ArticlePloS one2012
Lack of p53 affects the expression of several brain mitochondrial proteins: insights from proteomics into important pathways regulated by p53.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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
11 citing papers in PubMed, 16 citations in OpenAlex.
- EDR Peptide: Possible Mechanism of Gene Expression and Protein Synthesis Regulation Involved in the Pathogenesis of Alzheimer's Disease.Molecules (Basel, Switzerland) · 2020Review
- Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease.Antioxidants (Basel, Switzerland) · 2020Review
- Differential expression of skeletal muscle mitochondrial proteins in yak, dzo, and cattle: a proteomics-based study.The Journal of veterinary medical science · 2020Article
- Mutant huntingtin disrupts mitochondrial proteostasis by interacting with TIM23.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Article
- Oxidative Stress, Amyloid-β Peptide, and Altered Key Molecular Pathways in the Pathogenesis and Progression of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2018Review
- Article
- p53 and mitochondrial dysfunction: novel insight of neurodegenerative diseases.Journal of bioenergetics and biomembranes · 2016Review
- Activation of p53 in Down Syndrome and in the Ts65Dn Mouse Brain is Associated with a Pro-Apoptotic Phenotype.Journal of Alzheimer's disease : JAD · 2016Article
- Basal brain oxidative and nitrative stress levels are finely regulated by the interplay between superoxide dismutase 2 and p53.Journal of neuroscience research · 2015Article
- Annexin A1 complex mediates oxytocin vesicle transport.Journal of neuroendocrinology · 2013Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
The tumor suppressor protein p53 has been described "as the guardian of the genome" for its crucial role in regulating the transcription of numerous genes responsible for cells cycle arrest, senescence, or apoptosis in response to various stress signals. Although p53 promotes longevity by decreasing the risk of cancer through activation of apoptosis or cellular senescence, several findings suggest that an increase of its activity may have deleterious effects leading to selected aspects of the aging phenotype and neurodegenerative diseases. There is the link between p53 and oxidative stress, the latter a crucial factor that contributes to neurodegenerative processes like Alzheimer disease (AD). In the present study, using a proteomics approach, we analyzed the impact of lack of p53 on the expression of several brain mitochondrial proteins involved in different pathways, and how lack of p53 may present a target to restore neuronal impairments. Our investigation on isolated brain mitochondria from p53((-/-)) mice also provides a better understanding of the p53-mitochondria relationship and its involvement in the development of many diseases.
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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.