ArticleOncogene2004
Functional contribution of EEN to leukemogenic transformation by MLL-EEN fusion protein.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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
13 citing papers in PubMed, 28 citations in OpenAlex.
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- Impact of Endocytosis Mechanisms for the Receptors Targeted by the Currently Approved Antibody-Drug Conjugates (ADCs)-A Necessity for Future ADC Research and Development.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Evolution of AF6-RAS association and its implications in mixed-lineage leukemia.Nature communications · 2017Article
- Essential role of SH3GL1 in interleukin-6(IL-6)- and vascular endothelial growth factor (VEGF)-triggered p130Human cell · 2017Article
- Endocytosis and signaling: cell logistics shape the eukaryotic cell plan.Physiological reviews · 2012Review
- Endocytic proteins in the regulation of nuclear signaling, transcription and tumorigenesis.Molecular oncology · 2009Review
- Analysis of phenotype-genotype connection: the story of dissecting disease pathogenesis in genomic era in China, and beyond.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2007Review
- Complex MLL rearrangements in t(4;11) leukemia patients with absent AF4.MLL fusion allele.Leukemia · 2007Article
- Article
- Article
- Molecular pathogenesis of MLL-associated leukemias.International journal of hematology · 2005Review
- Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The EEN (extra eleven nineteen) gene was originally cloned from a case of acute myeloid leukemia M5 subtype with translocation t (11; 19)(q23; p13), in which EEN was fused with MLL. To explore the involvement of EEN in leukemogenesis caused by MLL-EEN, we studied the transformation potential of the MLL-EEN fusion protein. MLL-EEN had oncogenic features, while, as a control, MLLDelta, the truncated form of MLL lacking the EEN moiety, did not show any oncogenic potential. MLL-EEN exerted a dominant-negative effect over wild-type EEN in terms of subcellular localization. Normally, EEN was found in the cytoplasm, but the MLL-EEN fusion protein was located in the nucleus, and EEN could be delocalized by MLL-EEN. This interaction is via a coiled-coil dimerization domain of EEN, which is reserved in the fusion protein. In addition, MLL-EEN might act as a potential transcriptional factor with the MLL part providing the DNA-binding domain and the EEN part providing the transcription activation domain, though EEN seems to have no direct role in transcriptional regulation. As an aberrant transcriptional factor, MLL-EEN could transactivate the promoter of HoxA7, a potential target gene of MLL.
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Registered trials
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