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

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Development of T-leukaemias in CD45 tyrosine phosphatase-deficient mutant lck mice.

The CD45 tyrosine phosphatase lowers T-cell antigen receptor signalling thresholds by its positive actions on p56(lck) tyrosine kinase function. We now show that mice expressing active lck(F505) at non-oncogenic levels develop aggressive thymic lymphomas on a CD45(-/-) background. CD45 suppresses the tumorigenic potential of the kinase by dephosphorylation of the Tyr394 autophosphorylation site. In CD45(-/-) thymocytes the kinase is switched to a hyperactive oncogenic state, resulting in increased resistance to apoptosis. Transformation occurs in early CD4(-)CD8(-) thymocytes during the process of TCR-beta chain rearrangement by a recombinase-independent mechanism. Our findings represent the first example in which a tyrosine phosphatase in situ prevents the oncogenic actions of a SRC: family tyrosine kinase.[1]

References

  1. Development of T-leukaemias in CD45 tyrosine phosphatase-deficient mutant lck mice. Baker, M., Gamble, J., Tooze, R., Higgins, D., Yang, F.T., O'Brien, P.C., Coleman, N., Pingel, S., Turner, M., Alexander, D.R. EMBO J. (2000) [Pubmed]
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