ArticleBlood2013
Histone deacetylase 1 and 2 are essential for normal T-cell development and genomic stability in mice.
Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 145 citations in OpenAlex.
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- HDAC1 acts as a tumor suppressor in ALK-positive anaplastic large cell lymphoma: implications for HDAC inhibitor therapy.Leukemia · 2025Article
- Hdac1 as an early determinant of intermediate-exhausted CD8Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Therapeutic targeting of TGF-β in lung cancer.The FEBS journal · 2025Review
- Rapid degradation of histone deacetylase 1 (HDAC1) reveals essential roles in both gene repression and active transcription.Nucleic acids research · 2025Article
- Chromatin conformation, gene transcription, and nucleosome remodeling as an emergent system.Science advances · 2025Article
- Article
- Repurposing Histone Deacetylase Inhibitors for Management of Solid Organ Transplant Rejection.Results and problems in cell differentiation · 2025Review
- Histone deacetylases maintain expression of the pluripotent gene network via recruitment of RNA polymerase II to coding and noncoding loci.Genome research · 2024Article
- Dysregulation of histone deacetylases in ocular diseases.Archives of pharmacal research · 2024Review
- A multicenter phase Ib trial of the histone deacetylase inhibitor entinostat in combination with pembrolizumab in patients with myelodysplastic syndromes/neoplasms or acute myeloid leukemia refractory to hypomethylating agents.Annals of hematology · 2024Article
- Update on histone deacetylase inhibitors in peripheral T-cell lymphoma (PTCL).Clinical epigenetics · 2023Review
- Collateral lethality between HDAC1 and HDAC2 exploits cancer-specific NuRD complex vulnerabilities.Nature structural & molecular biology · 2023Article
- Comprehensive Transcriptomic Analysis of Novel Class I HDAC Proteolysis Targeting Chimeras (PROTACs).Biochemistry · 2023Article
- Article
- A toolbox for class I HDACs reveals isoform specific roles in gene regulation and protein acetylation.PLoS genetics · 2022Article
- Role of Histone Deacetylases in T-Cell Development and Function.International journal of molecular sciences · 2022Review
- Proximity-dependent biotin identification (BioID) reveals a dynamic LSD1-CoREST interactome during embryonic stem cell differentiation.Molecular omics · 2022Article
- The synergistic interaction landscape of chromatin regulators reveals their epigenetic regulation mechanisms across five cancer cell lines.Computational and structural biotechnology journal · 2022Article
- The Bidirectional Link Between RNA Cleavage and Polyadenylation and Genome Stability: Recent Insights From a Systematic Screen.Frontiers in genetics · 2022Review
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
Histone deacetylase 1 and 2 (HDAC1/2) regulate chromatin structure as the catalytic core of the Sin3A, NuRD and CoREST co-repressor complexes. To better understand the key pathways regulated by HDAC1/2 in the adaptive immune system and inform their exploitation as drug targets, we have generated mice with a T-cell specific deletion. Loss of either HDAC1 or HDAC2 alone has little effect, while dual inactivation results in a 5-fold reduction in thymocyte cellularity, accompanied by developmental arrest at the double-negative to double-positive transition. Transcriptome analysis revealed 892 misregulated genes in Hdac1/2 knock-out thymocytes, including down-regulation of LAT, Themis and Itk, key components of the T-cell receptor (TCR) signaling pathway. Down-regulation of these genes suggests a model in which HDAC1/2 deficiency results in defective propagation of TCR signaling, thus blocking development. Furthermore, mice with reduced HDAC1/2 activity (Hdac1 deleted and a single Hdac2 allele) develop a lethal pathology by 3-months of age, caused by neoplastic transformation of immature T cells in the thymus. Tumor cells become aneuploid, express increased levels of c-Myc and show elevated levels of the DNA damage marker, γH2AX. These data demonstrate a crucial role for HDAC1/2 in T-cell development and the maintenance of genomic stability.
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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.