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J Biol Chem, Vol. 274, Issue 2, 567-570, January 8, 1999
From the Division of Radiation Oncology and Department of
Immunology, Mayo Foundation, Rochester, Minnesota 55905
DNA damage activates cell cycle checkpoints in
yeast and human cells. In the yeasts Saccharomyces
cerevisiae and Schizosaccharomyces pombe
checkpoint-deficient mutants have been characterized, and the
corresponding genes have been cloned. Searches for human homologs of
S. pombe rad1, rad9, and hus1 genes
identified the potential human homologs hRad1, hRad9, and hHus1;
however, little is known about the roles of these proteins in human
cells. The present studies demonstrate that hRad1 and hHus1 associate
in a complex that interacts with a highly modified form of hRad9, but
hHus1 and hRad1 do not associate with hRad17. In addition to being a key participant in complex formation, hRad9 is phosphorylated in
response to DNA damage. Together, these results suggest that hRad9,
hRad1, and hHus1 are central components of a DNA damage-responsive protein complex in human cells.
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