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Changing anthropological behaviour, climate change and high mutation frequency are important determinants of arbovirus emergence.
The top genes by mutation frequency are shown in Table S2.
Additionally, in vitro assessments of antibiotic resistance mutation frequency are not accurate predictors of clinical resistance (Thulin et al., 2015).
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The U2AF1 mutation frequency was higher, with different frequencies in the mutated sites of U2AF1 (S34Y, 6/25; S34F, 11/25; and Q157P 8/25).
The HPRT mutation frequency was evaluated as described (van der Kuip et al., 2004).
Moreover, this mutation frequency was dependent on the ability of Cas9 to introduce a dsDNA break at the target site.
As shown in Figure 1c, HPRT mutation frequency was consistently elevated in cells lacking c-Abl kinase activity.
As expected, in cells expressing imatinib-resistant Bcr-Abl and imatinib-sensitive c-Abl, the HPRT mutation frequency is significantly enhanced in the presence of imatinib (Figure 1b).
However, in both young and old SCCs, the mutation frequency was lower than expected in exons and regulatory regions (Fig. 2b, c).
Concordantly, the highest KRAS/NRAS/BRAF mutation frequency was found in CLL patients with concomitant UM IGHV and trisomy 12-only (38/133, 28.6%).
This mutation frequency is above the empty vector control (~4 × 10−7), suggesting that C. difficile R20291 can use homology-directed repair to replace ssDNA breaks, but not efficiently.
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