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Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
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PI3K signaling controls cell fate at many points in B lymphocyte development and activation
Amber C Donahue1, David A Fruman
1Department of Molecular Biology and Biochemistry, University of California, Irvine, 3242 McGaugh Hall, Irvine, CA 92697-3900, USA. adonahue@uci.edu
Abstract:
Many receptors on diverse cell types activate phosphoinositide 3-kinase (PI3K). The lipid products of PI3K, termed 3-phosphoinositides, regulate numerous cellular processes by recruiting specific proteins to membrane signaling complexes. In the B lymphocyte lineage, PI3K activation is a critical control point at various stages of development, proliferation and differentiation. PI3K signaling is promoted by stimulatory receptors such as surface immunoglobulin, CD40, Toll-like receptors and cytokine receptors, and opposed by the inhibitory receptor FcgammaRIIB1. Genetic dissection of the PI3K pathway in mice has indicated that certain B cell functions are regulated by a limited set of PI3K isoforms and downstream effectors. Here we review our current understanding of how signals are relayed to and from PI3K in B cells.
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