ArticleMolecular and cellular biology2008
The absence of Ser389 phosphorylation in p53 affects the basal gene expression level of many p53-dependent genes and alters the biphasic response to UV exposure in mouse embryonic fibroblasts.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 34 citations in OpenAlex.
- Unaffected Li-Fraumeni Syndrome Carrier Parent Demonstrates Allele-Specific mRNA Stabilization of Wild-TypeGenes · 2022Article
- Inferring clonal composition from multiple tumor biopsies.NPJ systems biology and applications · 2020Article
- Evidence for allosteric effects on p53 oligomerization induced by phosphorylation.Protein science : a publication of the Protein Society · 2018Article
- Serine 392 phosphorylation modulates p53 mitochondrial translocation and transcription-independent apoptosis.Cell death and differentiation · 2018Article
- Allele-specific wild-type TP53 expression in the unaffected carrier parent of children with Li-Fraumeni syndrome.Cancer genetics · 2017Article
- A Novel Naphthalimide Compound Restores p53 Function in Non-small Cell Lung Cancer by Reorganizing the Bak·Bcl-xl Complex and Triggering Transcriptional Regulation.The Journal of biological chemistry · 2016Article
- Valuable lessons-learned in transcriptomics experimentation.Transcription · 2015Review
- PPARγ ligand production is tightly linked to clonal expansion during initiation of adipocyte differentiation.Journal of lipid research · 2014Article
- A range finding protocol to support design for transcriptomics experimentation: examples of in-vitro and in-vivo murine UV exposure.PloS one · 2014Article
- Requirement for phosphorylation of P53 at Ser312 in suppression of chemical carcinogenesis.Scientific reports · 2013Article
- Article
- Met acts through Abl to regulate p53 transcriptional outcomes and cell survival in the developing liver.Journal of hepatology · 2012Article
- p53 basic C terminus regulates p53 functions through DNA binding modulation of subset of target genes.The Journal of biological chemistry · 2012Article
- Induction and activation of the p53 pathway: a role for the protein kinase CK2?Molecular and cellular biochemistry · 2011Review
- A novel p53 phosphorylation site within the MDM2 ubiquitination signal: II. a model in which phosphorylation at SER269 induces a mutant conformation to p53.The Journal of biological chemistry · 2010Article
- A novel p53 phosphorylation site within the MDM2 ubiquitination signal: I. phosphorylation at SER269 in vivo is linked to inactivation of p53 function.The Journal of biological chemistry · 2010Article
- Serious complications in gene-expression studies with stress perturbation: An example of UV-exposed p53-mutant mouse embryonic fibroblasts.Transcription · 2010Article
- p53 post-translational modification: deregulated in tumorigenesis.Trends in molecular medicine · 2010Review
- Tumour suppression by p53: a role for the DNA damage response?Nature reviews. Cancer · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Phosphorylation is important in p53-mediated DNA damage responses. After UV irradiation, p53 is phosphorylated specifically at murine residue Ser389. Phosphorylation mutant p53.S389A cells and mice show reduced apoptosis and compromised tumor suppression after UV irradiation. We investigated the underlying cellular processes by time-series analysis of UV-induced gene expression responses in wild-type, p53.S389A, and p53(-/-) mouse embryonic fibroblasts. The absence of p53.S389 phosphorylation already causes small endogenous gene expression changes for 2,253, mostly p53-dependent, genes. These genes showed basal gene expression levels intermediate to the wild type and p53(-/-), possibly to readjust the p53 network. Overall, the p53.S389A mutation lifts p53-dependent gene repression to a level similar to that of p53(-/-) but has lesser effect on p53-dependently induced genes. In the wild type, the response of 6,058 genes to UV irradiation was strictly biphasic. The early stress response, from 0 to 3 h, results in the activation of processes to prevent the accumulation of DNA damage in cells, whereas the late response, from 12 to 24 h, relates more to reentering the cell cycle. Although the p53.S389A UV gene response was only subtly changed, many cellular processes were significantly affected. The early response was affected the most, and many cellular processes were phase-specifically lost, gained, or altered, e.g., induction of apoptosis, cell division, and DNA repair, respectively. Altogether, p53.S389 phosphorylation seems essential for many p53 target genes and p53-dependent processes.
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.