-transparent.png){kind=logo}
Three genetic complementation groups of rodent cells are defective for both repair of x-ray-induced double-strand breaks and V(D)J recombination. Cells from one group lack a DNA end-binding activity that is biochemically and antigenically similar to the Ku autoantigen. Transfection of complementary DNA (cDNA) that encoded the 86-kilodalton subunit of Ku rescued these mutant cells for DNA end-binding activity, x-ray resistance, and V(D)J recombination activity. These results establish a role for Ku in DNA repair and recombination. Furthermore, as a component of a DNA-dependent protein kinase, Ku may initiate a signaling pathway induced by DNA damage.
Related Publications
V Smider, and
W K Rathmell, and
M R Lieber, and
G Chu
May 1996,
Mutation research,
V Smider, and
W K Rathmell, and
M R Lieber, and
G Chu
November 1994,
Mutation research,
V Smider, and
W K Rathmell, and
M R Lieber, and
G Chu
January 1996,
Current topics in microbiology and immunology,
V Smider, and
W K Rathmell, and
M R Lieber, and
G Chu
August 2004,
Immunological reviews,
V Smider, and
W K Rathmell, and
M R Lieber, and
G Chu
November 1999,
Current biology : CB,
V Smider, and
W K Rathmell, and
M R Lieber, and
G Chu
January 2009,
Advances in experimental medicine and biology,
V Smider, and
W K Rathmell, and
M R Lieber, and
G Chu
January 2009,
Advances in experimental medicine and biology,
V Smider, and
W K Rathmell, and
M R Lieber, and
G Chu
March 2000,
The Journal of biological chemistry,
V Smider, and
W K Rathmell, and
M R Lieber, and
G Chu
January 1996,
Advances in immunology,
V Smider, and
W K Rathmell, and
M R Lieber, and
G Chu
January 1999,
Nature,
