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. 2015 Feb 24;43(5):2716–2729. doi: 10.1093/nar/gkv139

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© The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 2. — Specific complexes of hTDG-R275A at G:U^F lesion sites. (A) AFM image of hTDG-R275A on DNA substrate containing a G:U^F mismatch at 46% of DNA fragment length. Arrows point to specific hTDG-R275A–DNA complexes bound to the target site (yellow) and nonspecific complexes (white). (B) A Gaussian fit to the hTDG-R275A binding position distributions on G:U^F DNA revealed a lesion specificity of S = (358 ± 101). (C) Distribution of DNA bend angles induced by hTDG-R275A at G:U^F sites. A triple Gaussian fit (R² = 0.89) centered at (0 ± 12), (37 ± 12) and (66 ± 12)°. (D) Distribution of intrinsic DNA bend angles at the G:U^F mismatch in the absence of protein revealed a similar slightly bent state (33 ± 12)° as in (C) and a predominant linear state (2 ± 12)°. Results were pooled from three individual experiments (n = total data points) and are summarized in Table 3.