ArticleInternational journal of molecular sciences2021
Differential Role of p53 in Oligodendrocyte Survival in Response to Various Stresses: Experimental Autoimmune Encephalomyelitis, Cuprizone Intoxication or White Matter Stroke.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Neuroprotective effects of rutin against cuprizone-induced multiple sclerosis in mice.Inflammopharmacology · 2024Article
- Magnetic resonance elastography captures a transient benefit of exercise intervention on forebrain stiffness in a rat model of fetal alcohol spectrum disorders.Alcohol, clinical & experimental research · 2024Article
- Low-dose brain radiation: lowering hyperphosphorylated-tau without increasing DNA damage or oncogenic activation.Scientific reports · 2023Article
- Transient regulation of focal adhesion via Tensin3 is required for nascent oligodendrocyte differentiation.eLife · 2022Article
- Molecular Mechanisms of Cerebrovascular Diseases.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Promoting oligodendrocyte viability has been proposed as a therapeutic strategy for alleviating many neuronal diseases, such as multiple sclerosis and stroke. However, molecular pathways critical for oligodendrocyte survival under various stresses are still not well known. p53 is a strong tumor suppressor and regulates cell cycle, DNA repair and cell death. Our previous studies have shown that p53 plays an important role in promoting neuronal survival after insults, but its specific role in oligodendrocyte survival is not known. Here, we constructed the mice with oligodendrocyte-specific p53 loss by crossing TRP53
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Registered trials
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