ArticleMolecular and cellular biology2014
ELL inhibits E2F1 transcriptional activity by enhancing E2F1 deacetylation via recruitment of histone deacetylase 1.
Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Phosphorylation-dependent regulation of Eleven Lysine Rich Leukemia (ELL) uncovered by quantitative global phosphoproteomic analysis.Molecular genetics and genomics : MGG · 2026Article
- Phosphatidic acid-enabled MKL1 contributes to liver regeneration: Translational implication in liver failure.Acta pharmaceutica Sinica. B · 2024Article
- Review
- The Role of Post-Translational Acetylation and Deacetylation of Signaling Proteins and Transcription Factors after Cerebral Ischemia: Facts and Hypotheses.International journal of molecular sciences · 2021Review
- ELL targets c-Myc for proteasomal degradation and suppresses tumour growth.Nature communications · 2016Article
- Human MageB2 Protein Expression Enhances E2F Transcriptional Activity, Cell Proliferation, and Resistance to Ribotoxic Stress.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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Abstract
ELL (eleven-nineteen lysine-rich leukemia protein) was first identified as a translocation partner of MLL in acute myeloid leukemia; however, the exact mechanism of its action has remained elusive. In this study, we identified ELL as a direct downstream target gene of E2F1. Coimmunoprecipitation assays showed that ELL interacted with E2F1 in vitro and in vivo, leading to inhibition of E2F1 transcriptional activity. In addition, ELL enhanced E2F1 deacetylation via recruitment of histone deacetylase 1 (HDAC1). Notably, the MLL-ELL fusion protein lost the inhibitory role of ELL in E2F1 transcriptional activity. Furthermore, DNA damage induced ELL in an E2F1-dependent manner and ELL protected cells against E2F1-dependent apoptosis. Our findings not only connect ELL to E2F1 function and uncover a novel role of ELL in response to DNA damage but also provide an insight into the mechanism for MLL-ELL-associated leukemogenesis.
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Registered trials
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