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. 2020 Nov 2;11:5540. doi: 10.1038/s41467-020-19264-0

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© The Author(s) 2020, corrected publication 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — a Module-trait relationships between modules and APOE genotype, and between modules and AD status are shown. b, c Top gene ontologies and interaction of genes enriched in the yellow module genes. Purple nodes are hub genes (top 10 highest connectivity). d The mRNA expressions of ERCC4 (APOE4: p = 0.0576, AD: p = 0.0064, APOE4 x AD: p = 0.0742, Con-E3 vs. AD-E4: p = 0.0164, Con-E4 vs. AD-E4: p = 0.0049), DGCR8 (APOE4: p = 0.1088, AD: p = 0.0469, APOE4 x AD: p = 0.3298, Con-E4 vs. AD-E3: p = 0.0409), POLR3A (APOE4: p = 0.3926, AD: p = 0.0004, APOE4 x AD: p = 0.1349, Con-E3 vs. AD-E3: p = 0.0048, Con-E3 vs. AD-E4: p = 0.0084, Con-E4: AD-E3: p = 0.0221, Con-E4 vs. AD-E4: p = 0.0484), CLP1 (APOE4: p = 0.0953, AD: p = 0.0039, APOE4 x AD: p = 0.1831, Con-E3 vs. AD-E4: p = 0.0157, Con-E4 vs. AD-E4: p = 0.0066), HSPA4 (APOE4: p = 0.0501, AD: p = 0.0077, APOE4 x AD: p = 0.0410, Con-E3 vs. AD-E4: p = 0.0171, Con-E4 vs. AD-E4: p = 0.0038, AD-E3 vs. AD-E4: p = 0.0339), and PNO1 (APOE4: p = 0.8087, AD: p = 0.0022, APOE4 x AD: p = 0.1706, Con-E4 vs. AD-E3: p = 0.0218, Con-E4 vs. AD-E4: p = 0.0038) were quantified by RT-qPCR. e Representative images of the immunostaining for G3BP and Tuj1. Scale bar: 50 μm. f–i G3BP, EEA1, and LAMP1 levels were analyzed by western blotting. The levels of G3BP (g; APOE4: p = 0.6345, AD: p < 0.0001, APOE4 x AD: p = 0.0133, Con-E3 vs. AD-E4: p = 0.0025, Con-E4 vs. AD-E3: p = 0.0019, Con-E4 vs. AD-E4: p < 0.0001), EEA1 (h; APOE4: p = 0.2792, AD: p = 0.6789, APOE4 x AD: p = 0.0671), and LAMP1 (I; APOE4: p = 0.2558, AD: p = 0.0954, APOE4 x AD: p = 0.5646) were normalized to β-actin. j–l ERCC4, POLR3A, and HSPA4 were analyzed by western blotting. The levels of ERCC4 (j; APOE4: p = 0.9762, AD: p = 0.0016, APOE4 x AD: p = 0.3378, Con-E4 vs. AD-E3: p = 0.0241, Con-E4 vs. AD-E4: p = 0.0054), POLR3A (k; APOE4: p = 0.2095, AD: p = 0.0018, APOE4 x AD: p = 0.7764, Con-E4 vs. AD-E3: p = 0.0048, Con-E4 vs. AD-E4: p = 0.0149), and HSPA4 (l; APOE4: p = 0.6526, AD: p = 0.0152, APOE4 x AD: p = 0.2371) were normalized to β-actin. All data are expressed as mean ± SEM (N = 5). ANCOVA for APOE4, AD status, and APOE4 x AD status was performed by including sex, sampling age, and source of iPSCs as co-variables, which was followed by two-sided Tukey–Kramer tests to compare between the groups with two factors (APOE4 and AD status). *p < 0.05, **p < 0.01, ****p < 0.0001.