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. 2021 Nov 12;49(21):12252–12267. doi: 10.1093/nar/gkab1022

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© The Author(s) 2021. 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-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 6. — G4 structure reduces OG occurrence. (A) Metaprofiles of OG around TSSs with G4P peaks (G4+, n = 7173) and without G4P peaks (G4–, n = 7140). The shadow represents mean ± S.E.M. (B) Quantification of OGs in G4+ and G4– TSS surrounding regions (±500 bp). Endo, P value < 2.2e^–88; Exo-C, P value < 3.5e^–251; Exo-N, P value < 5.0e^–228. (C) Normalized OG signals around promoter-proximal G4P peaks (n = 12 311) and promoter-distal G4P peaks (n = 5476). (D) OG distributions around PQSs within G4P peaks (G4-PQSs, n = 31 623) and out of G4P peaks (non-G4-PQSs, n = 1 474 730). Replicates 1 are presented for A–D. (E) The profiles of PQSs around G4-PQSs and non-G4-PQSs. (F) The model illustrating the relationship between OG formation and G4 regulation. G4s can prevent OG formation to protect genome stability. On the other hand, non-G4-PQSs are hotspots of OGs which can stimulate the transformation of duplex to G4 and regulate downstream transcription through OGG1 and APE1.