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. 2019 Jan 25;41:2. doi: 10.1186/s41021-019-0119-6

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© The Author(s) 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 1 — A model for DNA damage recognition and verification in mammalian GG-NER. The XPC protein complex recognizes and binds to DNA sites with disrupted/destabilized base pair(s) regardless of the presence (left) or absence (right) of relevant lesions. After loading of the TFIIH complex, the XPD helicase subunit in TFIIH scans a DNA strand in 5′-3′ direction in conjunction with XPA, and the presence of a lesion is finally verified by blockage of this translocation. Even though a lesion is not present exactly at the XPC-bound site, this scanning mechanism may provide NER with a chance to find some nearby lesions