期刊
CELL
卷 139, 期 3, 页码 573-586出版社
CELL PRESS
DOI: 10.1016/j.cell.2009.08.041
关键词
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资金
- NIH [AI054636, CA092625, AI014782-31]
- Leukemia and Lymphoma Society
- European Union through MUGEN
- Hematology and Transfusion Medicine at Harvard Medical School
- Portuguese Foundation for Science and Technology
- Robert A. and Renee E. Belfer Foundation
Previous work has shown that mature B cells depend upon survival signals delivered to the cells by their antigen receptor (BCR). To identify the molecular nature of this survival signal, we have developed a genetic approach in which ablation of the BCR is combined with the activation of specific, BCR dependent signaling cascades in mature B cells in vivo. Using this system, we provide evidence that the survival of BCR deficient mature B cells can be rescued by a single signaling pathway downstream of the BCR, namely PI3K signaling, with the FOXO1 transcription factor playing a central role.
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