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This would result from using the T-containing strand as the repair template (see section, 'The mutational spectrum, sequence context, and fate of the bases mutated in response to DNA repair are consistent with APOBEC-mediated mutagenesis').
There is also some evidence, he adds, that pertussis strains have mutated in response to vaccination campaigns, rendering antibodies less effective.
Furthermore, 454 sequencing was used to study how a specific region of the HIV envelope mutated in response to treatment with a CCR5 agonist and to detect HIV that utilizes the CXC receptor 4, allowing for the phenotyping of specific HIV strains [17], [18].
Fraction of bases (in terms of top strand sequence) that were mutated in response to the repair of the indicated lesions on the bottom strand on FM1.
(C ) Fraction of bases (in terms of top strand sequence) that were mutated in response to the repair (i.e., either restored to C/G or, with respect to T/G, converted to T/A) of the indicated lesions on the top strand of FM1 (pooled according to the type of lesion).
(A ) Fraction of the bases (in terms of top strand sequence) that were mutated in response to the repair of the indicated lesions on the top (top two panels) or bottom (bottom two panels) strand of FM1 for the clustered (more than one mutations per sequence) or unclustered (one mutation per sequence).
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Therefore, there may be unknown pathways of apoptosis that function preferentially in colorectal cancer cells with the mutated TP53-P72 in response to 5-FU based postoperative chemotherapy.
CHEK2 functions downstream of ATM (ataxia telangiectasia-mutated protein) in response to DNA damage (Chaturvedi et al, 1999) to phosphorylate TP53 (Chehab et al, 2000) and BRCA1 (Lee et al, 2000), therefore regulating the tumour suppressor functions of these proteins.
CHK2 functions downstream of ATM (ataxia telangiectasia-mutated protein) in response to DNA damage to phosphorylate p53 and BRCA1 and thereby regulate the tumour suppressor functions of these proteins (Chehab et al, 2000; Lee et al, 2000; Matsuoka et al, 2000).
Furthermore, each of these three mutated proteins is phosphorylated in response to DNA damage generated by the topoisomerase I poison camptothecin (CPT, Fig. 1D).
Many proteins (e.g. gamma histone 2AX, BRCA1, and 53BP1) aggregating into the foci are phosphorylated on S/TQ sites (serine or threonine followed by glutamine) by the ataxia-telangiectasia mutated gene (ATM) kinase in response to DNA damage.
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