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. 2024 May 30;27(8):1555–1564. doi: 10.1038/s41593-024-01654-y

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© The Author(s) 2024

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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Extended Data Fig. 6 — (a) Heterozygous Kras loss rescues RAS hyperactivation in heterozygous Nf1-mutant mice. Brown-Forsythe ANOVA test (F = 1582) with Dunnett’s T3 multiple comparisons. **, P = 0.0012 (WT vs Nf1^+/neo mice), 0.001 (Nf1^+/neo vs Kras^+/- mice), 0.0018 (Nf1^+/neo vs Kras^+/-;Nf1^+/neo mice). N = 3 per group. (b) Kras heterozygous loss rescues RAS hyperactivation in mice heterozygous for the R1809C Nf1 gene mutation (1809; 5425 C > T)³⁵. Brown-Forsythe ANOVA test (F = 610) with Dunnett’s T3 multiple comparisons. ***, P = 0.0003; ****, P < 0.0001. (c) The percentage of the forebrain covered by focal OPC hyperdensities revealed no difference between Nf1^+/neo and Kras^+/-; Nf1^+/neo mice. Kruskal-Wallis test with Dunn’s multiple comparisons. **, P = 0.0071. N = 4,4,6 (left to right). Data shown as mean ± SEM; each point = one mouse (a-c); two-sided; ns, not significant (P > 0.05).

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