ArticleNucleic acids research2018
ZBTB24 is a transcriptional regulator that coordinates with DNMT3B to control DNA methylation.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 65 citations in OpenAlex.
- Functional characterization of UHRF1 variants in facilitating DNA methylation.The Journal of biological chemistry · 2026Article
- CDCA7 targets LSH to DNA maintenance methylation in S phase and transcription regulation in interphase via two distinct DNA-binding modes.Nucleic acids research · 2026Article
- Structure of human lymphoid-specific helicase HELLS in its autoinhibited state.Nucleic acids research · 2026Article
- Missense substitutions in the BTB domain of ZBTB24 can lead to protein instability and cause ICF2 syndrome.Human molecular genetics · 2026Article
- ICF syndrome: An epigenetic paradigm for primary immunodeficiencies.Journal of human immunity · 2026Review
- Structure of human lymphoid-specific helicase HELLS in its autoinhibitory state.bioRxiv : the preprint server for biology · 2025Article
- The ZBTB24-CDCA7-HELLS axis suppresses the totipotent 2C-like reprogramming by maintaining Dux methylation and repression.Nucleic acids research · 2025Article
- ZBTB24 is a conserved multifaceted transcription factor at genes and centromeres that governs the DNA methylation state and expression of satellite repeats.Human molecular genetics · 2025Article
- In-depth immune profiling of a patient with immunodeficiency, centromeric instability, and facial anomalies syndrome type 2 caused by a novel mutation in ZBTB24.Clinical and experimental immunology · 2025Article
- Case report: Novel multi-exon homozygous deletion ofFrontiers in immunology · 2025Article
- The ICF2 gene Zbtb24 specifically regulates the differentiation of B1 cells via promoting heme synthesis.Cellular & molecular biology letters · 2024Article
- 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 · 2024Article
- SETD2 loss in renal epithelial cells drives epithelial-to-mesenchymal transition in a TGF-β-independent manner.Molecular oncology · 2024Article
- The epigenetic modification of DNA methylation in neurological diseases.Frontiers in immunology · 2024Review
- A novel iPSC-based model of ICF syndrome subtype 2 recapitulates the molecular phenotype of ZBTB24 deficiency.Frontiers in immunology · 2024Article
- Enhanced CD19 activity in B cells contributes to immunodeficiency in mice deficient in the ICF syndrome gene Zbtb24.Cellular & molecular immunology · 2023Article
- Seminars in cell and development biology on histone variants remodelers of H2A variants associated with heterochromatin.Seminars in cell & developmental biology · 2023Review
- Rare diseases of epigenetic origin: Challenges and opportunities.Frontiers in genetics · 2023Review
- The remodeling of Z-DNA in the mammalian germ line.Biochemical Society transactions · 2022Article
- DNMT3B overexpression downregulates genes with CpG islands, common motifs, and transcription factor binding sites that interact with DNMT3B.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
The interplay between transcription factors and epigenetic writers like the DNA methyltransferases (DNMTs), and the role of this interplay in gene expression, is being increasingly appreciated. ZBTB24, a poorly characterized zinc-finger protein, or the de novo methyltransferase DNMT3B, when mutated, cause Immunodeficiency, Centromere Instability, and Facial anomalies (ICF) syndrome, suggesting an underlying mechanistic link. Chromatin immunoprecipitation coupled with loss-of-function approaches in model systems revealed common loci bound by ZBTB24 and DNMT3B, where they function to regulate gene body methylation. Genes coordinately regulated by ZBTB24 and DNMT3B are enriched for molecular mechanisms essential for cellular homeostasis, highlighting the importance of the ZBTB24-DNMT3B interplay in maintaining epigenetic patterns required for normal cellular function. We identify a ZBTB24 DNA binding motif, which is contained within the promoters of most of its transcriptional targets, including CDCA7, AXIN2, and OSTC. Direct binding of ZBTB24 at the promoters of these genes targets them for transcriptional activation. ZBTB24 binding at the promoters of RNF169 and CAMKMT, however, targets them for transcriptional repression. The involvement of ZBTB24 targets in diverse cellular programs, including the VDR/RXR and interferon regulatory pathways, suggest that ZBTB24's role as a transcriptional regulator is not restricted to immune cells.
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