ArticleProceedings of the National Academy of Sciences of the United States of America2016
Regulation of normal B-cell differentiation and malignant B-cell survival by OCT2.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 110 citations in OpenAlex.
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- BRWD1 directs B cell epigenetic states required for germinal center initiation, maintenance and function.Nature communications · 2026Article
- Clonotypic characterization defines B-cell drivers of clonal expansion and intratumor heterogeneity in IgM monoclonal gammopathies.HemaSphere · 2026Article
- Malignant B-cell States Orchestrate Spatially Organized Immune Ecosystems in B-cell Lymphomas.Research square · 2026Article
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- Single-cell epigenetic and transcriptomic states across the continuum of monoclonal B cell lymphocytosis to chronic lymphocytic leukemia.Genome biology · 2026Article
- BAF complexes maintain accessibility at stimulus-responsive chromatin and are required for transcriptional stimulus responses.bioRxiv : the preprint server for biology · 2026Article
- Evidence for chronological diversification of spinal neuron subtypes by a shared sequence of transcription factors.Science advances · 2026Article
- Splice-site mutations in POU2AF1 are associated with B-cell lymphomagenesis and therapeutic response.Scientific reports · 2026Article
- BARTsc identifies key transcriptional regulators from single-cell omics data.bioRxiv : the preprint server for biology · 2026Article
- Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation.bioRxiv : the preprint server for biology · 2026Article
- Regulation of B cell development and lymphocyte function by transcriptional coactivator OCA-B.Frontiers in immunology · 2026Review
- Unraveling the molecular landscape of Erdheim-Chester disease: new insights from methylome and transcriptome integration.Leukemia · 2025Article
- BayesCNet: Bayesian inference for cell type-specific regulatory networks leveraging cell type hierarchy in single-cell data.bioRxiv : the preprint server for biology · 2025Article
- OCT-2 Is Associated With Pro-Metastatic Epigenomic Properties of Triple-Negative Breast Cancer Cells.Cancer science · 2025Article
- Article
20 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
The requirement for the B-cell transcription factor OCT2 (octamer-binding protein 2, encoded by Pou2f2) in germinal center B cells has proved controversial. Here, we report that germinal center B cells are formed normally after depletion of OCT2 in a conditional knockout mouse, but their proliferation is reduced and in vivo differentiation to antibody-secreting plasma cells is blocked. This finding led us to examine the role of OCT2 in germinal center-derived lymphomas. shRNA knockdown showed that almost all diffuse large B-cell lymphoma (DLBCL) cell lines are addicted to the expression of OCT2 and its coactivator OCA-B. Genome-wide chromatin immunoprecipitation (ChIP) analysis and gene-expression profiling revealed the broad transcriptional program regulated by OCT2 that includes the expression of STAT3, IL-10, ELL2, XBP1, MYC, TERT, and ADA. Importantly, genetic alteration of OCT2 is not a requirement for cellular addiction in DLBCL. However, we detected amplifications of the POU2F2 locus in DLBCL tumor biopsies and a recurrent mutation of threonine 223 in the DNA-binding domain of OCT2. This neomorphic mutation subtly alters the DNA-binding preference of OCT2, leading to the transactivation of noncanonical target genes including HIF1a and FCRL3 Finally, by introducing mutations designed to disrupt the OCT2-OCA-B interface, we reveal a requirement for this protein-protein interface that ultimately might be exploited therapeutically. Our findings, combined with the predominantly B-cell-restricted expression of OCT2 and the absence of a systemic phenotype in our knockout mice, suggest that an OCT2-targeted therapeutic strategy would be efficacious in both major subtypes of DLBCL while avoiding systemic toxicity.
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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.