ArticleScientific reports2017
RNA sequencing of synaptic and cytoplasmic Upf1-bound transcripts supports contribution of nonsense-mediated decay to epileptogenesis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- RNA Granules at the Crossroads of Synaptic Dysfunction and Neurodegeneration.Journal of neurochemistry · 2025Review
- UPF1-From mRNA Degradation to Human Disorders.Cells · 2023Review
- Progression of the pluripotent epiblast depends upon the NMD factor UPF2.Development (Cambridge, England) · 2022Article
- ALS-associated KIF5A mutations abolish autoinhibition resulting in a toxic gain of function.Cell reports · 2022Article
- Article
- NMD abnormalities during brain development in the Fmr1-knockout mouse model of fragile X syndrome.Genome biology · 2021Article
- Enrichment of Circular RNA Expression Deregulation at the Transition to Recurrent Spontaneous Seizures in Experimental Temporal Lobe Epilepsy.Frontiers in genetics · 2021Article
- Poison exons in neurodevelopment and disease.Current opinion in genetics & development · 2020Review
- UPF2 leads to degradation of dendritically targeted mRNAs to regulate synaptic plasticity and cognitive function.Molecular psychiatry · 2020Article
- Article
- Bi-directional genetic modulation of GSK-3β exacerbates hippocampal neuropathology in experimental status epilepticus.Cell death & disease · 2018Article
- Continuous Monitoring via Tethered Electroencephalography of Spontaneous Recurrent Seizures in Mice.Frontiers in behavioral neuroscience · 2017Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nonsense mediated decay (NMD) pathway is a critical surveillance mechanism for identifying aberrant mRNA transcripts. It is unknown, however, whether the NMD system is affected by seizures in vivo and whether changes confer beneficial or maladaptive responses that influence long-term outcomes such the network alterations that produce spontaneous recurrent seizures. Here we explored the responses of the NMD pathway to prolonged seizures (status epilepticus) and investigated the effects of NMD inhibition on epilepsy in mice. Status epilepticus led to increased protein levels of Up-frameshift suppressor 1 homolog (Upf1) within the mouse hippocampus. Upf1 protein levels were also higher in resected hippocampus from patients with intractable temporal lobe epilepsy. Immunoprecipitation of Upf1-bound RNA from the cytoplasmic and synaptosomal compartments followed by RNA sequencing identified unique populations of NMD-associated transcripts and altered levels after status epilepticus, including known substrates such as Arc as well as novel targets including Inhba and Npas4. Finally, long-term video-EEG recordings determined that pharmacologic interference in the NMD pathway after status epilepticus reduced the later occurrence of spontaneous seizures in mice. These findings suggest compartment-specific recruitment and differential loading of transcripts by NMD pathway components may contribute to the process of epileptogenesis.
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