ArticleThe Journal of biological chemistry2011
Oct1 is a switchable, bipotential stabilizer of repressed and inducible transcriptional states.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 70 citations in OpenAlex.
- Regulation of B cell development and lymphocyte function by transcriptional coactivator OCA-B.Frontiers in immunology · 2026Review
- Transcriptional co-regulator OCA-B/Pou2af1 restricts Th2 differentiation.Frontiers in immunology · 2025Article
- IκBζ is a dual-use coactivator of NF-κB and POU transcription factors.Molecular cell · 2024Article
- A SWI/SNF-dependent transcriptional regulation mediated by POU2AF2/C11orf53 at enhancer.Nature communications · 2024Article
- OCA-B/Pou2af1 is sufficient to promote CD4Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- High expression of transcription factor POU2F1 confers improved survival on smokers with lung adenocarcinoma: a retrospective study of two cohorts.Translational lung cancer research · 2023Article
- Oct1 cooperates with the Smad family of transcription factors to promote mesodermal lineage specification.Science signaling · 2023Article
- Long-Distance Repression by Human Silencers: Chromatin Interactions and Phase Separation in Silencers.Cells · 2022Review
- ABCB10 Loss Reduces CD4Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Efficient induction and sustenance of pluripotent stem cells from bovine somatic cells.Biology open · 2021Article
- Targeting transcriptional coregulator OCA-B/Pou2af1 blocks activated autoreactive T cells in the pancreas and type 1 diabetes.The Journal of experimental medicine · 2021Article
- Pathological matrix stiffness promotes cardiac fibroblast differentiation through the POU2F1 signaling pathway.Science China. Life sciences · 2021Article
- Estrogen Receptor Alpha Mutations in Breast Cancer Cells Cause Gene Expression Changes through Constant Activity and Secondary Effects.Cancer research · 2021Article
- Article
- Transcription factor Oct1 protects against hematopoietic stress and promotes acute myeloid leukemia.Experimental hematology · 2019Article
- T cell-selective deletion of Oct1 protects animals from autoimmune neuroinflammation while maintaining neurotropic pathogen response.Journal of neuroinflammation · 2019Article
- Oct1/Pou2f1 is selectively required for colon regeneration and regulates colon malignancy.PLoS genetics · 2019Article
- CKIP-1 limits foam cell formation and inhibits atherosclerosis by promoting degradation of Oct-1 by REGγ.Nature communications · 2019Article
- Nubbin isoform antagonism governs Drosophila intestinal immune homeostasis.PLoS pathogens · 2018Article
- BRCA1 through Its E3 Ligase Activity Regulates the Transcription Factor Oct1 and Carbohydrate Metabolism.Molecular cancer research : MCR · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Little is known regarding how the Oct1 transcription factor regulates target gene expression. Using murine fibroblasts and two target genes, Polr2a and Ahcy, we show that Oct1 recruits the Jmjd1a/KDM3A lysine demethylase to catalyze the removal of the inhibitory histone H3K9 dimethyl mark and block repression. Using purified murine T cells and the Il2 target locus, and a colon cancer cell line and the Cdx2 target locus, we show that Oct1 recruits the NuRD chromatin-remodeling complex to promote a repressed state, but in a regulated manner can switch to a different capacity and mediate Jmjd1a recruitment to block repression. These findings indicate that Oct1 maintains repression through a mechanism involving NuRD and maintains poised gene expression states through an antirepression mechanism involving Jmjd1a. We propose that, rather than acting as a primary trigger of gene activation or repression, Oct1 is a switchable stabilizer of repressed and inducible states.
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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.