We skip to work: alternative splicing in normal and malignant myelopoiesis.
Full text not available from this repository.Item Type: | Article |
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Status: | Published |
Official URL: | https://doi.org/10.1038/s41375-018-0021-4 |
Journal or Publication Title: | Leukemia |
Volume: | 32 |
Number: | 5 |
Page Range: | pp. 1081-1093 |
Date: | 2018 |
Divisions: | Epigenetics and RNA Biology Gene and Stem Cell Therapy |
Depositing User: | General Admin |
Identification Number: | 10.1038/s41375-018-0021-4 |
ISSN: | 0887-6924 |
Date Deposited: | 04 Jan 2021 04:33 |
Abstract: | Alternative splicing expands the transcriptome thereby promoting protein diversity. It governs critical cellular processes such as differentiation, proliferation and apoptosis in a tissue-specific manner. Aberrant splicing consequent to mutations in splicing factors and disruption of isoform ratios in key regulatory genes provides an important contribution to the pathogenesis of the myelodysplastic syndromes and myeloid leukemia. We review here the central role of alternative splicing in regulating myelopoiesis, and provide clear examples of how global splicing disruption or specific aberrant splicing events might promote leukemogenesis. We discuss the growing number of mechanistic links between epigenetic factors and alternative splicing. Finally, we address the potential utility of alternatively spliced isoforms as biomarkers and the development of novel therapies that modulate alternative splicing in myeloid and other malignancies. |
Creators: | Creators Email Wong, Alex C. H. UNSPECIFIED Rasko, John E. J. UNSPECIFIED Wong, Justin J.-L. UNSPECIFIED |
Last Modified: | 04 Jan 2021 04:33 |
URI: | https://eprints.centenary.org.au/id/eprint/612 |
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