Abstract
Bcl11a (also called Evi9) functions as a myeloid or B cell proto-oncogene in mice and humans, respectively. Here we show that Bcl11a is essential for postnatal development and normal lymphopoiesis. Bcl11a mutant embryos lack B cells and have alterations in several types of T cells. Phenotypic and expression studies show that Bcl11a functions upstream of the transcription factors Ebf1 and Pax5 in the B cell pathway. Transplantation studies show that these defects in Bcl11a mutant mice are intrinsic to fetal liver precursor cells. Mice transplanted with Bcl11a-deficient cells died from T cell leukemia derived from the host. Thus, Bcl11a may also function as a non-autonomous T cell tumor suppressor gene.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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B-Lymphocytes / immunology*
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Carrier Proteins*
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DNA-Binding Proteins
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Leukemia, T-Cell / genetics
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Leukemia, T-Cell / immunology
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Lymphopoiesis / genetics
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Lymphopoiesis / immunology*
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Membrane Proteins / immunology
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Neoplasm Proteins / genetics
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Neoplasm Proteins / immunology*
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Nuclear Proteins*
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Proto-Oncogene Mas
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Receptor, Notch1
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Receptors, Cell Surface*
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Repressor Proteins
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Signal Transduction
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Transcription Factors*
Substances
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Bcl11a protein, mouse
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Carrier Proteins
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DNA-Binding Proteins
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MAS1 protein, human
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Membrane Proteins
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Neoplasm Proteins
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Notch1 protein, mouse
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Nuclear Proteins
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Proto-Oncogene Mas
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Receptor, Notch1
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Receptors, Cell Surface
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Repressor Proteins
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Transcription Factors