ArticleProceedings of the National Academy of Sciences of the United States of America2008
Specific requirement of the chromatin modifier mSin3B in cell cycle exit and cellular differentiation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
85 citing papers in PubMed, 123 citations in OpenAlex.
- Intragenic loss-of-function variants in transcription factorsJournal of medical genetics · 2026Article
- Mutations on the surface of HDAC1 reveal molecular determinants of specific complex assembly and their requirement for gene regulation.Nucleic acids research · 2025Article
- BAHCC1 promotes gene expression in neuronal cells by antagonizing SIN3A-HDAC1.Nucleic acids research · 2025Article
- Loss of GATA2 promotes invasion and predicts cancer recurrence and survival in uterine serous carcinoma.JCI insight · 2025Article
- 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
- Chromatin accessibility and cell cycle progression are controlled by the HDAC-associated Sin3B protein in murine hematopoietic stem cells.Epigenetics & chromatin · 2024Article
- SIN-3 acts in distinct complexes to regulate the germline transcriptional program in Caenorhabditis elegans.Development (Cambridge, England) · 2023Article
- 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
- Chromatin-Associated SIN3B Protects Cancer Cells from Genotoxic Stress-Induced Apoptosis and Dictates DNA Damage Repair Pathway Choice.Molecular cancer research : MCR · 2023Article
- Mechanism of assembly, activation and lysine selection by the SIN3B histone deacetylase complex.Nature communications · 2023Article
- Suppression of SIN3A by miR-183 Promotes Breast Cancer Metastasis.Molecular cancer research : MCR · 2022Article
- Impaired Neurodevelopmental Genes in Slovenian Autistic Children Elucidate the Comorbidity of Autism With Other Developmental Disorders.Frontiers in molecular neuroscience · 2022Article
- Haploinsufficiency of the Sin3/HDAC corepressor complex member SIN3B causes a syndromic intellectual disability/autism spectrum disorder.American journal of human genetics · 2021Article
- Soft repression: Subtle transcriptional regulation with global impact.BioEssays : news and reviews in molecular, cellular and developmental biology · 2021Article
- Article
- ARID4B is critical for mouse embryonic stem cell differentiation towards mesoderm and endoderm, linking epigenetics to pluripotency exit.The Journal of biological chemistry · 2020Article
- Differential Complex Formation via Paralogs in the Human Sin3 Protein Interaction Network.Molecular & cellular proteomics : MCP · 2020Article
25 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
6 authors at 3 institutions in 1 country.
Funding
Abstract
The Sin3-histone deacetylase (HDAC) corepressor complex is conserved from yeast to humans. Mammals possess two highly related Sin3 proteins, mSin3A and mSin3B, which serve as scaffolds tethering HDAC enzymatic activity, and numerous sequence-specific transcription factors to enable local chromatin regulation at specific gene targets. Despite broad overlapping expression of mSin3A and mSin3B, mSin3A is cell-essential and vital for early embryonic development. Here, genetic disruption of mSin3B reveals a very different phenotype characterized by the survival of cultured cells and lethality at late stages of embryonic development with defective differentiation of multiple lineages-phenotypes that are strikingly reminiscent of those associated with loss of retinoblastoma family members or E2F transcriptional repressors. Additionally, we observe that, whereas mSin3B(-/-) cells cycle normally under standard growth conditions, they show an impaired ability to exit the cell cycle with limiting growth factors. Correspondingly, mSin3B interacts physically with the promoters of known E2F target genes, and its deficiency is associated with derepression of these gene targets in vivo. Together, these results reveal a critical role for mSin3B in the control of cell cycle exit and terminal differentiation in mammals and establish contrasting roles for the mSin3 proteins in the growth and development of specific lineages.
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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.