ArticleiScience2025
A CHD8-TRRAP axis facilitates MYC and E2F target gene regulation in human neural stem cells.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- CHD8-Dependent Chromatin Licensing Sustains Trophoblast Stem Cell Transcriptional Programs.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Defective Neural Stem and Progenitor Cell Proliferation in Neurodevelopmental Disorders.Journal of developmental biology · 2025Review
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Authors and funding
12 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Mutations in ATP-dependent chromatin remodeler CHD8 cause one of the most frequent monogenetic forms of autism and are associated with brain overgrowth. Nevertheless, the activities of CHD8 in autism-relevant cell types are still poorly understood. Here, we purify the CHD8 protein from human neural stem cells and determine its interaction partners using mass spectrometry. We identify the TRRAP complex, a coactivator of MYC and E2F transcription factors, as a prominent CHD8 interaction partner. CHD8 colocalizes genome-wide with TRRAP and binds together at MYC and E2F target gene promoters in human neural stem cells. Depletion of CHD8 or TRRAP in human neural stem cells shows downregulation of MYC and E2F target genes as the most prominent gene-regulatory events. Depletion of CHD8 diminishes cell-cycle entry into S-phase. MYC and E2F transcription factors are established oncogenes and regulate cell growth. Our results link CHD8 to TRRAP in facilitating the regulation of MYC and E2F target genes in human neural stem cells.
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