ArticleThe Prostate2007
Apoptosis induction and growth suppression by U19/Eaf2 is mediated through its ELL-binding domain.
Article in The Prostate, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Long-term exercise enhances meningeal lymphatic vessel plasticity and drainage in a mouse model of Alzheimer's disease.Translational neurodegeneration · 2025Article
- EAF2: a tumor suppressor gene with multi-aspect functions.Frontiers in pharmacology · 2024Review
- Overview of research on fusion genes in prostate cancer.Translational cancer research · 2020Review
- FOXA1 modulates EAF2 regulation of AR transcriptional activity, cell proliferation, and migration in prostate cancer cells.The Prostate · 2015Article
- Identification of a genetic interaction between the tumor suppressor EAF2 and the retinoblastoma protein (Rb) signaling pathway in C. elegans and prostate cancer cells.Biochemical and biophysical research communications · 2014Article
- Pirin down-regulates the EAF2/U19 protein and alleviates its growth inhibition in prostate cancer cells.The Prostate · 2014Article
- Evidence for a genomic mechanism of action for progesterone receptor membrane component-1.Steroids · 2012Review
- Regulation of fertility, survival, and cuticle collagen function by the Caenorhabditis elegans eaf-1 and ell-1 genes.The Journal of biological chemistry · 2011Article
- Article
- ELL is an HIF-1alpha partner that regulates and responds to hypoxia response in PC3 cells.The Prostate · 2010Article
- Elongation factor ELL (Eleven-Nineteen Lysine-rich Leukemia) acts as a transcription factor for direct thrombospondin-1 regulation.The Journal of biological chemistry · 2009Article
- Dynamic intracellular distribution of Eaf2 and its potential involvement in UV-Induced DNA damage response.DNA and cell biology · 2008Article
- FB1, an E2A fusion partner in childhood leukemia, interacts with U19/EAF2 and inhibits its transcriptional activity.Cancer letters · 2007Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundU19/Eaf2 is an androgen-response gene and its downregulation is frequently observed in advanced human prostate cancer. U19/Eaf2 interacts with ELL, a fusion partner of MLL in the (11;19) (q23;p13.1) translocation in acute myeloid leukemia. U19/Eaf2 overexpression induces apoptosis and suppresses xenograft tumor growth.
methodsTransfection and colony formation were used to assay for apoptosis and growth suppression of various U19/Eaf2 mutants. Co-immunoprecipitation was performed to test the interaction between the U19/Eaf2 constructs and ELL.
resultsThe region of U19/Eaf2 essential for apoptosis and growth suppression was mapped to amino acids 68-113. This region was necessary and sufficient for binding ELL. Co-expression of U19/Eaf2 and ELL in 293 cells lead to significant increase in cell death and growth suppression.
conclusionsThese observations argue that the interaction with ELL is essential for the induction of apoptosis and growth suppression by U19/Eaf2.
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