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. 2023 Oct 18;14:6570. doi: 10.1038/s41467-023-42445-6

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — a Examples of models by which vTRs can affect human TF (hTF) binding. vTRs can cooperate with hTFs to bind to DNA elements or a vTR can sequester an hTF, preventing its binding to DNA. b Number of hTF-vTR pairs tested for binding to 83 cancer gene promoters. hTF-vTR pairs were selected based on known PPIs between the two proteins or homology with known pairs. hTFs are classified by TF families. c Network of relationships between hTFs and vTRs at 83 cancer gene promoters. d Examples of RBPJ-EBNA3B cooperative binding to the TRIP11 and SGK1 promoters, and of EBNA3C antagonism of RBPJ binding to the DCC promoter. Source data are provided as a Source Data file.