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Wnt Signaling in Lymphopoiesis

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Grosschedl,  R.
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Timm, A., & Grosschedl, R. (2005). Wnt Signaling in Lymphopoiesis. In H. Singh, R. Grosschedl, & Springer Science (Eds.), Molecular Analysis of B Lymphocyte Development and Activation (pp. 225-252). Berlin, Germany: Spring- Verlag.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002B-93F4-5
Abstract
Wnt signaling elicits changes in gene expression and cell physiology through β-catenin and LEF1/TCF proteins. The signal transduction pathway regulates many cellular and developmental processes, including cell proliferation, cell fate decisions and differentiation. In cells that have been stimulated by a Wnt protein, cytoplasmic β-catenin is stabilized and transferred to the nucleus, where it interacts with the nuclear mediators of Wnt signaling, the LEF1/TCF proteins, to elicit a transcriptional response. Loss-of-function and gain-of-function experiments in the mouse have provided insight into the role of this signaling pathway in lymphopoiesis. The self-renewal and maintenance of hematopoietic stem cells is regulated by Wnt signals. Differentiation of T cells and natural killer cells is blocked in the absence of LEF1/TCF proteins, and pro-B cell proliferation is regulated by Wnt signaling.