期刊
BLOOD
卷 111, 期 6, 页码 2999-3004出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2007-04-087213
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资金
- NCI NIH HHS [5R01CA026038-30, R01 CA026038] Funding Source: Medline
Transcription factors known as CCAAT enhancer binding proteins (C/EBPs) are involved in hematopoietic differentiation, including myelopolesis and granulopolesis. C/EBP beta-deficient mice develop normally; however, they exhibit detective macrophage function, resulting in increased susceptibility to infection. Little is known about the role of G/EBP beta in granulopoiesis; therefore, we examined granulopoiesis in C/EBP beta-deficient mice. Morphology, the number of peripheral blood and bone marrow cells, and the expression of genes specific for the myeloid lineage were normal in C/EBP beta-deficient mice. Interestingly, the hematopoietic progenitor cells of C/EBP beta-deficient mice did not respond normally to granulocyte/macrophage-colony stimulating factor and granulocyte colony stimulating factor. In addition, C/EBP beta-deficient neutrophils displayed enhanced apoptosis compared with wild-type neutrophils. Our present results indicate that C/EBP beta helps regulate survival of neutrophils, downstream of the granulocyte colony stimulating factor receptor.
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