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. 2021 Mar 4;11:5154. doi: 10.1038/s41598-021-84647-2

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© The Author(s) 2021

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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USP7 haploinsufficiency uniquely promotes cellular growth in Jurkat and Molt-4 cell lines. (A) USP7 haploinsufficiency generated by CRISPR genome editing targeting USP7’s exon 6. (B) ATP monitoring system cellular growth assay for the USP7 homozygous KO, USP7 heterozygous KO, and USP7 wild-type control in Jurkat cells. (C) Cellular growth assay of the wild-type and CRISPR clones in Molt-4. (D) GSEA analysis showing that genes down-regulated in the USP7-heterozygous-KO Jurkat cells compared to USP7-wt control are enriched for E-protein targets negatively regulated by TAL1. (E) GSEA analysis showing that genes down-regulated in the USP7 50% KD Molt-4 cells compared to wild-type are enriched for E-protein targets negatively regulated by TAL1.