ArticleInternational journal of biological sciences2019
p53 Mutant p53
Article in International journal of biological sciences, 2019. 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
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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
10 citing papers in PubMed, 17 citations in OpenAlex.
- Oncogenic and teratogenic effects ofeLife · 2025Article
- Sex Disparities in P53 Regulation and Functions: Novel Insights for Personalized Cancer Therapies.Cells · 2025Review
- Untargeted Metabolomics Reveals Metabolic Link Between Histone H3K27 Demethylase UTX and Neurodevelopment.Journal of cellular and molecular medicine · 2025Article
- Identification of potential key ferroptosis- and autophagy-related genes in myelomeningocele through bioinformatics analysis.Heliyon · 2024Article
- Melatonin alleviates valproic acid-induced neural tube defects by modulating Src/PI3K/ERK signaling and oxidative stress.Acta biochimica et biophysica Sinica · 2024Article
- Emodin Protects SH-SY5Y Cells Against Zinc-Induced Synaptic Impairment and Oxidative Stress Through the ERK1/2 Pathway.Frontiers in pharmacology · 2022Article
- Micronutrient imbalance and common phenotypes in neural tube defects.Genesis (New York, N.Y. : 2000) · 2021Review
- Article
- Review
- Regulating tumor suppressor genes: post-translational modifications.Signal transduction and targeted therapy · 2020Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The p53 is one of the most important tumor suppressors through surveillance of DNA damages and abnormal proliferation signals, and activation the cell cycle arrest and apoptosis in response to stress. However, the mutation of p53 is known to be oncogenic by both loss of function in inhibiting cell cycle progress and gain of function in promoting abnormal proliferation. In the present study, we have established a knock in mouse model containing an Asn-to-Ser substitution at p53 amino acid 236 by homologous recombination (p53N236S). Other than tumorigenesis phenotype, we found that
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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.