ArticleMolecular cell2022
APC7 mediates ubiquitin signaling in constitutive heterochromatin in the developing mammalian brain.
Article in Molecular cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Review
- Ki-67 regulates heterochromatin organization in neurons and forms condensates with heterochromatic components.Nature communications · 2026Article
- The APC/C subunit APC7 promotes hepatocellular carcinoma progression by mediating ubiquitination and degradation of LATS1 to activate YAP/TAZ.Biology direct · 2026Article
- The APC/C subunit APC7 exerts antiviral effects by targeting the adaptor protein MAVS.Frontiers in immunology · 2026Article
- Anapc5 and Anapc7 as genetic modifiers of KIF18A function in fertility and mitotic progression.Scientific reports · 2025Article
- Notch controls APC/CScience advances · 2025Article
- The Hao-Fountain syndrome protein USP7 regulates neuronal connectivity in the brain via a novel p53-independent ubiquitin signaling pathway.Cell reports · 2025Article
- Multichannel 3D-Printed Bioactive Scaffold Combined with Small Interfering RNA Delivery to Promote Neurological Recovery after Spinal Cord Injury.Research (Washington, D.C.) · 2025Article
- Current advances in cancer immunohistochemistry: a new perspective for the Ki-67 biomarker.Ecancermedicalscience · 2025Review
- A comparative study of the cryo-EM structures ofeLife · 2024Article
- The anaphase-promoting complex controls a ubiquitination-phosphoprotein axis in chromatin during neurodevelopment.Developmental cell · 2023Article
- Identification and validation of a PD-L1-related signature from mass spectrometry in gastric cancer.Journal of cancer research and clinical oncology · 2023Article
- Artificial intelligence and bioinformatics analyze markers of children's transcriptional genome to predict autism spectrum disorder.Frontiers in neurology · 2023Article
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Authors and funding
21 authors at 9 institutions in 2 countries.
Funding
Abstract
Neurodevelopmental cognitive disorders provide insights into mechanisms of human brain development. Here, we report an intellectual disability syndrome caused by the loss of APC7, a core component of the E3 ubiquitin ligase anaphase promoting complex (APC). In mechanistic studies, we uncover a critical role for APC7 during the recruitment and ubiquitination of APC substrates. In proteomics analyses of the brain from mice harboring the patient-specific APC7 mutation, we identify the chromatin-associated protein Ki-67 as an APC7-dependent substrate of the APC in neurons. Conditional knockout of the APC coactivator protein Cdh1, but not Cdc20, leads to the accumulation of Ki-67 protein in neurons in vivo, suggesting that APC7 is required for the function of Cdh1-APC in the brain. Deregulated neuronal Ki-67 upon APC7 loss localizes predominantly to constitutive heterochromatin. Our findings define an essential function for APC7 and Cdh1-APC in neuronal heterochromatin regulation, with implications for understanding human brain development and disease.
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