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Growth Control and Cancer Group [E. N. L., R. S. P.] and Laboratory of Molecular Carcinogenesis [D. A. A.], National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709; Department of Pathology [W. K. K.] and Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina 27599-7295 [W. K. K., R. S. P.]; and Fred Hutchinson Cancer Center, Seattle, Washington 98104 [D. A. G.]
We have previously reported that the immediate G2 checkpoint delay of normal human fibroblasts in response to ionizing radiation is correlated with inhibition of p34CDC2/cyclin B kinase activity. Here, we observed increased amounts of the cyclin-dependent protein kinase inhibitor p21CIP1 associated with p34CDC2/cyclin B protein complexes from irradiated normal human fibroblasts. Since wild-type p53 function is not required for the early G2 checkpoint response to ionizing radiation, we investigated whether a p53-independent induction of p21CIP1 was required for the G2 checkpoint. Early passage human fibroblasts expressing the E6 oncoprotein of human papilloma virus-type 16 (NHF4 E6) were analyzed. It has been demonstrated earlier that inactivation of wild-type p53 function in these cells by E6 protein does not alter their intact early G2 checkpoint response to 
-rays. p21CIP1 was found to be undetectable in p34CDC2/cyclin B protein complexes and in total extracts from the E6-expressing cells, with or without exposure to ionizing radiation. These data indicate that p21CIP1 is not required for the immediate G2 checkpoint response and is not induced by a p53-independent pathway in G2 phase following exposure to -rays.
1 To whom requests for reprints should be addressed, at Growth Control and Cancer Group, National Institute of Environmental Health Sciences, Mail Drop C1-09, P. O. Box 12233, Research Triangle Park, NC 27709.
Received 3/ 3/95. Accepted 5/ 3/95.
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