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

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Growth retardation and leaky SCID phenotype of Ku70-deficient mice.

Ku70, Ku80, and DNA-PKcs are subunits of the DNA-dependent protein kinase (DNA-PK), an enzyme implicated in DNA double-stranded break repair and V(D)J recombination. Our Ku70-deficient mice were about 50% the size of control littermates, and their fibroblasts were ionizing radiation sensitive and displayed premature senescence associated with the accumulation of nondividing cells. Ku70-deficient mice lacked mature B cells or serum immunoglobulin but, unexpectedly, reproducibly developed small populations of thymic and peripheral alpha/beta T lineage cells and had a significant incidence of thymic lymphomas. In association with B and T cell developmental defects, Ku70-deficient cells were severely impaired for joining of V(D)J coding and recombination signal sequences. These unanticipated features of the Ku70-deficient phenotype with respect to lymphocyte development and V(D)J recombination may reflect differential functions of the three DNA-PK components.[1]

References

  1. Growth retardation and leaky SCID phenotype of Ku70-deficient mice. Gu, Y., Seidl, K.J., Rathbun, G.A., Zhu, C., Manis, J.P., van der Stoep, N., Davidson, L., Cheng, H.L., Sekiguchi, J.M., Frank, K., Stanhope-Baker, P., Schlissel, M.S., Roth, D.B., Alt, F.W. Immunity (1997) [Pubmed]
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