Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
Seidel, MG; Look, AT.
E2A-HLF usurps control of evolutionarily conserved survival pathways.
Oncogene. 2001; 20(40):5718-5725
Doi: 10.1038/sj.onc.1204591
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- Abstract:
- E2A-HLF, the chimeric fusion protein resulting from the leukemogenic translocation t(17;19), appears to employ evolutionarily conserved signaling cascades for its transforming and antiapoptotic functions. These arise from both impairment of normal E2A function and activation of a survival pathway triggered through the HLF bZip DNA binding and dimerization domain. Recent reports identify wild-type E2A as a tumor suppressor in T lymphocytes. Moreover, E2A-HLF has been shown to activate SLUG, a mammalian homologue of the cell death specification protein CES-1 in Caenorhabditis elegans, which appears to regulate an evolutionarily conserved cell survival program. Recently, several key mouse models have been generated, enabling further elucidation of these pathways on a molecular genetic level in vivo. In this review, we discuss the characteristics of both components of the fusion protein with regard to their contribution to the regulation of cell fate and the oncogenic potential of E2A-HLF.
- Find related publications in this database (using NLM MeSH Indexing)
- Animals -
- Apoptosis -
- Basic-Leucine Zipper Transcription Factors -
- Caenorhabditis elegans -
- Cell Lineage -
- Cell Survival -
- DNA-Binding Proteins - chemistry DNA-Binding Proteins - metabolism DNA-Binding Proteins - physiology
- Evolution, Molecular -
- Humans -
- Leukemia - etiology Leukemia - genetics
- Mice -
- Models, Biological -
- Oncogene Proteins, Fusion - chemistry Oncogene Proteins, Fusion - metabolism Oncogene Proteins, Fusion - physiology
- Protein Structure, Tertiary -
- Signal Transduction -
- Transcription Factors -
- Translocation, Genetic -
- Find related publications in this database (Keywords)
- apoptosis
- acute leukemia
- chromosomal translocation
- circadian rhythm
- hepatic leukemia factor
- developmental cell fate