Abstract
PML is a tumour suppressor inactivated in Acute Promyelocytic Leukaemia (APL). PML is the essential component of a subnuclear structure called the PML nuclear body (PML-NB), which is disrupted in APL. By targeting different cellular proteins to this structure, PML can either hamper or potentiate their functions. The PML transcript undergoes alternative splicing to generate both nuclear and cytoplasmic isoforms. Most of the research in this field has focused its attention on studying nuclear PML. Nevertheless, new exciting studies show that cytoplasmic PML may control essential cellular functions, thus opening new avenues for investigation.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Active Transport, Cell Nucleus
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Adaptor Proteins, Signal Transducing / metabolism
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Alternative Splicing
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Animals
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Cell Cycle
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Cell Nucleus / metabolism
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Cytoplasm / metabolism*
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Gene Expression Regulation, Neoplastic*
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Humans
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Interferons / metabolism
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Leukemia, Promyelocytic, Acute / genetics
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Leukemia, Promyelocytic, Acute / metabolism*
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Membrane Proteins / metabolism
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Neoplasm Proteins / genetics
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Neoplasm Proteins / metabolism*
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Nuclear Proteins / genetics
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Nuclear Proteins / metabolism*
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Oncogene Proteins, Fusion / metabolism
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Promyelocytic Leukemia Protein
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Protein Isoforms / metabolism
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Signal Transduction*
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Transcription Factors / genetics
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Transcription Factors / metabolism*
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Transforming Growth Factor beta / metabolism
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Tumor Suppressor Proteins / genetics
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Tumor Suppressor Proteins / metabolism*
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Virus Diseases / metabolism
Substances
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Adaptor Proteins, Signal Transducing
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Membrane Proteins
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Neoplasm Proteins
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Nuclear Proteins
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Oncogene Proteins, Fusion
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Promyelocytic Leukemia Protein
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Protein Isoforms
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TRAT1 protein, human
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Transcription Factors
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Transforming Growth Factor beta
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Tumor Suppressor Proteins
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promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
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PML protein, human
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Interferons