ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Cdh1/Hct1-APC is essential for the survival of postmitotic neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 159 citations in OpenAlex.
- A standardized randomized 6-month aerobic exercise-training down-regulated pro-inflammatory genes, but up-regulated anti-inflammatory, neuron survival and axon growth-related genes.Experimental gerontology · 2015Trial
- Uncovering Cell Cycle Dysregulations and Associated Mechanisms in Cancer and Neurodegenerative Disorders: A Glimpse of Hope for Repurposed Drugs.Molecular neurobiology · 2024Review
- Dopaminergic neuron metabolism: relevance for understanding Parkinson's disease.Metabolomics : Official journal of the Metabolomic Society · 2024Review
- APC/C prevents a noncanonical order of cyclin/CDK activity to maintain CDK4/6 inhibitor-induced arrest.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Weak neuronal glycolysis sustains cognition and organismal fitness.Nature metabolism · 2024Article
- Deletion of a core APC/C component reveals APC/C function in regulating neuronal USP1 levels and morphology.Frontiers in molecular neuroscience · 2024Article
- APC/C prevents non-canonical order of cyclin/CDK activity to maintain CDK4/6 inhibitor-induced arrest.bioRxiv : the preprint server for biology · 2023Article
- Apoptosis in Alzheimer's disease: insight into the signaling pathways and therapeutic avenues.Apoptosis : an international journal on programmed cell death · 2023Review
- Cross-talk between energy and redox metabolism in astrocyte-neuron functional cooperation.Essays in biochemistry · 2023Review
- MAD2B Blunts Chronic Unpredictable Stress and Corticosterone Stimulation-Induced Depression-Like Behaviors in Mice.The international journal of neuropsychopharmacology · 2023Article
- HN1 Is Enriched in the S-Phase, Phosphorylated in Mitosis, and Contributes to Cyclin B1 Degradation in Prostate Cancer Cells.Biology · 2023Article
- A pilot investigation of differential hydroxymethylation levels in patient-derived neural stem cells implicates altered cortical development in bipolar disorder.Frontiers in psychiatry · 2023Article
- Cdk5 Promotes Mitochondrial Fission via Drp1 Phosphorylation at S616 in Chronic Ethanol Exposure-Induced Cognitive Impairment.Molecular neurobiology · 2022Article
- Adult Neural Stem Cell Migration Is Impaired in a Mouse Model of Alzheimer's Disease.Molecular neurobiology · 2022Article
- Conditional deletion of MAD2B in forebrain neurons enhances hippocampus-dependent learning and memory in mice.Frontiers in cellular neuroscience · 2022Article
- Amyloid-β Induces Cdh1-Mediated Rock2 Stabilization Causing Neurodegeneration.Frontiers in pharmacology · 2022Article
- APC/C-Cdh1-targeted substrates as potential therapies for Alzheimer's disease.Frontiers in pharmacology · 2022Review
- Rapid initiation of cell cycle reentry processes protects neurons from amyloid-β toxicity.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Nuclear Lamina: Protein Accumulation and Disease.Biomedicines · 2020Review
- Does APC/CJournal of neurochemistry · 2019Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell division at the end of mitosis and G1 is controlled by Cdh1/Hct1, an activator of the E3-ubiquitin ligase anaphase-promoting complex (APC) that promotes the ubiquitylation and degradation of mitotic cyclins and other substrates. Cdh1-APC is active in postmitotic neurons, where it regulates axonal growth and patterning in the developing brain. However, it remains unknown whether Cdh1-APC is involved in preventing cell-cycle progression in terminally differentiated neurons. To address this issue, we used the small hairpin RNA strategy to deplete Cdh1 in postmitotic neurons. We observed that Cdh1 silencing rapidly triggered apoptotic neuronal death. To investigate the underlying mechanism, we focused on cyclin B1, a major Cdh1-APC substrate. Our results demonstrate that Cdh1 is required to prevent the accumulation of cyclin B1 in terminally differentiated neurons. Moreover, by keeping cyclin B1 low, Cdh1 prevented these neurons from entering an aberrant S phase that led to apoptotic cell death. These results provide an explanation for the mechanism of cyclin B1 reactivation that occurs in the brain of patients suffering from neurodegenerative diseases, such as Alzheimer's disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.