ArticleThe Journal of experimental medicine2016
In vivo conditional deletion of HDAC7 reveals its requirement to establish proper B lymphocyte identity and development.
Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- Integrated Genomic and Epigenomic Analysis Reveals Epigenetic Plasticity in Disease Progression and Multidrug Resistance in Multiple Myeloma.Cancer research · 2026Article
- HDAC7 induction combined with standard-of-care chemotherapy provides a therapeutic advantage in t(4;11) infant B-cell acute lymphoblastic leukemia.Biomarker research · 2025Article
- Class IIa HDACs Are Important Signal Transducers with Unclear Enzymatic Activities.Biomolecules · 2025Review
- HDAC7 promotes cardiomyocyte proliferation by suppressing myocyte enhancer factor 2.Journal of molecular cell biology · 2025Article
- Epigenetic Plasticity Drives Carcinogenesis and Multi-Therapy Resistance in Multiple Myeloma.Research square · 2025Article
- Discovery of a potential hematologic malignancies therapy: Selective and potent HDAC7 PROTAC degrader targeting non-enzymatic function.Acta pharmaceutica Sinica. B · 2025Article
- YY1 knockout in pro-B cells impairs lineage commitment, enabling unusual hematopoietic lineage plasticity.Genes & development · 2024Article
- Deacetylation of FOXP1 by HDAC7 potentiates self-renewal of mesenchymal stem cells.Stem cell research & therapy · 2023Article
- Histone deacetylase 7: a signalling hub controlling development, inflammation, metabolism and disease.The FEBS journal · 2023Review
- Alternative splicing of HDAC7 regulates its interaction with 14-3-3 proteins to alter histone marks and target gene expression.Cell reports · 2023Article
- Epigenetic regulation in hematopoiesis and its implications in the targeted therapy of hematologic malignancies.Signal transduction and targeted therapy · 2023Review
- The HDAC7-TET2 epigenetic axis is essential during early B lymphocyte development.Nucleic acids research · 2022Article
- Corticosterone-mediated regulation and functions of miR-218-5p in rat brain.Scientific reports · 2022Article
- Comprehensive Analysis of the Differential Expression and Prognostic Value of Histone Deacetylases in Glioma.Frontiers in cell and developmental biology · 2022Article
- Deletion of Mettl3 at the Pro-B Stage Marginally Affects B Cell Development and Profibrogenic Activity of B Cells in Liver Fibrosis.Journal of immunology research · 2022Article
- HDAC7 is a major contributor in the pathogenesis of infant t(4;11) proB acute lymphoblastic leukemia.Leukemia · 2021Article
- HDAC4 degradation during senescence unleashes an epigenetic program driven by AP-1/p300 at selected enhancers and super-enhancers.Genome biology · 2021Article
- Interplay between cofactors and transcription factors in hematopoiesis and hematological malignancies.Signal transduction and targeted therapy · 2021Review
- Expression of histone deacetylase (HDAC) family members in bortezomib-refractory multiple myeloma and modulation by panobinostat.Cancer drug resistance (Alhambra, Calif.) · 2021Article
- The black sheep of class IIa: HDAC7 SIKens the heart.The Journal of clinical investigation · 2020Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Class IIa histone deacetylase (HDAC) subfamily members are tissue-specific gene repressors with crucial roles in development and differentiation processes. A prominent example is HDAC7, a class IIa HDAC that shows a lymphoid-specific expression pattern within the hematopoietic system. In this study, we explored its potential role in B cell development by generating a conditional knockout mouse model. Our study demonstrates for the first time that HDAC7 deletion dramatically blocks early B cell development and gives rise to a severe lymphopenia in peripheral organs, while also leading to pro-B cell lineage promiscuity. We find that HDAC7 represses myeloid and T lymphocyte genes in B cell progenitors through interaction with myocyte enhancer factor 2C (MEFC2). In B cell progenitors, HDAC7 is recruited to promoters and enhancers of target genes, and its absence leads to increased enrichment of histone active marks. Our results prove that HDAC7 is a bona fide transcriptional repressor essential for B cell development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.