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. 2022 Jan 12;8(2):eabi6180. doi: 10.1126/sciadv.abi6180

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Copyright © 2022 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC).

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Fig. 2. — (A and B) Enrichment of DNM-affected genes within coexpression modules in (A) prenatal and (B) postnatal human brains (left) and Gene Ontology (GO) biological process (BP) enrichment results according to Metascape for corresponding modules (right). Heatmaps indicate the P values of the degree of enrichment. (C) Integrative analysis of the potential pathogenicity of coding DNM-affected genes. Thirteen independent sources of evidence were used to rank DNM-affected genes. (D) Schematic of the chromatin-regulating activities of SETD5, KDM3B, and ASXL3. (E) Western blot result (left) and cross-species conservation at the discovered mutation site (right). (F) qPCR validation of mutation of (E). CHD8, chromodomain helicase DNA binding protein 8; FMRP, fragile X mental retardation protein; RBFOX, RNA binding fox-1 homolog 1; G2C, the genes to cognition program.