Abstract
Acute promyelocytic leukemia (APL) cells carry a mutated gene that is the result of a translocation in which the retinoic acid receptor alpha (RAR alpha) gene is fused to the promyelocytic leukemia (PML) gene, coding for a fusion protein, PML/RAR alpha. Its presence is the single event that causes APL in transgenic mice. All-trans-retinoic acid (atRA) induces the proteolytic degradation of PML/RAR alpha by ubiquitination and proteolysis. RAR alpha itself is also degraded by atRA treatment, a process representing a possible feedback mechanism to turn off RAR alpha's stimulation of transcription.
MeSH terms
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Antineoplastic Agents / pharmacology
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Artificial Gene Fusion
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Humans
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Leukemia, Promyelocytic, Acute / drug therapy
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Leukemia, Promyelocytic, Acute / genetics
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Neoplasm Proteins / genetics*
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Nuclear Proteins*
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Promyelocytic Leukemia Protein
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Receptors, Retinoic Acid / genetics*
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Transcription Factors / genetics*
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Translocation, Genetic / genetics
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Tretinoin / pharmacology
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Tretinoin / physiology*
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Tumor Suppressor Proteins
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Vitamin A / therapeutic use
Substances
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Antineoplastic Agents
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Neoplasm Proteins
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Nuclear Proteins
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Promyelocytic Leukemia Protein
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Receptors, Retinoic Acid
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Transcription Factors
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Tumor Suppressor Proteins
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Vitamin A
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PML protein, human
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Tretinoin