Abstract
The PML gene, involved in the t(15;17) chromosomal translocation of acute promyelocytic leukemia (APL), encodes a protein which localizes to the PML-nuclear body, a subnuclear macromolecular structure. PML controls apoptosis, cell proliferation, and senescence. Here, we review the current understanding of its role in tumor suppression.
MeSH terms
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Adaptor Proteins, Signal Transducing
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Animals
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Apoptosis / physiology*
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Carrier Proteins / metabolism
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Cell Division
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Cell Transformation, Neoplastic*
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Cellular Senescence
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Co-Repressor Proteins
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Genes, Tumor Suppressor / physiology*
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Humans
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Intracellular Signaling Peptides and Proteins*
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Molecular Chaperones
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Neoplasm Proteins / genetics*
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Neoplasm Proteins / metabolism
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Neoplasm Proteins / physiology*
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Neoplasms / genetics
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Neoplasms / physiopathology
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Nuclear Proteins / genetics
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Nuclear Proteins / metabolism
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Oncogene Proteins, Fusion / genetics
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Oncogene Proteins, Fusion / metabolism*
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Promyelocytic Leukemia Protein
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Receptors, Retinoic Acid / genetics
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Receptors, Retinoic Acid / metabolism
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Retinoic Acid Receptor alpha
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Transcription Factors / genetics*
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Transcription Factors / metabolism
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Transcription Factors / physiology*
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Tumor Suppressor Protein p53 / metabolism
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Tumor Suppressor Proteins
Substances
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Adaptor Proteins, Signal Transducing
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Carrier Proteins
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Co-Repressor Proteins
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DAXX protein, human
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Intracellular Signaling Peptides and Proteins
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Molecular Chaperones
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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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RARA protein, human
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Receptors, Retinoic Acid
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Retinoic Acid Receptor alpha
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Transcription Factors
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Tumor Suppressor Protein p53
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Tumor Suppressor Proteins
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PML protein, human