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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Involvement of SLP-65 and Btk in tumor suppression and malignant transformation of pre-B cells.

Signals from the precursor-B cell receptor (pre-BCR) are essential for selection and clonal expansion of pre-B cells that have performed productive immunoglobulin heavy chain V(D)J recombination. In the mouse, the downstream signaling molecules SLP-65 and Btk cooperate to limit proliferation and induce differentiation of pre-B cells, thereby acting as tumor suppressors to prevent pre-B cell leukemia. In contrast, recent observations in human BCR-ABL1(+) pre-B lymphoblastic leukemia cells demonstrate that Btk is constitutively phosphorylated and activated by the BCR-ABL1 fusion protein. As a result, activated Btk transmits survival signals that are essential for the transforming activity of oncogenic Abl tyrosine kinase.[1]

References

  1. Involvement of SLP-65 and Btk in tumor suppression and malignant transformation of pre-B cells. Hendriks, R.W., Kersseboom, R. Semin. Immunol. (2006) [Pubmed]
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