Abstract
Hematopoietic stem cells (HSC) are tightly regulated through, as yet, undefined mechanisms that balance self-renewal and differentiation. We have identified a role for the transcriptional coactivators CREB-binding protein (CBP) and p300 in such HSC fate decisions. A full dose of CBP, but not p300, is crucial for HSC self-renewal. Conversely, p300, but not CBP, is essential for proper hematopoietic differentiation. Furthermore, in chimeric mice, hematologic malignancies emerged from both CBP(-/-) and p300(-/-) cell populations. Thus, CBP and p300 play essential but distinct roles in maintaining normal hematopoiesis, and, in mice, both are required for preventing hematologic tumorigenesis.
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.
MeSH terms
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Alleles
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Animals
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Blastocyst / cytology*
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CREB-Binding Protein
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Cell Culture Techniques / methods
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Cell Differentiation
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Cell Division
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Cell Line
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Crosses, Genetic
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Cyclic AMP Response Element-Binding Protein / genetics
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Cyclic AMP Response Element-Binding Protein / metabolism*
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E1A-Associated p300 Protein
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Hematologic Neoplasms / prevention & control
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Hematopoietic Stem Cells / cytology*
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Nuclear Proteins / metabolism*
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Sequence Deletion
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Trans-Activators / metabolism*
Substances
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Cyclic AMP Response Element-Binding Protein
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Nuclear Proteins
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Trans-Activators
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CREB-Binding Protein
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Crebbp protein, mouse
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E1A-Associated p300 Protein
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Ep300 protein, mouse