ArticleMolecular and cellular biology2009
The p53 tumor suppressor causes congenital malformations in Rpl24-deficient mice and promotes their survival.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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
65 citing papers in PubMed, 94 citations in OpenAlex.
- Nucleolus as a cornerstone linking proliferation and metabolism to cellular responses to stress: involvement of transcription factors MYC and p53.Frontiers in molecular biosciences · 2026Review
- All these screens that we've done: how functional genetic screens have informed our understanding of ribosome biogenesis.Bioscience reports · 2023Review
- Ribosomal protein mutations and cell competition: autonomous and nonautonomous effects on a stress response.Genetics · 2023Article
- RPL24 as a potential prognostic biomarker for cervical cancer treated by Cisplatin and concurrent chemoradiotherapy.Frontiers in oncology · 2023Article
- Eukaryotic Elongation Factor 2 Kinase Activity Is Required for the Phenotypes of the Rpl24The Journal of investigative dermatology · 2022Article
- Cell autonomous and non-autonomous consequences of deviations in translation machinery on organism growth and the connecting signalling pathways.Open biology · 2022Review
- RNA-interference screen for p53 regulators unveils a role of WDR75 in ribosome biogenesis.Cell death and differentiation · 2022Article
- Mutations in Hcfc1 and Ronin result in an inborn error of cobalamin metabolism and ribosomopathy.Nature communications · 2022Article
- Article
- Puma- and Caspase9-mediated apoptosis is dispensable for p53-driven neural crest-based developmental defects.Cell death and differentiation · 2021Article
- Article
- Disruption of entireeLife · 2021Article
- Transcriptomic Profiling of Human Pluripotent Stem Cell-derived Retinal Pigment Epithelium over Time.Genomics, proteomics & bioinformatics · 2021Article
- The p53 family reaches the final frontier: the variegated regulation of the dark matter of the genome by the p53 family in cancer.RNA biology · 2020Article
- Knockdown of GINS2 inhibits proliferation and promotes apoptosis through the p53/GADD45A pathway in non-small-cell lung cancer.Bioscience reports · 2020Observational
- Inhibition of the 60S ribosome biogenesis GTPase LSG1 causes endoplasmic reticular disruption and cellular senescence.Aging cell · 2019Article
- Review
- The role of p53 in developmental syndromes.Journal of molecular cell biology · 2019Review
- p53 pathway is involved in cell competition during mouse embryogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- A knowledge-based approach for predicting gene-disease associations.Bioinformatics (Oxford, England) · 2016Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypomorphic mutation in one allele of ribosomal protein l24 gene (Rpl24) is responsible for the Belly Spot and Tail (Bst) mouse, which suffers from defects of the eye, skeleton, and coat pigmentation. It has been hypothesized that these pathological manifestations result exclusively from faulty protein synthesis. We demonstrate here that upregulation of the p53 tumor suppressor during the restricted period of embryonic development significantly contributes to the Bst phenotype. However, in the absence of p53 a large majority of Rpl24(Bst/+) embryos die. We showed that p53 promotes survival of these mice via p21-dependent mechanism. Our results imply that activation of a p53-dependent checkpoint mechanism in response to various ribosomal protein deficiencies might also play a role in the pathogenesis of congenital malformations in humans.
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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.