ArticleProceedings of the National Academy of Sciences of the United States of America2017
Formation of neurodegenerative aggresome and death-inducing signaling complex in maternal diabetes-induced neural tube defects.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Research advances on the impact of gestational diabetes mellitus on offspring neurodevelopment.Diabetology & metabolic syndrome · 2026Review
- Impact of ATF6 deletion on the embryonic brain development.iScience · 2025Article
- Study and validation on mitochondrial and immune-related hub genes in gestational diabetes mellitus based on bioinformatics.Frontiers in endocrinology · 2025Article
- Spatial sequestration of activated-caspase 3 in aggresomes mediates resistance of neuroblastoma cell to bortezomib treatment.Scientific reports · 2024Article
- Supramolecular organizing centers at the interface of inflammation and neurodegeneration.Frontiers in immunology · 2022Review
- Update and Potential Opportunities in CBP [Cyclic Adenosine Monophosphate (cAMP) Response Element-Binding Protein (CREB)-Binding Protein] Research Using Computational Techniques.The protein journal · 2021Review
- PERK participates in cardiac valve development via fatty acid oxidation and endocardial-mesenchymal transformation.Scientific reports · 2020Article
- Identification of histone malonylation in the human fetal brain and implications for diabetes-induced neural tube defects.Molecular genetics & genomic medicine · 2020Article
- 4-Phenylbutyrate ameliorates apoptotic neural cell death in Down syndrome by reducing protein aggregates.Scientific reports · 2020Article
- Hsp90 and complex birth defects: A plausible mechanism for the interaction of genes and environment.Neuroscience letters · 2020Review
- Rare mutations in apoptosis related genes APAF1, CASP9, and CASP3 contribute to human neural tube defects.Cell death & disease · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Diabetes mellitus in early pregnancy increases the risk in infants of birth defects, such as neural tube defects (NTDs), known as diabetic embryopathy. NTDs are associated with hyperglycemia-induced protein misfolding and Caspase-8-induced programmed cell death. The present study shows that misfolded proteins are ubiquitinylated, suggesting that ubiquitin-proteasomal degradation is impaired. Misfolded proteins form aggregates containing ubiquitin-binding protein p62, suggesting that autophagic-lysosomal clearance is insufficient. Additionally, these aggregates contain the neurodegenerative disease-associated proteins α-Synuclein, Parkin, and Huntingtin (Htt). Aggregation of Htt may lead to formation of a death-inducing signaling complex of Hip1, Hippi, and Caspase-8. Treatment with chemical chaperones, such as sodium 4-phenylbutyrate (PBA), reduces protein aggregation in neural stem cells in vitro and in embryos in vivo. Furthermore, treatment with PBA in vivo decreases NTD rate in the embryos of diabetic mice, as well as Caspase-8 activation and cell death. Enhancing protein folding could be a potential interventional approach to preventing embryonic malformations in diabetic pregnancies.
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