ArticleMolecular and cellular biology2004
c-Jun-deficient cells undergo premature senescence as a result of spontaneous DNA damage accumulation.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 62 citations in OpenAlex.
- Tfcp2l1 as a central integrator of hypoxia, dedifferentiation, and tumor progression.Journal of experimental & clinical cancer research : CR · 2025Review
- Inactivation of JNK signalling results in polarity loss and cell senescence of Sertoli cell.Cell proliferation · 2025Article
- EWS-FLI1 and Activator Protein-1 (AP-1) Reciprocally Regulate Extracellular-Matrix Proteins in Ewing sarcoma Cells.International journal of molecular sciences · 2024Article
- Signalling inhibition by ponatinib disrupts productive alternative lengthening of telomeres (ALT).Nature communications · 2023Article
- The potential of activator protein 1 (AP-1) in cancer targeted therapy.Frontiers in immunology · 2023Review
- Role of p53 in Regulating Radiation Responses.Life (Basel, Switzerland) · 2022Review
- AP-1 is a temporally regulated dual gatekeeper of reprogramming to pluripotency.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Cross-Talk Between Sphingolipids and Insulin-Like Growth Factor Signaling: Significance for Aging and Neurodegeneration.Molecular neurobiology · 2019Review
- Review
- Gadd45b deficiency promotes premature senescence and skin aging.Oncotarget · 2016Article
- Functional characterization of RAD52 as a lung cancer susceptibility gene in the 12p13.33 locus.Molecular carcinogenesis · 2016Article
- The role of c-Jun in controlling the EPAC1-dependent induction of the SOCS3 gene in HUVECs.FEBS letters · 2014Article
- ATM regulates insulin-like growth factor 1-secretory clusterin (IGF-1-sCLU) expression that protects cells against senescence.PloS one · 2014Article
- JNK signaling is needed to tolerate chromosomal instability.Cell cycle (Georgetown, Tex.) · 2014Article
- Mitogen-activated protein kinases and their role in radiation response.Genes & cancer · 2013Review
- Linking JNK Activity to the DNA Damage Response.Genes & cancer · 2013Review
- Differential regulation of c-Jun protein plays an instrumental role in chemoresistance of cancer cells.The Journal of biological chemistry · 2013Article
- A distal enhancer controls cytokine-dependent human cPLA2α gene expression.Journal of lipid research · 2013Article
- The NRF2 activation and antioxidative response are not impaired overall during hyperoxia-induced lung epithelial cell death.Oxidative medicine and cellular longevity · 2013Article
- Nucleolar AATF regulates c-Jun-mediated apoptosis.Molecular biology of the cell · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mouse embryo fibroblasts deficient for the c-Jun proto-oncogene (c-Jun-/- MEF) undergo p53-dependent premature senescence in conventional culture. This phenotype becomes evident only after several cell divisions, suggesting that senescence may result from exposure to unknown environmental factors. Here, we show that c-Jun-/- MEF can proliferate successfully in low oxygen (3% O2), indicating that premature senescence under conventional culture conditions is a consequence of hyperoxic stress. c-Jun-/- MEF exhibit higher basal levels of DNA damage compared to normal fibroblasts in high but not low oxygen, implying that senescence results from chronic accumulation of spontaneous DNA damage. This accumulation may be attributable, at least in part, to inefficient repair, since DNA damage induced by gamma ionizing radiation and H2O2 persists for longer in c-Jun-/- MEF than in wild-type MEF. Unexpectedly, p53 expression, phosphorylation, and transcriptional activity are largely unaffected by oxygen exposure, indicating that the accumulation of spontaneous DNA damage does not result in chronic activation of p53 as judged by conventional criteria. Finally, we find that c-Jun associates with nuclear foci containing gammaH2AX and ATM following irradiation, suggesting a potential role for c-Jun in DNA repair processes per se.
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.