ArticleMolecular immunology2017
Selective expression of the transcription elongation factor ELL3 in B cells prior to ELL2 drives proliferation and survival.
Article in Molecular immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- Programmed-Cell-Death-Related Signature Reveals Immune Microenvironment Characteristics and Predicts Therapeutic Response in Diffuse Large B Cell Lymphoma.Biomedicines · 2025Article
- InSituCor: exploring spatially correlated genes conditional on the cell type landscape.Genome biology · 2025Article
- Article
- Transcriptome Profiling Reveals Features of Immune Response and Metabolism of Acutely Infected, Dead and Asymptomatic Infection of African Swine Fever Virus in Pigs.Frontiers in immunology · 2021Article
- Histone deacetylase 8 inhibition suppresses mantle cell lymphoma viability while preserving natural killer cell function.Biochemical and biophysical research communications · 2021Article
- Role of ETS1 in the Transcriptional Network of Diffuse Large B Cell Lymphoma of the Activated B Cell-Like Type.Cancers · 2020Article
- ELL2 Is Required for the Growth and Survival of AR-Negative Prostate Cancer Cells.Cancer management and research · 2020Article
- Data supporting the functional role of Eleven-nineteen Lysine-rich Leukemia 3 (ELL3) in B cell lymphoma cell line cells.Data in brief · 2017Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
B cell activation is dependent on a large increase in transcriptional output followed by focused expression on secreted immunoglobulin as the cell transitions to an antibody producing plasma cell. The rapid transcriptional induction is facilitated by the release of poised RNA pol II into productive elongation through assembly of the super elongation complex (SEC). We report that a SEC component, the Eleven -nineteen Lysine-rich leukemia (ELL) family member 3 (ELL3) is dynamically up-regulated in mature and activated human B cells followed by suppression as B cells transition to plasma cells in part mediated by the transcription repressor PRDM1. Burkitt's lymphoma and a sub-set of Diffuse Large B cell lymphoma cell lines abundantly express ELL3. Depletion of ELL3 in the germinal center derived lymphomas results in severe disruption of DNA replication and cell division along with increased DNA damage and cell death. This restricted utilization and survival dependence reveal a key step in B cell activation and indicate a potential therapeutic target against B cell lymphoma's with a germinal center origin.
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