Affinage

CDCA7

Cell division cycle-associated protein 7 · UniProt Q9BWT1

Length
371 aa
Mass
42.6 kDa
Annotated
2026-06-09
39 papers in source corpus 25 papers cited in narrative 23 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

CDCA7 is a hemimethylated CpG-sensing chromatin adaptor that, together with the SNF2-family ATPase HELLS/LSH, forms a bipartite nucleosome remodeling complex required for maintenance of DNA methylation at heterochromatin (PMID:29339483, PMID:39178260, PMID:38187757). Its evolutionarily conserved C-terminal cysteine-rich/4CXXC-type zinc-finger domain folds into a unique zinc-binding structure that recognizes hemimethylated CpG within nucleosomal DNA, providing the specificity that directs the complex to replicating heterochromatin (PMID:39178260, PMID:38187757, PMID:39178265, PMID:38168392). The central region of CDCA7 binds and activates the HELLS ATPase to drive nucleosome sliding, while the zinc-finger domain confers the complex's preference for hemimethylated CpG; both are needed for replication-dependent pericentromeric heterochromatin foci (PMID:39142653). Through this activity CDCA7 promotes loading of the DNMT1/UHRF1 maintenance methylation machinery and facilitates UHRF1-mediated H3 ubiquitylation on nascent DNA, and its loss produces aberrant pericentromeric R-loops and DNA damage (PMID:39178260, PMID:38187757, PMID:33082427). In vivo, CDCA7 loss causes large hypomethylated domains and acts as a DNA-methylation-dependent transcriptional repressor, silencing clustered protocadherin isoforms and, within a ZBTB24-CDCA7-HELLS axis, the Dux cluster to restrain 2C-like reprogramming (PMID:38335290, PMID:40226918). CDCA7 also has methylation-independent roles, binding CG-rich promoters in interphase and recruiting HELLS there to regulate transcription, and supporting Ku70/Ku80-dependent classical non-homologous end joining (PMID:42234582, PMID:30307408). CDCA7 expression is driven by c-Myc, E2F, and Notch and is directly controlled by ZBTB24, while AKT phosphorylation at Thr163 promotes 14-3-3 binding and cytoplasmic sequestration away from MYC (PMID:11598121, PMID:16580749, PMID:25385755, PMID:27466202, PMID:23166294). ICF syndrome type 3 is caused by CDCA7 mutations that abolish hemimethylated DNA/chromatin binding and HELLS recruitment, disrupting maintenance methylation (PMID:39178260, PMID:38187757, PMID:39178265, PMID:38168392, PMID:42234582).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2001 Medium

    Established the first functional context for CDCA7 by linking it genetically to c-Myc, framing it as a Myc-responsive nuclear effector relevant to transformation.

    Evidence Representational difference analysis, inducible c-Myc systems, and Rat1a transformation complementation assay

    PMID:11598121

    Open questions at the time
    • Did not define a molecular activity for the protein
    • Mechanism of how CDCA7 complements Myc Box II function unresolved
  2. 2006 Medium

    Extended transcriptional control of CDCA7 to the cell-cycle machinery, identifying it as a direct E2F target and noting intrinsic transactivation potential in its C-terminal region.

    Evidence Adenoviral E2F1 overexpression, promoter-reporter deletion assays, ChIP, and mammalian one-hybrid assay

    PMID:16580749

    Open questions at the time
    • One-hybrid transactivation not tied to endogenous target genes
    • No chromatin or DNA-binding mechanism defined
  3. 2012 High

    Showed how CDCA7 activity is post-translationally gated, revealing AKT-Thr163 phosphorylation as a switch controlling its partitioning between nuclear MYC association and cytoplasmic 14-3-3 sequestration.

    Evidence In vitro AKT kinase assay, phospho-mutants, co-IP, subcellular fractionation, and apoptosis/transformation assays

    PMID:23166294

    Open questions at the time
    • Relationship of the MYC-apoptosis role to the later chromatin/methylation function unresolved
    • Upstream signals controlling Thr163 phosphorylation in vivo not defined
  4. 2014 High

    Added a developmental dimension, placing CDCA7 downstream of Notch as a direct RBPj/Notch1 target required for hematopoietic stem cell emergence.

    Evidence ChIP-on-chip and ChIP in AGM, shRNA knockdown, zebrafish morpholino loss-of-function, and human ESC differentiation

    PMID:25385755

    Open questions at the time
    • Molecular function of CDCA7 in HSC emergence not mechanistically defined
    • Whether the chromatin remodeling activity underlies this role unknown
  5. 2016 High

    Connected CDCA7 to the ICF-syndrome regulatory network by establishing ZBTB24 as a direct transcriptional activator of CDCA7, linking two ICF disease genes in one pathway.

    Evidence Zbtb24 BTB-deletion mouse, RNA-seq, ChIP at the CDCA7 promoter, ectopic rescue, and patient cell analysis

    PMID:27466202

    Open questions at the time
    • Did not establish the downstream biochemical role of CDCA7
    • How reduced CDCA7 produces ICF phenotypes not yet mechanistic
  6. 2018 High

    Defined the core biochemical function of CDCA7: it is required to load HELLS onto chromatin, and the CDCA7-HELLS complex possesses nucleosome remodeling activity absent in either protein alone, with ICF mutations abolishing recruitment.

    Evidence Xenopus egg extract chromatin proteomics, co-IP, in vitro nucleosome remodeling assay, and ICF mutant analysis

    PMID:29339483

    Open questions at the time
    • DNA-sequence/modification specificity of recruitment not yet defined
    • Structural basis of CDCA7-nucleosome recognition unknown
  7. 2018 High

    Broadened CDCA7 function to genome stability, showing nuclease-sensitive association with Ku70/Ku80 and a requirement for CDCA7/HELLS in classical NHEJ.

    Evidence Nuclease-sensitive co-IP, laser-induced damage Ku80 recruitment imaging, and NHEJ reporter assays in knockout cells

    PMID:30307408

    Open questions at the time
    • Whether NHEJ defect is direct or secondary to chromatin remodeling unresolved
    • Mechanism by which CDCA7/HELLS accelerates Ku recruitment unclear
  8. 2020 Medium

    Linked CDCA7/HELLS remodeling to maintenance methylation and R-loop suppression, showing the complex enables accumulation of DNMT1/UHRF1 and R-loop resolution factors on nascent DNA.

    Evidence iPOND nascent-DNA proteomics, S9.6 R-loop detection, and RNASEH1 rescue of DNA damage in ICF-mutant cells

    PMID:33082427

    Open questions at the time
    • Causal order between methylation loss and R-loop accumulation not fully resolved
    • Single-lab nascent-DNA proteomics
  9. 2024 High

    Resolved the molecular specificity of CDCA7: cryo-EM and structural studies showed the C-terminal zinc-finger/CRD recognizes hemimethylated CpG in nucleosomal and non-B DNA, explaining how the complex is targeted to replicating heterochromatin and how ICF mutations disrupt it.

    Evidence Cryo-EM of the CDCA7-nucleosome complex, CRD zinc-fold determination, hemimethylated-CpG binding assays, S-phase localization imaging, and UHRF1 ubiquitylation assays

    PMID:39178260 PMID:39178265

    Open questions at the time
    • How hemimethylated-DNA sensing is coupled to HELLS ATPase activation not fully integrated
    • In vivo dynamics of foci formation only partially defined
  10. 2024 High

    Dissected the domain architecture functionally, assigning HELLS binding and ATPase activation to the central region, autoinhibition to the N-terminus, and hemimethylated-CpG preference to the zinc finger.

    Evidence In vitro ATPase and nucleosome sliding assays with CDCA7 domain mutants plus replication-foci imaging in mESCs

    PMID:39142653

    Open questions at the time
    • Conformational basis of N-terminal autoinhibition not structurally defined
    • Regulation of the autoinhibition in cells unknown
  11. 2024 High

    Demonstrated the in vivo consequences of CDCA7 loss as a methylation-dependent transcriptional repressor, with hypomethylation of B-compartment and protocadherin loci independent of H3K9me3.

    Evidence Pathogenic Cdca7 missense knock-in mouse, whole-genome bisulfite sequencing, histone-mark and CTCF ChIP, and transcriptomics

    PMID:38335290

    Open questions at the time
    • Mechanism linking protocadherin hypomethylation to CTCF/H3K4me3 gain not fully causal
    • Tissue-specific selectivity of affected domains unexplained
  12. 2025 High

    Defined a ZBTB24-CDCA7-HELLS axis maintaining Dux-cluster methylation to suppress 2C-like totipotent reprogramming, integrating CDCA7's upstream regulation with its chromatin-targeting role.

    Evidence Genetic KO of ZBTB24/CDCA7/HELLS in mESCs, CDCA7 ChIP at Dux, bisulfite sequencing, and dCas9-targeted re-methylation rescue

    PMID:40226918

    Open questions at the time
    • How CDCA7 selects the Dux locus among many repeats unclear
    • Relative contributions of CDCA7 vs HELLS to silencing not separated
  13. 2026 High

    Distinguished two cell-cycle-dependent DNA-binding modes, showing interphase CG-rich promoter binding versus late-S-phase hemimethylated heterochromatin localization, with both directing HELLS recruitment and methylation-independent transcriptional effects.

    Evidence Genome-wide CDCA7 ChIP-seq, in vitro CG-rich vs hemimethylated binding assays, cell-cycle-resolved live imaging, methylome and transcriptome analysis, and G294V ICF mutant

    PMID:42234582

    Open questions at the time
    • Switch mechanism between the two binding modes not defined
    • Functional importance of interphase promoter binding in disease unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how CDCA7's conserved chromatin-remodeling/methylation function mechanistically gives rise to its many reported context-specific oncogenic transcriptional activities (e.g., CCNA2, TGF-β/Smad, STAT3/HK2, autophagy genes) and partner interactions (EZH2, STAT3).
  • Several cancer-context partnerships rest on single non-reciprocal co-IPs
  • Whether these transcriptional effects are direct or downstream of methylation changes is untested
  • Integration of cytoskeletal/migration phenotype with chromatin function unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 3 GO:0060090 molecular adaptor activity 3 GO:0140110 transcription regulator activity 2 GO:0140657 ATP-dependent activity 2
Localization
GO:0000228 nuclear chromosome 3 GO:0005634 nucleus 3 GO:0005829 cytosol 1
Pathway
R-HSA-4839726 Chromatin organization 5 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-73894 DNA Repair 2
Partners
DNMT1EZH2HELLSMYCUHRF1XRCC5XRCC6YWHA
Complex memberships
CDCA7-HELLS nucleosome remodeling complex

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2018 CDCA7 and HELLS form a stoichiometric bipartite nucleosome remodeling complex on chromatin; CDCA7 is essential for loading HELLS onto chromatin, and the HELLS-CDCA7 complex together possesses nucleosome remodeling activity that neither protein has alone. ICF-mutant CDCA7 fails to recruit the complex to chromatin. Xenopus egg extract chromatin proteomics, co-immunoprecipitation, in vitro nucleosome remodeling assay, Aurora B inhibitor treatment, ICF patient mutation analysis Proceedings of the National Academy of Sciences of the United States of America High 29339483
2024 The C-terminal zinc-finger domain (HMZF/zf-4CXXC_R1) of CDCA7 is an evolutionarily conserved hemimethylated CpG sensor. Cryo-EM structural analysis of the CDCA7-nucleosome complex reveals this domain recognizes hemimethylated CpG in the outward-facing DNA major groove within the nucleosome core particle. CDCA7 recruits HELLS to hemimethylated chromatin and facilitates UHRF1-mediated H3 ubiquitylation associated with replication-uncoupled maintenance DNA methylation. ICF disease mutations abolish hemimethylated DNA binding. Cryo-EM structure determination, in vitro DNA binding assays (hemimethylated vs. unmethylated vs. fully methylated CpG), ICF mutant functional analysis, UHRF1 ubiquitylation assay Science advances High 38187757 39178260
2024 The CDCA7 C-terminal cysteine-rich domain (CRD) adopts a unique zinc-binding structure that recognizes a CpG dyad in a non-B DNA formed by two sequence motifs, with strand-specific preference for hemimethylated CpG. ICF mutant CDCA7 loses this binding. During S phase, CDCA7 concentrates in constitutive heterochromatin foci in a CRD-dependent manner, and this localization can be outcompeted by exogenous hemi-methylated non-B DNA. Structural determination of CRD zinc-binding fold, in vitro DNA binding assays with non-B DNA substrates, live-cell imaging of S-phase localization, ICF mutant analysis, competition assay with exogenous DNA Science advances High 38168392 39178265
2024 The central region of CDCA7 is critical for binding HELLS, activating HELLS ATPase activity, and enabling nucleosome sliding by the HELLS-CDCA7 complex. The N-terminal region tends to inhibit ATPase activity. The C-terminal 4CXXC-type zinc finger domain confers preference for hemimethylated CpG DNA in HELLS-CDCA7 ATPase activity, and replication-dependent pericentromeric heterochromatin foci formation of CDCA7 with HELLS requires an intact zinc finger domain. In vitro ATPase assay, nucleosome sliding assay, domain-deletion/mutant CDCA7 proteins, live-cell imaging of replication foci in mouse embryonic stem cells Nucleic acids research High 39142653
2018 CDCA7 co-immunoprecipitates with C-NHEJ proteins Ku80 and Ku70 as well as HELLS; this interaction is sensitive to nuclease treatment and to an ICF3 mutation in CDCA7 that impairs chromatin binding. Loss of CDCA7 or HELLS compromises classical NHEJ activity and delays Ku80 accumulation at DNA damage sites. Co-immunoprecipitation (nuclease-sensitive), live-cell imaging of Ku80 recruitment to laser-induced DNA damage, NHEJ reporter assay in CDCA7/HELLS-deficient HEK293 cells The Journal of clinical investigation High 30307408
2012 AKT phosphorylates CDCA7 at threonine 163, promoting its binding to 14-3-3 proteins, dissociation from MYC, and cytoplasmic sequestration. Dephosphorylated CDCA7 associates with MYC in the nucleus and sensitizes cells to apoptosis upon serum withdrawal; CDCA7 knockdown reduces MYC-dependent apoptosis, and CDCA7 co-expression reduces MYC-mediated transformation of fibroblasts. In vitro kinase assay (AKT phosphorylation of Thr163), co-immunoprecipitation (CDCA7-MYC, CDCA7-14-3-3), phospho-mimetic/phospho-dead mutants, subcellular fractionation, apoptosis assays, Rat1a transformation assay Molecular and cellular biology High 23166294
2001 CDCA7 (JPO1) is a direct transcriptional target of c-Myc, encodes a 47-kDa nuclear protein, and complements a transformation-defective Myc Box II mutant in the Rat1a fibroblast transformation assay, establishing a functional genetic link between c-Myc and CDCA7. Representational difference analysis to identify Myc-responsive gene, inducible c-Myc systems, Rat1a transformation assay, clonogenicity assay in human lymphoblastoid cells The Journal of biological chemistry Medium 11598121
2006 CDCA7 is a direct transcriptional target of E2F1 (and E2F2/E2F4 but not E2F5/E2F6), as demonstrated by E2F-responsive element requirement in the CDCA7 promoter and ChIP showing E2F1/E2F2/E2F4 binding. The C-terminal cysteine-rich region of CDCA7 harbors intrinsic transcriptional activator activity in a mammalian one-hybrid assay. Adenoviral E2F1 overexpression, promoter-reporter assays with deletion constructs, chromatin immunoprecipitation (ChIP) of E2F binding, mammalian one-hybrid transcriptional activity assay Biochimica et biophysica acta Medium 16580749
2016 ZBTB24 directly controls transcription of CDCA7: ZBTB24 is enriched at the CDCA7 promoter by ChIP, loss of functional Zbtb24 in mouse ESCs downregulates Cdca7 as the top affected gene, and ectopic ZBTB24 expression restores Cdca7 levels. CDCA7 protein levels are reduced in patients with ZBTB24 nonsense mutations. Zbtb24 BTB-domain deletion mouse model, transcriptome analysis (RNAseq), ChIP at CDCA7 promoter, ectopic ZBTB24 rescue experiment, patient lymphoblastoid cell analysis Human molecular genetics High 27466202
2014 CDCA7 is a direct Notch transcriptional target in the aorta-gonad-mesonephros (AGM): RBPj and Notch1 are recruited to the Cdca7 promoter by ChIP. CDCA7 expression is restricted to hematopoietic clusters in the aorta and is required for hematopoietic stem cell emergence; its knockdown in zebrafish reduces HSC formation, and its downregulation in AGM cells promotes hematopoietic differentiation and loss of progenitors. ChIP-on-chip for RBPj in AGM, ChIP for Notch1, shRNA knockdown in AGM cells, zebrafish loss-of-function experiment (morpholinos), human ESC hematopoietic differentiation with Notch inhibition The Journal of experimental medicine High 25385755
2020 The CDCA7/HELLS complex is required for the accumulation of proteins on nascent DNA, including the DNMT1/UHRF1 maintenance methylation complex and R-loop resolution factors. Loss of CDCA7/HELLS leads to increased transcription and aberrant DNA:RNA hybrid (R-loop) formation at pericentromeric repeats, and ectopic RNASEH1 expression reduces DNA damage accumulation at these loci in ICF mutant cells. iPOND (nascent DNA proteomics), R-loop detection (S9.6 antibody), RNASEH1 rescue experiment in CDCA7/HELLS-deficient cells, γH2AX quantification Scientific reports Medium 33082427
2019 CDCA7 knockdown in lymphoma cells disrupts actomyosin and tubulin cytoskeleton polarization required for migration, increases filamentous actin formation, and induces myosin activation, impairing migration on fibronectin without affecting adhesion. Inhibitors of actin polymerization, myosin II, or ROCK restore migration capacity of CDCA7-silenced lymphoma cells. shRNA knockdown, matrigel transwell invasion assay, mouse xenograft invasion model, zebrafish invasion model, phalloidin staining of F-actin, myosin phosphorylation assays, pharmacological rescue with actin/myosin/ROCK inhibitors Haematologica Medium 31221787
2021 CDCA7 directly binds the CCNA2 (Cyclin A2) gene promoter and upregulates its expression; knockdown of CCNA2 reverses the proliferative phenotype induced by CDCA7 overexpression in esophageal squamous cell carcinoma cells. ChIP assay (CDCA7 binding to CCNA2 promoter), luciferase reporter assay, CCNA2 rescue/knockdown experiments, cell cycle analysis Frontiers in oncology Medium 34737951
2022 CDCA7 transcriptionally regulates Smad4 and Smad7 expression to modulate the TGF-β signaling pathway and promote EMT in esophageal squamous cell carcinoma; dual-luciferase reporter assays and rescue experiments established this regulatory link. Dual-luciferase reporter assay, ChIP, CDCA7 knockdown/overexpression, rescue assay with Smad4/Smad7, EMT marker Western blot Cancer science Medium 36056599
2019 ZBTB24 regulates human T-cell apoptosis via CDCA7: ZBTB24 deficiency reduces CDCA7 expression, and CDCA7 knockdown phenocopies ZBTB24 loss (increased TRAIL/TRAIL-R expression, apoptosis). Overexpression of CDCA7 rescues the increased apoptosis in ZBTB24-depleted Jurkat T cells. shRNA knockdown of ZBTB24 and CDCA7 in Jurkat and primary T cells, CDCA7 overexpression rescue, TRAIL/TRAIL-R expression analysis, flow cytometry apoptosis assay Biochemical and biophysical research communications Medium 31030944
2021 CDCA7 physically interacts with EZH2 in ovarian cancer cells, as verified by co-immunoprecipitation; CDCA7 knockdown suppresses EZH2 expression and reduces in vitro angiogenesis. Co-immunoprecipitation (CDCA7–EZH2), shRNA knockdown, HUVEC tube formation assay Bioengineered Low 34551671
2025 CDCA7 interacts with STAT3 and affects STAT3-dependent transcriptional regulation of hexokinase 2 (HK2), thereby promoting aerobic glycolysis in pancreatic cancer cells. Co-immunoprecipitation (CDCA7–STAT3), luciferase reporter for HK2 promoter, CDCA7 knockdown/overexpression with metabolic assays Cell death & disease Low 39905019
2024 METTL3 enhances CDCA7 mRNA stability via N6-methyladenosine (m6A) modification, as demonstrated by methylated RNA immunoprecipitation (MeRIP) confirming METTL3-dependent m6A on CDCA7 mRNA in colon adenocarcinoma cells. Methylated RNA immunoprecipitation (MeRIP), METTL3 knockdown with CDCA7 mRNA stability measurement Pathology, research and practice Low 38959625
2024 CDCA7 loss in vivo causes large aberrantly hypomethylated domains overlapping the B genomic compartment without affecting H3K9me3 deposition. In brain tissue, CDCA7 acts as a transcriptional repressor of clustered protocadherin isoforms via DNA methylation; hypomethylation at protocadherin loci upon CDCA7 loss is accompanied by gain of H3K4me3 and increased CTCF binding. Pathogenic Cdca7 missense knock-in mouse, whole-genome bisulfite sequencing across multiple tissues, H3K9me3/H3K4me3 ChIP, CTCF ChIP, transcriptome analysis Science advances High 38335290
2025 CDCA7 and HELLS constitute a ZBTB24-CDCA7-HELLS axis that suppresses totipotent 2C-like reprogramming in mESCs by maintaining DNA methylation of the Dux cluster. CDCA7 is enriched at the Dux cluster chromatin and recruits HELLS there; disruption leads to Dux hypomethylation, derepression, and upregulation of 2C-specific genes, reversible by site-specific re-methylation at the Dux promoter. Genetic KO of ZBTB24, CDCA7, and HELLS in mESCs, ChIP (CDCA7 enrichment at Dux cluster), bisulfite sequencing, dCas9-targeted methylation rescue, transcriptome analysis Nucleic acids research High 40226918
2026 CDCA7 exhibits two distinct DNA-binding modes and subcellular localization patterns: diffuse nuclear distribution in interphase (binding CG-rich promoter regions) and pericentromeric heterochromatin localization in late S phase (hemimethylated DNA-dependent). An ICF-causing G294V mutation abolishes both CG-rich DNA binding and heterochromatin localization. CDCA7 recruits LSH/HELLS to both CG-rich promoters in interphase and heterochromatin domains in late S phase, and both proteins can regulate transcription independently of DNA methylation. Genome-wide CDCA7 ChIP-seq, in vitro DNA binding assays (CG-rich vs. hemimethylated probes), live-cell imaging of cell-cycle-dependent localization, whole-genome DNA methylation analysis, transcriptome analysis, G294V ICF mutant comparison Nucleic acids research High 42234582
2026 CDCA7 physically interacts with HELLS in gastric cancer cells (co-immunoprecipitation), promotes HELLS recruitment to chromatin (ChIP), and knockdown of CDCA7 reduces global 5hmC/5mC levels and histone methylation marks H3K9me3 and H4K20me3; HELLS overexpression partially reverses these effects and the antiproliferative/proapoptotic consequences of CDCA7 knockdown. Co-immunoprecipitation (CDCA7-HELLS), ChIP (HELLS chromatin recruitment), dot blot for 5mC/5hmC, Western blot for histone marks, HELLS overexpression rescue in CDCA7 KD cells Oncology research Medium 42065057
2026 CDCA7 transcriptionally activates autophagy-related genes ULK1, ATG2A, and ATG3 in breast cancer drug-tolerant persister (DTP) cells, as identified by ChIP-seq and validated by dual-luciferase assay with site-directed mutagenesis of binding sites. CDCA7 knockdown reduces autophagic flux and restores chemosensitivity. ChIP-seq (CDCA7 binding at ULK1, ATG2A, ATG3), dual-luciferase assay with mutagenesis, transmission electron microscopy of autolysosomes, mRFP-GFP-LC3 autophagic flux assay, drug resistance (CCK-8), in vivo xenograft Frontiers in immunology Medium 41890763

Source papers

Stage 0 corpus · 39 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2015 Mutations in CDCA7 and HELLS cause immunodeficiency-centromeric instability-facial anomalies syndrome. Nature communications 151 26216346
2018 HELLS and CDCA7 comprise a bipartite nucleosome remodeling complex defective in ICF syndrome. Proceedings of the National Academy of Sciences of the United States of America 109 29339483
2018 CDCA7 and HELLS mutations undermine nonhomologous end joining in centromeric instability syndrome. The Journal of clinical investigation 75 30307408
2019 Long noncoding RNA FGD5-AS1 promotes colorectal cancer cell proliferation, migration, and invasion through upregulating CDCA7 via sponging miR-302e. In vitro cellular & developmental biology. Animal 64 31332696
2018 Comparative methylome analysis of ICF patients identifies heterochromatin loci that require ZBTB24, CDCA7 and HELLS for their methylated state. Human molecular genetics 64 29659838
2012 The MYC-associated protein CDCA7 is phosphorylated by AKT to regulate MYC-dependent apoptosis and transformation. Molecular and cellular biology 62 23166294
2005 The Myc target gene JPO1/CDCA7 is frequently overexpressed in human tumors and has limited transforming activity in vivo. Cancer research 58 15994934
2001 A novel c-Myc-responsive gene, JPO1, participates in neoplastic transformation. The Journal of biological chemistry 54 11598121
2016 Converging disease genes in ICF syndrome: ZBTB24 controls expression of CDCA7 in mammals. Human molecular genetics 53 27466202
2014 Identification of Cdca7 as a novel Notch transcriptional target involved in hematopoietic stem cell emergence. The Journal of experimental medicine 43 25385755
2006 JPO1/CDCA7, a novel transcription factor E2F1-induced protein, possesses intrinsic transcriptional regulator activity. Biochimica et biophysica acta 38 16580749
2020 CDCA7 and HELLS suppress DNA:RNA hybrid-associated DNA damage at pericentromeric repeats. Scientific reports 34 33082427
2019 CDCA7 promotes lung adenocarcinoma proliferation via regulating the cell cycle. Pathology, research and practice 26 31570276
2024 CDCA7 is an evolutionarily conserved hemimethylated DNA sensor in eukaryotes. Science advances 21 39178260
2021 CDCA7 Facilitates Tumor Progression by Directly Regulating CCNA2 Expression in Esophageal Squamous Cell Carcinoma. Frontiers in oncology 19 34737951
2019 CDCA7 finely tunes cytoskeleton dynamics to promote lymphoma migration and invasion. Haematologica 19 31221787
2018 CDCA7 is a critical mediator of lymphomagenesis that selectively regulates anchorage-independent growth. Haematologica 19 29880607
2023 Coevolution of the CDCA7-HELLS ICF-related nucleosome remodeling complex and DNA methyltransferases. eLife 18 37769127
2020 LncRNA LEF1-AS1 silencing diminishes EZH2 expression to delay hepatocellular carcinoma development by impairing CEBPB-interaction with CDCA7. Cell cycle (Georgetown, Tex.) 18 32178558
2024 CDCA7-associated global aberrant DNA hypomethylation translates to localized, tissue-specific transcriptional responses. Science advances 17 38335290
2024 The C-terminal 4CXXC-type zinc finger domain of CDCA7 recognizes hemimethylated DNA and modulates activities of chromatin remodeling enzyme HELLS. Nucleic acids research 17 39142653
2022 CDCA7 promotes TGF-β-induced epithelial-mesenchymal transition via transcriptionally regulating Smad4/Smad7 in ESCC. Cancer science 17 36056599
2021 CDCA7-regulated inflammatory mechanism through TLR4/NF-κB signaling pathway in stomach adenocarcinoma. BioFactors (Oxford, England) 16 34339079
2021 Downregulation of cell division cycle-associated protein 7 (CDCA7) suppresses cell proliferation, arrests cell cycle of ovarian cancer, and restrains angiogenesis by modulating enhancer of zeste homolog 2 (EZH2) expression. Bioengineered 16 34551671
2024 The ICF syndrome protein CDCA7 harbors a unique DNA binding domain that recognizes a CpG dyad in the context of a non-B DNA. Science advances 15 39178265
2025 CDCA7 enhances STAT3 transcriptional activity to regulate aerobic glycolysis and promote pancreatic cancer progression and gemcitabine resistance. Cell death & disease 10 39905019
2019 ZBTB24 regulates the apoptosis of human T cells via CDCA7/TRAIL-receptor axis. Biochemical and biophysical research communications 9 31030944
2025 The ZBTB24-CDCA7-HELLS axis suppresses the totipotent 2C-like reprogramming by maintaining Dux methylation and repression. Nucleic acids research 4 40226918
2025 CircASH1L inhibits ferroptosis and enhances cisplatin resistance by sponging miR-515-5p to regulate cell cycle-related CDCA7/RRM2 in ovarian cancer cells. Frontiers in pharmacology 3 40630134
2023 CDCA7 is a hemimethylated DNA adaptor for the nucleosome remodeler HELLS. bioRxiv : the preprint server for biology 3 38187757
2025 CDCA7 facilitates MET1-mediated CG DNA methylation maintenance in centromeric heterochromatin via linker histone H1. Proceedings of the National Academy of Sciences of the United States of America 2 41370347
2023 The ICF syndrome protein CDCA7 harbors a unique DNA-binding domain that recognizes a CpG dyad in the context of a non-B DNA. bioRxiv : the preprint server for biology 2 38168392
2023 Coevolution of the CDCA7-HELLS ICF-related nucleosome remodeling complex and DNA methyltransferases. bioRxiv : the preprint server for biology 1 36778482
2026 CDCA7 promotes chemoresistance of drug-tolerant persister cells in breast cancer by upregulating the expression of autophagy-related protein genes. Frontiers in immunology 0 41890763
2026 CDCA7 Promotes Proliferation and Suppresses Apoptosis in Gastric Cancer via HELLS-Mediated Chromatin Remodeling. Oncology research 0 42065057
2026 CDCA7 Promotes Neuroblastoma Proliferation via Regulating the Cell Cycle. Iranian journal of biotechnology 0 42145973
2026 CDCA7 targets LSH to DNA maintenance methylation in S phase and transcription regulation in interphase via two distinct DNA-binding modes. Nucleic acids research 0 42234582
2024 METTL3-mediated m6A modification of CDCA7 mRNA promotes COAD progression. Pathology, research and practice 0 38959625
2024 Circ_0006220 (circ-TADA2A) accelerates prostate cancer cell malignant behaviors through miR-520f-3p/CDCA7 axis. Cellular and molecular biology (Noisy-le-Grand, France) 0 39097891

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