期刊
BLOOD
卷 115, 期 14, 页码 2796-2805出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2009-08-239210
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资金
- National Health and Medical Research Council (NHMRC) of Australia
- National Heart, Lung, and Blood Institute [R01 HL080019]
- Pfizer Australia Research Fellowship
- NHMRC
- Australian Research Council
- Leukemia Foundation of Australia
- University of Melbourne
- MRC [G0501688] Funding Source: UKRI
- Medical Research Council [G9818340B, G0501688] Funding Source: researchfish
c-Myb is a transcription factor with functions in many hematopoietic lineages. c-Myb-deficient mice display reduced numbers of B cells; however, it is unknown what role c-Myb plays in B lymphopoiesis because no critical target genes have been identified in the B-cell lineage. We demonstrate that conditional deletion of c-Myb in B-cell progenitors completely abolishes B-cell development. c-Myb is required for lymphoid progenitors to respond to the cytokines interleukin-7 and thymic stromal lymphopoietin; in the absence of sufficient c-Myb activity, mice display a B lymphopenia that closely resembles that observed in interleukin-7 receptor alpha-deficient animals. Analysis of the multipotent progenitor compartment indicates that c-Myb is also required for up-regulation of multiple lymphoidassociated genes, including Il7r, and for the subsequent development of the common lymphoid progenitor population. These data show that c-Myb plays a critical role in the regulatory pathways governing lymphoid specification and early B-cell differentiation. (Blood. 2010; 115(14): 2796-2805)
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