ArticleOncogene2004
Limited role of N-terminal phosphoserine residues in the activation of transcription by p53.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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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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.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- Conserved oncogenic behavior of the FAM83 family regulates MAPK signaling in human cancer.Molecular cancer research : MCR · 2014Article
- Hyperactivation of EGFR and downstream effector phospholipase D1 by oncogenic FAM83B.Oncogene · 2014Article
- DNA damage signaling induced by the G-quadruplex ligand 12459 is modulated by PPM1D/WIP1 phosphatase.Nucleic acids research · 2013Article
- Hypoxia-induced cytotoxic drug resistance in osteosarcoma is independent of HIF-1Alpha.PloS one · 2013Article
- FAM83B mediates EGFR- and RAS-driven oncogenic transformation.The Journal of clinical investigation · 2012Article
- Article
- A p53-independent role for the MDM2 antagonist Nutlin-3 in DNA damage response initiation.BMC cancer · 2011Article
- Regulation of Chk2 ubiquitination and signaling through autophosphorylation of serine 379.Molecular and cellular biology · 2008Article
- Dissecting the role of p53 phosphorylation in homologous recombination provides new clues for gain-of-function mutants.Nucleic acids research · 2008Article
- The C/H3 domain of p300 is required to protect VRK1 and VRK2 from their downregulation induced by p53.PloS one · 2008Article
- Nutlin-3a activates p53 to both down-regulate inhibitor of growth 2 and up-regulate mir-34a, mir-34b, and mir-34c expression, and induce senescence.Cancer research · 2008Article
- 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.Molecular and cellular biology · 2008Article
- Mdm2 is required for inhibition of Cdk2 activity by p21, thereby contributing to p53-dependent cell cycle arrest.Molecular and cellular biology · 2007Article
- The MDM2 ubiquitination signal in the DNA-binding domain of p53 forms a docking site for calcium calmodulin kinase superfamily members.Molecular and cellular biology · 2007Article
- Macrophage inhibitory cytokine 1 mediates a p53-dependent protective arrest in S phase in response to starvation for DNA precursors.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Defect in serine 46 phosphorylation of p53 contributes to acquisition of p53 resistance in oral squamous cell carcinoma cells.Oncogene · 2006Article
- p53 Stabilization and accumulation induced by human vaccinia-related kinase 1.Molecular and cellular biology · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The p53 tumor suppressor is phosphorylated in response to various cellular stress signals, such as DNA damage, leading to its release from MDM2 and consequent stabilization and activation as a transcription factor. In human U2OS cells, treatment with adriamycin causes p53 to be phosphorylated on all six serine residues tested, leading to the dissociation of p53 from MDM2 and transcription of the p21 and mdm2 genes. In contrast, in these cells, IPTG-dependent induction of p14ARF, which sequesters MDM2 away from p53, does not lead to detectable phosphorylation of any of the five N-terminal serine residues tested (6, 9, 15, 20, 37). Only C-terminal serine 392 is phosphorylated. However, the increase of p21 and mdm2 mRNAs was indistinguishable following treatment with adriamycin or induction of p14ARF. By using cDNA arrays to examine global p53-dependent gene expression in response to adriamycin or p14ARF, we found that most genes were regulated similarly by the two treatments. However, a subset of p53-regulated genes whose products have proliferative roles or regulate VEGF activity, newly described here, are repressed by p14ARF much more than by adriamycin. We conclude that the phosphorylation of p53 on N-terminal serine residues is not required for increased transcription of the great majority of p53-responsive genes and that the induction of p53 by p14ARF, with little phosphorylation, leads to substantial repression of genes whose products have roles in proliferation.
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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.