Abstract
p300, which was originally cloned as a nuclear binding target of the adenovirus E1A oncoprotein, forms a family with cyclic-AMP response element binding protein (CREB)-binding protein (CBP). p300/CBP are considered to be transcriptional coactivators that connect the basal transcriptional machinery to various DNA-binding transcriptional factors. p300/CBP are implicated in both cell differentiation and regulation of cell-cycle. We identify here that the p300 gene is fused to the MLL gene and that in-frame MLL-p300 fusion protein is generated in acute myeloid leukemia (AML) with t(11; 22)(q23; q13). These findings suggest that the basis for the leukemogenesis of t(11; 22)-AML is the inability of p300 to regulate cell-cycle and cell differentiation after fusion with MLL.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Sequence
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Base Sequence
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CREB-Binding Protein
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Child, Preschool
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Chromosomes, Human, Pair 11*
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Chromosomes, Human, Pair 22*
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DNA-Binding Proteins / analysis
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DNA-Binding Proteins / genetics
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Gene Rearrangement
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Histone-Lysine N-Methyltransferase
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Humans
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Male
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Molecular Sequence Data
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Myeloid-Lymphoid Leukemia Protein
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Nuclear Proteins / physiology*
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Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics*
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Proto-Oncogenes*
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Trans-Activators*
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Transcription Factors / physiology*
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Translocation, Genetic*
Substances
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DNA-Binding Proteins
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KMT2A protein, human
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Nuclear Proteins
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Trans-Activators
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Transcription Factors
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Myeloid-Lymphoid Leukemia Protein
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Histone-Lysine N-Methyltransferase
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CREB-Binding Protein
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CREBBP protein, human