ArticleOncogene2008
hSMG-1 and ATM sequentially and independently regulate the G1 checkpoint during oxidative stress.
Article in Oncogene, 2008. 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
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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.
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, 58 citations in OpenAlex.
- Two stress-responsive kinases suppress ferroptosis by activating antioxidant programs under mild oxidative stress.Signal transduction and targeted therapy · 2026Article
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- Stress-Induced Eukaryotic Translational Regulatory Mechanisms.Journal of clinical and medical sciences · 2024Article
- Progression of the pluripotent epiblast depends upon the NMD factor UPF2.Development (Cambridge, England) · 2022Article
- A Novel Role of SMG1 in Cholesterol Homeostasis That Depends Partially on p53 Alternative Splicing.Cancers · 2022Article
- Cellular variability of nonsense-mediated mRNA decay.Nature communications · 2021Article
- SMG1 heterozygosity exacerbates haematopoietic cancer development in Atm null mice by increasing persistent DNA damage and oxidative stress.Journal of cellular and molecular medicine · 2019Article
- A region-based gene association study combined with a leave-one-out sensitivity analysis identifies SMG1 as a pancreatic cancer susceptibility gene.PLoS genetics · 2019Article
- The loss of SMG1 causes defects in quality control pathways in Physcomitrella patens.Nucleic acids research · 2018Article
- Neonatal hyperoxia depletes pulmonary vein cardiomyocytes in adult mice via mitochondrial oxidation.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Nonsense-mediated mRNA decay: a 'nonsense' pathway makes sense in stem cell biology.Nucleic acids research · 2018Review
- Hyperoxia activates ATM independent from mitochondrial ROS and dysfunction.Redox biology · 2015Article
- A critical role of RBM8a in proliferation and differentiation of embryonic neural progenitors.Neural development · 2015Article
- PNAS-4, an Early DNA Damage Response Gene, Induces S Phase Arrest and Apoptosis by Activating Checkpoint Kinases in Lung Cancer Cells.The Journal of biological chemistry · 2015Article
- SMG-1 suppresses CDK2 and tumor growth by regulating both the p53 and Cdc25A signaling pathways.Cell cycle (Georgetown, Tex.) · 2013Article
- The C-terminal residues of Saccharomyces cerevisiae Mec1 are required for its localization, stability, and function.G3 (Bethesda, Md.) · 2013Article
- Abnormal mitosis triggers p53-dependent cell cycle arrest in human tetraploid cells.Chromosoma · 2013Article
- The proteasome activator PA200 regulates tumor cell responsiveness to glutamine and resistance to ionizing radiation.Molecular cancer research : MCR · 2012Article
- SMG-1 and mTORC1 act antagonistically to regulate response to injury and growth in planarians.PLoS genetics · 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
5 authors at 1 institution in 1 country.
Funding
Abstract
Genotoxic stress activates the phosphatidylinositol 3-kinase-like kinases (PIKKs) that phosphorylate proteins involved in cell cycle arrest, DNA repair and apoptosis. Previous work showed that the PIKK ataxia telangiectasia mutated (ATM) but not ATM and Rad3 related phosphorylates p53 (Ser15) during hyperoxia, a model of prolonged oxidative stress and DNA damage. Here, we show hSMG-1 is responsible for the rapid and early phosphorylation of p53 (Ser15) and that ATM helps maintain phosphorylation after 24 h. Despite reduced p53 phosphorylation and abundance in cells depleted of hSMG-1 or ATM, levels of the p53 target p21 were still elevated and the G(1) checkpoint remained intact. Conditional overexpression of p21 in p53-deficient cells revealed that hyperoxia also stimulates wortmannin-sensitive degradation of p21. siRNA depletion of hSMG-1 or ATM restored p21 stability and the G(1) checkpoint during hyperoxia. These findings establish hSMG-1 as a proximal regulator of DNA damage signaling and reveal that the G(1) checkpoint is tightly regulated during prolonged oxidative stress by both PIKK-dependent synthesis and proteolysis of p21.
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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.