ArticleFrontiers in genetics2018
p53-Sensitive Epileptic Behavior and Inflammation in
Article in Frontiers in genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Convpaint-Interactive pixel classification using pretrained neural networks.Cell reports methods · 2026Article
- Article
- Seizures in brain tumors: pathogenesis, risk factors and management (Review).International journal of molecular medicine · 2025Review
- Nedl1 knockout ameliorates cognitive impairment and improves epilepsy threshold in pilocarpine-induced epileptic mice.Acta epileptologica · 2025Article
- Impact of diffused versus vasculature targeted DNA damage on the heart of mice depleted of telomeric factor Ft1.Aging cell · 2023Article
- Causal relationship between telomere length and epilepsy: A bidirectional Mendelian randomization study.Epilepsia open · 2023Observational
- Combined alteration of lamin and nuclear morphology influences the localization of the tumor-associated factor AKTIP.Journal of experimental & clinical cancer research : CR · 2022Article
- AKTIP interacts with ESCRT I and is needed for the recruitment of ESCRT III subunits to the midbody.PLoS genetics · 2021Article
- Cellular Senescence in Brain Aging.Frontiers in aging neuroscience · 2021Review
- Interplay of the nuclear envelope with chromatin in physiology and pathology.Nucleus (Austin, Tex.) · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epilepsy is a complex clinical condition characterized by repeated spontaneous seizures. Seizures have been linked to multiple drivers including DNA damage accumulation. Investigation of epilepsy physiopathology in humans imposes ethical and practical limitations, for this reason model systems are mostly preferred. Among animal models, mouse mutants are particularly valuable since they allow conjoint behavioral, organismal, and genetic analyses. Along with this, since aging has been associated with higher frequency of seizures, prematurely aging mice, simulating human progeroid diseases, offer a further useful modeling element as they recapitulate aging over a short time-window. Here we report on a mouse mutant with progeroid traits that displays repeated spontaneous seizures. Mutant mice were produced by reducing the expression of the gene
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.