ArticleNucleic acids research2018
The SIN3A histone deacetylase complex is required for a complete transcriptional response to hypoxia.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.
- Hypoxia classifier for transcriptome datasets.BMC bioinformatics · 2022Pooled it
- Transglutaminase 2 Deletion Enhances Astrocyte-to-Neuron Metabolic Support and Attenuates Subacute Pathology Following Repetitive Mild Traumatic Brain Injury.bioRxiv : the preprint server for biology · 2026Article
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation.Cell death & disease · 2026Article
- HIF sustain a transcriptional regulatory circuit of EPAS1 expression in renal clear cell carcinoma.Nature communications · 2026Article
- Sotatercept Reverses SIN3a Deficiency-Driven PAH by Reprogramming BMPR2/TGF-β-HIF-1α Signaling Pathways.bioRxiv : the preprint server for biology · 2026Article
- NF-κB is a central regulator of hypoxia-induced gene expression.EMBO reports · 2026Article
- BAP18, as a corepressor of AR together with the SIN3A/HDAC complex, promotes AR-positive triple-negative breast cancer progression.Cell & bioscience · 2025Article
- HypoxamiRs: the hidden architects of tissue adaptation in hypoxia.Cell death & disease · 2025Review
- HIF1A facilitates hypoxia-induced changes in H3K27ac modification to promote myometrial contractility.Communications biology · 2025Article
- REST missense mutations reveal disrupted Re1 motif binding and co-repressor interactions in uterine fibroids.Frontiers in bioinformatics · 2025Article
- Article
- Pharmacological inhibition of astrocytic transglutaminase 2 facilitates the expression of a neurosupportive astrocyte reactive phenotype in association with increased histone acetylation.bioRxiv : the preprint server for biology · 2024Article
- Validation of a Paralimbic-Related Subcortical Brain Dysmaturation MRI Score in Infants with Congenital Heart Disease.Journal of clinical medicine · 2024Article
- Bhlhe40 Regulates Proliferation and Angiogenesis in Mouse Embryoid Bodies under Hypoxia.International journal of molecular sciences · 2024Article
- PDK1 promotes breast cancer progression by enhancing the stability and transcriptional activity of HIF-1α.Genes & diseases · 2024Article
- Rescuing lung development through embryonic inhibition of histone acetylation.Science translational medicine · 2024Article
- Transcription factors regulating vasculogenesis and angiogenesis.Developmental dynamics : an official publication of the American Association of Anatomists · 2024Review
- T-regulatory cells require Sin3a for stable expression of Foxp3.Frontiers in immunology · 2024Article
- Oxygen-regulated post-translation modifications as master signalling pathway in cells.EMBO reports · 2023Review
- Sleep Disorder Kleine-Levin Syndrome (KLS) Joins the List of Polygenic Brain Disorders Associated with Obstetric Complications.Cellular and molecular neurobiology · 2023Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
Abstract
Cells adapt to environmental changes, including fluctuations in oxygen levels, through the induction of specific gene expression programs. To identify genes regulated by hypoxia at the transcriptional level, we pulse-labeled HUVEC cells with 4-thiouridine and sequenced nascent transcripts. Then, we searched genome-wide binding profiles from the ENCODE project for factors that correlated with changes in transcription and identified binding of several components of the Sin3A co-repressor complex, including SIN3A, SAP30 and HDAC1/2, proximal to genes repressed by hypoxia. SIN3A interference revealed that it participates in the downregulation of 75% of the hypoxia-repressed genes in endothelial cells. Unexpectedly, it also blunted the induction of 47% of the upregulated genes, suggesting a role for this corepressor in gene induction. In agreement, ChIP-seq experiments showed that SIN3A preferentially localizes to the promoter region of actively transcribed genes and that SIN3A signal was enriched in hypoxia-repressed genes, prior exposure to the stimulus. Importantly, SINA3 occupancy was not altered by hypoxia in spite of changes in H3K27ac signal. In summary, our results reveal a prominent role for SIN3A in the transcriptional response to hypoxia and suggest a model where modulation of the associated histone deacetylase activity, rather than its recruitment, determines the transcriptional output.
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