ArticleCellular and molecular neurobiology2017
The O-GlcNAc Modification of CDK5 Involved in Neuronal Apoptosis Following In Vitro Intracerebral Hemorrhage.
Article in Cellular and molecular neurobiology, 2017. 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, 20 citations in OpenAlex.
- Gabapentin Alleviates Brain Injury in Intracerebral Hemorrhage Through Suppressing Neuroinflammation and Apoptosis.Neurochemical research · 2022Article
- O-GlcNAc transferase regulates glioblastoma acetate metabolism via regulation of CDK5-dependent ACSS2 phosphorylation.Oncogene · 2022Article
- p75Neurotoxicity research · 2022Article
- The role of Cdk5 in neurological disorders.Frontiers in cellular neuroscience · 2022Review
- Role ofPhysiological reviews · 2021Review
- A simple lectin-based biochip might display the potential clinical value of glycomics in patients with spontaneous intracerebral hemorrhage.Annals of translational medicine · 2021Article
- MicroRNA-181c provides neuroprotection in an intracerebral hemorrhage model.Neural regeneration research · 2020Article
- The O-GlcNAc Modification on Kinases.ACS chemical biology · 2020Article
- Nutrient regulation of signaling and transcription.The Journal of biological chemistry · 2019Review
- Nutrient-driven O-GlcNAc in proteostasis and neurodegeneration.Journal of neurochemistry · 2018Review
- The emerging link between O-GlcNAcylation and neurological disorders.Cellular and molecular life sciences : CMLS · 2017Review
- Higher O-GlcNAc Levels Are Associated with Defects in Progenitor Proliferation and Premature Neuronal Differentiation duringFrontiers in cellular neuroscience · 2017Article
- Loss of O-GlcNAc glycosylation in forebrain excitatory neurons induces neurodegeneration.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Contrary to cell cycle-associated cyclin-dependent kinases, CDK5 is best known for its regulation of signaling processes in regulating mammalian CNS development. Studies of CDK5 have focused on its phosphorylation, although the diversity of CDK5 functions in the brain suggests additional forms of regulation. Here we expanded on the functional roles of CDK5 glycosylation in neurons. We showed that CDK5 was dynamically modified with O-GlcNAc in response to neuronal activity and that glycosylation represses CDK5-dependent apoptosis by impairing its association with p53 pathway. Blocking glycosylation of CDK5 alters cellular function and increases neuronal apoptosis in the cell model of the ICH. Our findings demonstrated a new role for O-glycosylation in neuronal apoptosis and provided a mechanistic understanding of how glycosylation contributes to critical neuronal functions. Moreover, we identified a previously unknown mechanism for the regulation of activity-dependent gene expression, neural development, and apoptosis.
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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.