ArticleMolecular and cellular biology2003
Molecular basis of p53 functional inactivation by the leukemic protein MLL-ELL.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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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
24 citing papers in PubMed, 45 citations in OpenAlex.
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- Silencing of Testin expression is a frequent event in spontaneous lymphomas from Trp53-mutant mice.Scientific reports · 2020Article
- Antitumor immunity augments the therapeutic effects of p53 activation on acute myeloid leukemia.Nature communications · 2019Article
- Opposing effects of acute versus chronic inhibition of p53 on decitabine's efficacy in myeloid neoplasms.Scientific reports · 2019Article
- Molecular mechanisms and pathobiology of oncogenic fusion transcripts in epithelial tumors.Oncotarget · 2019Review
- Atg5-dependent autophagy contributes to the development of acute myeloid leukemia in an MLL-AF9-driven mouse model.Cell death & disease · 2016Article
- TESTIN Induces Rapid Death and Suppresses Proliferation in Childhood B Acute Lymphoblastic Leukaemia Cells.PloS one · 2016Article
- Low-dose radiation exposure induces a HIF-1-mediated adaptive and protective metabolic response.Cell death and differentiation · 2014Article
- ELL inhibits E2F1 transcriptional activity by enhancing E2F1 deacetylation via recruitment of histone deacetylase 1.Molecular and cellular biology · 2014Article
- Regulation of fertility, survival, and cuticle collagen function by the Caenorhabditis elegans eaf-1 and ell-1 genes.The Journal of biological chemistry · 2011Article
- Flt3-ITD alters chemotherapy response in vitro and in vivo in a p53-dependent manner.Experimental hematology · 2011Article
- Article
- Elongation factor ELL (Eleven-Nineteen Lysine-rich Leukemia) acts as a transcription factor for direct thrombospondin-1 regulation.The Journal of biological chemistry · 2009Article
- Molecular targeting of MLL-rearranged leukemia cell lines with the synthetic peptide PFWT synergistically enhances the cytotoxic effect of established chemotherapeutic agents.Leukemia research · 2009Article
- The molecular biology of mixed lineage leukemia.Haematologica · 2009Review
- Review
- Mutational analysis of an RNA polymerase II elongation factor in Drosophila melanogaster.Molecular and cellular biology · 2005Article
- Molecular pathogenesis of MLL-associated leukemias.International journal of hematology · 2005Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The Eleven Lysine-rich Leukemia (ELL) gene undergoes translocation and fuses in frame to the Multiple Lineage Leukemia (MLL) gene in a substantial proportion of patients suffering from acute forms of leukemia. Molecular mechanisms of cellular transformation by the MLL-ELL fusion are not well understood. Although both MLL-ELL and wild-type ELL can reduce functional activity of p53 tumor suppressor, our data reveal that MLL-ELL is a much more efficient inhibitor of p53 than is wild-type ELL. We also demonstrate for the first time that ELL extreme C terminus [ELL(eCT)] is required for the recruitment of p53 into MLL-ELL nuclear foci and is both necessary and sufficient for the MLL-ELL inhibition of p53-mediated induction of p21 and apoptosis. Finally, our results demonstrate that MLL-ELL requires the presence of intact ELL(eCT) in order to disrupt p53 interactions with p300/CBP coactivator and thus significantly reduce p53 acetylation in vivo. Since ELL(eCT) has recently been shown to be both necessary and sufficient for MLL-ELL-mediated transformation of normal blood progenitors, our data correlate ELL(eCT) contribution to MLL-ELL transformative effects with its ability to functionally inhibit p53.
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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.