ArticleGenes and immunity2016
Downregulation of ZBTB24 hampers the G0/1- to S-phase cell-cycle transition via upregulating the expression of IRF-4 in human B cells.
Article in Genes and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- 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
- A novel iPSC-based model of ICF syndrome subtype 2 recapitulates the molecular phenotype of ZBTB24 deficiency.Frontiers in immunology · 2024Article
- T Cell Repertoire Abnormality in Immunodeficiency Patients with DNA Repair and Methylation Defects.Journal of clinical immunology · 2022Article
- ZBTB24 (Zinc Finger and BTB Domain Containing 24) prevents recurrent spontaneous abortion by promoting trophoblast proliferation, differentiation and migration.Bioengineered · 2022Article
- Case Report: Primary Immunodeficiencies, Massive EBV+ T-Cell Lympoproliferation Leading to the Diagnosis of ICF2 Syndrome.Frontiers in immunology · 2021Article
- ZBTB Transcription Factors: Key Regulators of the Development, Differentiation and Effector Function of T Cells.Frontiers in immunology · 2021Review
- Cell death pathologies: targeting death pathways and the immune system for cancer therapy.Genes and immunity · 2019Review
- Progressive Immunodeficiency with Gradual Depletion of B and CD4⁺ T Cells in Immunodeficiency, Centromeric Instability and Facial Anomalies Syndrome 2 (ICF2).Diseases (Basel, Switzerland) · 2019Article
- ZBTB24 is a transcriptional regulator that coordinates with DNMT3B to control DNA methylation.Nucleic acids research · 2018Article
- Article
- Regulation of the Development and Function of B Cells by ZBTB Transcription Factors.Frontiers in immunology · 2018Review
- Novel ZBTB24 Mutation Associated with Immunodeficiency, Centromere Instability, and Facial Anomalies Type-2 Syndrome Identified in a Patient with Very Early Onset Inflammatory Bowel Disease.Inflammatory bowel diseases · 2017Article
- Single-Cell RNA Analysis Reveals Reduced Frequency and Activity of CXCR5XenotransplantationArticle
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been recently identified that loss-of-function mutations in the uncharacterized gene ZBTB24 (zinc finger and BTB domain-containing 24) cause ICF2 (immunodeficiency, centromeric instability and facial anomalies syndrome 2) with immunological characteristics of greatly reduced serum antibodies and circulating memory B cells. ZBTB24 belongs to the large ZBTB family of transcriptional repressors with members like B-cell lymphoma 6 (BCL-6; ZBTB27) playing critical roles in B-cell functions. Given the genotype-phenotype correlation analyses in ICF2 patients and the high expression of ZBTB24 in human B cells, we, in the present study, investigated the function of ZBTB24 in human B-cell line Raji cells. Knockdown of endogenous ZBTB24 by small hairpin RNAs results in a significantly reduced proliferation through blocking the G0/1- to S-phase cell-cycle progression, but not apoptosis induction. Moreover, downregulation of ZBTB24 increases the expression of IRF-4 (interferon regulatory factor 4) and Blimp-1 (B lymphocyte-induced maturation protein 1), two crucial factors involved in the proliferation and differentiation of B cells. Importantly, ZBTB24 exerts these functions independent of BCL-6 as it does not affect the expression and function of BCL-6. Our study thus not only provides a molecular explanation for the B-cell and antibody defects observed in ZBTB24-deficient ICF2 patients, but also indicates that ZBTB24 represents a novel transcriptional factor essentially involved in human B-cell functions.
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