Abstract
The leukemia-associated fusion proteins share several structural or functional similarities, suggesting that they may impart a leukemic phenotype through common modes of transcriptional dysregulation. The fusion proteins generated by these translocations usually contain a DNA-binding domain, domains responsible for homo- or hetero-dimerization, and domains that interact with proteins involved in chromatin remodeling (e.g., co-repressor molecules or co-activator molecules). It is these shared features that constitute the 'variations on the theme' that underling the aberrant growth and differentiation that is the hallmark of acute leukemia cells.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Apoptosis
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Cell Cycle
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Cell Differentiation
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Cell Division
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Humans
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Leukemia, Myeloid, Acute / metabolism*
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Mice
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Models, Biological
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Nuclear Pore Complex Proteins / chemistry
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Oncogene Proteins, Fusion / chemistry*
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Oncogene Proteins, Fusion / metabolism*
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Receptors, Retinoic Acid / chemistry
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Retinoic Acid Receptor alpha
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Transcription Factors / metabolism*
Substances
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Nuclear Pore Complex Proteins
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Oncogene Proteins, Fusion
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RARA protein, human
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Rara protein, mouse
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Receptors, Retinoic Acid
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Retinoic Acid Receptor alpha
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Transcription Factors