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. 1999 Dec 21;96(26):15038–15043. doi: 10.1073/pnas.96.26.15038

Table 1.

Relative delay in nucleotide excision repair for LF041 skin fibroblasts, and for lung fibroblasts expressing the HPV E6, HPV E7, or both oncoproteins

Fibroblast type Strand Average 50% repair time, hr* Fold delay in repair No. and location of sites analyzed
Normal skin TS 3  (1, 8) 1 16 (exon 1 c-jun); 5 (exon 7 p53)
NTS 10  (4, 16) 1 10 (exon 5 p53)
LF041 skin TS 14  (4, 28) 6.1 ± 2.8 16 (exon 1 c-jun); 5 (exon 7 p53)
NTS 28  (16, 32) 3.1 ± 1.1 10 (exon 5 p53)
LXSN lung TS 3.5  (1, 8) 1  9 (c-jun promoter); 4 (exon 7 p53)
NTS 6 (2, 16) 1  7 (exon 5 p53); 9 (exon 8 p53)
E6 lung TS 12  (6, 24) 3.8 ± 1.4  9 (c-jun promoter); 4 (exon 7 p53)
NTS 18  (8, 24) 4.1 ± 1.3  7 (exon 5 p53); 9 (exon 8 p53)
E7 lung TS 4  (1, 8) 1.5 ± 0.8  9 (c-jun promoter); 4 (exon 7 p53)
NTS 16  (4, 32) 3.6 ± 1.9  5 (exon 5 p53); 5 (exon 8 p53)
E6E7 lung TS 13  (4, 28) 4.1 ± 0.9  9 (c-jun promoter); 4 (exon 7 p53)
NTS 17  (6, 32) 4.1 ± 1.3  5 (exon 5 p53); 5 (exon 8 p53)
*

Each value reflects the average time required to achieve 50% repair, and was extrapolated from repair-rate determinations for at least 10 different dipyrimidine sites pooled from different gels. For example (as indicated by the first entry in the column at the far right), the average 50% repair time for the TS strand of normal skin fibroblasts was calculated by pooling repair-rate calculations from 21 sites, i.e., 16 from exon 1 of c-jun and 5 from exon 7 of p53. The values in parentheses represent the slowest and fastest 50% repair times, to indicate the site-to-site variation in repair rates.