ArticleOncogene2003
Apoptosis or growth arrest: modulation of the cellular response to p53 by proliferative signals.
Article in Oncogene, 2003. 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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Who cites it
17 citing papers in PubMed, 39 citations in OpenAlex.
- Combination treatment of cordycepin and radiation induces MA-10 mouse Leydig tumor cell death via ROS accumulation and DNA damage.American journal of cancer research · 2023Article
- Synergistic Effects of Weightlessness, Isoproterenol, and Radiation on DNA Damage Response and Cytokine Production in Immune Cells.International journal of molecular sciences · 2018Article
- LRP1 Regulates Retinal Angiogenesis by Inhibiting PARP-1 Activity and Endothelial Cell Proliferation.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
- Article
- Apoptotic effect of cordycepin combined with cisplatin and/or paclitaxel on MA-10 mouse Leydig tumor cells.OncoTargets and therapy · 2015Article
- NF-κB1 p50 promotes p53 protein translation through miR-190 downregulation of PHLPP1.Oncogene · 2014Article
- Increased expression of the pro-apoptotic protein BIM, a mechanism for cAMP/protein kinase A (PKA)-induced apoptosis of immature T cells.The Journal of biological chemistry · 2011Article
- A rapid and optimization-free procedure allows the in vivo detection of subtle cell cycle and ploidy alterations in tissues by flow cytometry.Cell cycle (Georgetown, Tex.) · 2010Article
- Regression based predictor for p53 transactivation.BMC bioinformatics · 2009Article
- Article
- Dissecting microregulation of a master regulatory network.BMC genomics · 2008Article
- Article
- Epigenetic mechanisms affect mutant p53 transgene expression in WAP-mutp53 transgenic mice.Oncogene · 2005Article
- Oxidative stress attenuates Fas-mediated apoptosis in Jurkat T cell line through Bfl-1 induction.Oncogene · 2005Article
- Transcriptional networks and cellular senescence in human mammary fibroblasts.Molecular biology of the cell · 2005Article
- Article
- Effects of Photon Radiation on DNA Damage, Cell Proliferation, Cell Survival, and Apoptosis of Murine and Human Mesothelioma Cell Lines.Advances in radiation oncologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of the tumor suppressor p53 after genotoxic insults may result in two different responses: growth arrest or apoptosis. In this study, we analysed how mitogenic stimulation of primary mouse lymphocytes influences p53 signaling upon gamma-irradiation. We found that G(0) lymphocytes rapidly went into p53-dependent apoptosis, whereas stimulated lymphocytes went into a p53-dependent, p21-mediated growth arrest. The switch in p53 response upon stimulation did neither result from a switch in transcriptional activation of major p53 target genes, nor from the high level of p21 expressed in stimulated, irradiated cells. Growth stimulation, however, led to the upregulation of the antiapoptotic factors Bcl-x(L) and Bfl-1. In resting cells, p53 induced apoptosis after gamma-irradiation was accompanied by a breakdown of the mitochondrial membrane potential (psi(m)) that was counteracted by growth stimulation. We propose that growth stimulation intercepted p53 proapoptotic signaling at the level of mitochondrial integrity, most likely by upregulating the antiapoptotic factors Bcl-x(L) and Bfl-1. Upregulation of Bcl-x(L) and of Bfl-1 upon growth stimulation was mediated by the PKC-dependent activation of NF-kappaB. Consequently, blocking PKC activity restored apoptosis in stimulated, irradiated splenocytes. The inherent coupling of growth stimulation with antiapoptotic signaling in primary lymphocytes might provide hints as to how precancerous lymphocytes bypass the need for mutational inactivation of p53. Thus, our findings might explain the relatively low frequency of p53 mutations in lymphomas in comparison to other tumor entities.
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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.