstructive sleep apnoea syndrome, endothelial function and markers of endothelialization. Changes after CPAP. PloS one 24 25815511
2011 Effect of CPAP on oxidative stress and circulating progenitor cell levels in sleep patients with apnea-hypopnea syndrome. Respiratory care 24 21605479
2016 Phosphorylation of CPAP by Aurora-A Maintains Spindle Pole Integrity during Mitosis. Cell reports 23 26997271
2012 The non-intubated, spontaneously breathing, continuous positive airway pressure (CPAP) ventilated pre-term lamb: a unique animal model. Reproductive toxicology (Elmsford, N.Y.) 23 22659287
2022 Modeling Human Primary Microcephaly With hiPSC-Derived Brain Organoids Carrying CPAP-E1235V Disease-Associated Mutant Protein. Frontiers in cell and developmental biology 22 35309908
2019 Novel design of NIR-triggered plasmonic nanodots capped mesoporous silica nanoparticles loaded with natural capsaicin to inhibition of metastasis of human papillary thyroid carcinoma B-CPAP cells in thyroid cancer chemo-photothermal therapy. Journal of photochemistry and photobiology. B, Biology 22 31279897
2012 CPAP is required for cilia formation in neuronal cells. Biology open 22 23213448
2021 A 3D-printed microfluidic platform for simulating the effects of CPAP on the nasal epithelium. Biofabrication 20 33561837
2018 Plk1/Polo Phosphorylates Sas-4 at the Onset of Mitosis for an Efficient Recruitment of Pericentriolar Material to Centrosomes. Cell reports 20 30590037
2015 A pathway underlying the impact of CPAP adherence on intimate relationship with bed partner in men with obstructive sleep apnea. Sleep & breathing = Schlaf & Atmung 20 26265560
2012 Regular CPAP utilization reduces nasal inflammation assessed by nasal cytology in obstructive sleep apnea syndrome. Sleep medicine 20 22763015
2008 Short-term CPAP treatment induces a mild increase in inflammatory cells in patients with sleep apnoea syndrome. Rhinology 20 18575017
2022 A genome-wide CRISPR-Cas9 screen identifies CENPJ as a host regulator of altered microtubule organization during Plasmodium liver infection. Cell chemical biology 19 35738280
2014 Centrobin-centrosomal protein 4.1-associated protein (CPAP) interaction promotes CPAP localization to the centrioles during centriole duplication. The Journal of biological chemistry 19 24700465
2021 The Assessment of Endothelial Dysfunction among OSA Patients after CPAP Treatment. Medicina (Kaunas, Lithuania) 18 33806108
2016 Effects of nasal CPAP on exhaled SIRT1 and tumor necrosis factor-α in patients with obstructive sleep apnea. Respiratory physiology & neurobiology 18 26976689
2013 Human-specific hypomethylation of CENPJ, a key brain size regulator. Molecular biology and evolution 18 24288161
2009 Dimerization of CPAP orchestrates centrosome cohesion plasticity. The Journal of biological chemistry 17 19889632
2017 ROLE OF SPOUSAL INVOLVEMENT IN CONTINUOUS POSITIVE AIRWAY PRESSURE (CPAP) ADHERENCE IN PATIENTS WITH OBSTRUCTIVE SLEEP APNEA (OSA). Southwest journal of pulmonary & critical care 16 28725492

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