| First Author | Gu Y | Year | 1997 |
| Journal | Immunity | Volume | 7 |
| Issue | 5 | Pages | 653-65 |
| PubMed ID | 9390689 | Mgi Jnum | J:44361 |
| Mgi Id | MGI:1099942 | Doi | 10.1016/s1074-7613(00)80386-6 |
| Citation | Gu Y, et al. (1997) Growth retardation and leaky SCID phenotype of Ku70-deficient mice. Immunity 7(5):653-65 |
| abstractText | 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. |
