ArticleMolecular and cellular biology2005
The mSin3A chromatin-modifying complex is essential for embryogenesis and T-cell development.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 1 of them a synthesis that pooled it.
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Who cites it
92 citing papers in PubMed, 1 synthesis or guideline pooled it, 142 citations in OpenAlex.
- Histone and Histone Acetylation-Related Alterations of Gene Expression in Uninvolved Psoriatic Skin and Their Effects on Cell Proliferation, Differentiation, and Immune Responses.International journal of molecular sciences · 2023Pooled it
- A de novo missense variant in MIDEAS results in increased deacetylase activity of the MiDAC HDAC complex causing a neurodevelopmental syndrome.Nature communications · 2025Article
- The Allosteric Regulator Inositol Phosphate Dramatically Affects the Efficacy and Selectivity of Inhibitors for Different HDAC Complexes.Journal of the American Chemical Society · 2025Article
- Mutations on the surface of HDAC1 reveal molecular determinants of specific complex assembly and their requirement for gene regulation.Nucleic acids research · 2025Article
- Identification of glycolysis-related molecular subtypes and prognostic model in intrahepatic cholangiocarcinoma.Discover oncology · 2025Article
- BAHCC1 promotes gene expression in neuronal cells by antagonizing SIN3A-HDAC1.Nucleic acids research · 2025Article
- The histone modification regulator, SIN3, plays a role in the cellular response to changes in glycolytic flux.PloS one · 2025Article
- Common variants increase risk for congenital diaphragmatic hernia within the context of de novo variants.American journal of human genetics · 2024Article
- SIN3B Loss Heats up Cold Tumor Microenvironment to Boost Immunotherapy in Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- HDAC activity is dispensable for repression of cell-cycle genes by DREAM and E2F:RB complexes.Nature communications · 2024Article
- Rescuing lung development through embryonic inhibition of histone acetylation.Science translational medicine · 2024Article
- T-regulatory cells require Sin3a for stable expression of Foxp3.Frontiers in immunology · 2024Article
- Switch-Independent 3A: An Epigenetic Regulator in Cancer with New Implications for Pulmonary Arterial Hypertension.Biomedicines · 2023Review
- HDAC activity is dispensable for repression of cell-cycle genes by DREAM and E2F:RB complexes.bioRxiv : the preprint server for biology · 2023Article
- SAP30 promotes breast tumor progression by bridging the transcriptional corepressor SIN3 complex and MLL1.The Journal of clinical investigation · 2023Article
- A potential histone-chaperone activity for the MIER1 histone deacetylase complex.Nucleic acids research · 2023Article
- Histone H3 lysine 27 crotonylation mediates gene transcriptional repression in chromatin.Molecular cell · 2023Article
- The Fgf/Erf/NCoR1/2 repressive axis controls trophoblast cell fate.Nature communications · 2023Article
- The transcriptional regulator Sin3A balances IL-17A and Foxp3 expression in primary CD4 T cells.EMBO reports · 2023Article
- Mechanism of assembly, activation and lysine selection by the SIN3B histone deacetylase complex.Nature communications · 2023Article
32 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The corepressor mSin3A is the core component of a chromatin-modifying complex that is recruited by multiple gene-specific transcriptional repressors. In order to understand the role of mSin3A during development, we generated constitutive germ line as well as conditional msin3A deletions. msin3A deletion in the developing mouse embryo results in lethality at the postimplantation stage, demonstrating that it is an essential gene. Blastocysts derived from preimplantation msin3A null embryos and mouse embryo fibroblasts (MEFs) lacking msin3A display a significant reduction in cell division. msin3A null MEFs also show mislocalization of the heterochromatin protein, HP1alpha, without alterations in global histone acetylation. Heterozygous msin3A(+/-) mice with a systemic twofold decrease in mSin3A protein develop splenomegaly as well as kidney disease indicative of a disruption of lymphocyte homeostasis. Conditional deletion of msin3A from developing T cells results in reduced thymic cellularity and a fivefold decrease in the number of cytotoxic (CD8) T cells, while helper (CD4) T cells are unaffected. We show that CD8 development is dependent on mSin3A at a step downstream of T-cell receptor signaling and that loss of mSin3A specifically decreases survival of double-positive and CD8 T cells. Thus, msin3A is a pleiotropic gene which, in addition to its role in cell cycle progression, is required for the development and homeostasis of cells in the lymphoid lineage.
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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.