ArticleNucleic acids research2016
PKCα and HMGB1 antagonistically control hydrogen peroxide-induced poly-ADP-ribose formation.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Poly-ADP-ribosylation dynamics, signaling, and analysis.Environmental and molecular mutagenesis · 2024Review
- Converting cell death into senescence by PARP1 inhibition improves recovery from acute oxidative injury.Nature aging · 2024Article
- MyoD induces ARTD1 and nucleoplasmic poly-ADP-ribosylation during fibroblast to myoblast transdifferentiation.iScience · 2021Article
- Mitochondrial NADMolecular cell · 2021Article
- Engineering Af1521 improves ADP-ribose binding and identification of ADP-ribosylated proteins.Nature communications · 2020Article
- Vitamin C Promotes Apoptosis and Cell Cycle Arrest in Oral Squamous Cell Carcinoma.Frontiers in oncology · 2020Article
- Comprehensive ADP-ribosylome analysis identifies tyrosine as an ADP-ribose acceptor site.EMBO reports · 2018Article
- The Modulatory Properties of Li-Ru-Kang Treatment on Hyperplasia of Mammary Glands Using an Integrated Approach.Frontiers in pharmacology · 2018Article
- Proteomic analyses identify ARH3 as a serine mono-ADP-ribosylhydrolase.Nature communications · 2017Article
- Oxidative stress rapidly stabilizes promoter-proximal paused Pol II across the human genome.Nucleic acids research · 2017Article
- New Quantitative Mass Spectrometry Approaches Reveal Different ADP-ribosylation Phases Dependent On the Levels of Oxidative Stress.Molecular & cellular proteomics : MCP · 2017Article
- Article
- Proteome-wide identification of the endogenous ADP-ribosylome of mammalian cells and tissue.Nature communications · 2016Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Harmful oxidation of proteins, lipids and nucleic acids is observed when reactive oxygen species (ROS) are produced excessively and/or the antioxidant capacity is reduced, causing 'oxidative stress'. Nuclear poly-ADP-ribose (PAR) formation is thought to be induced in response to oxidative DNA damage and to promote cell death under sustained oxidative stress conditions. However, what exactly triggers PAR induction in response to oxidative stress is incompletely understood. Using reverse phase protein array (RPPA) and in-depth analysis of key stress signaling components, we observed that PAR formation induced by H2O2 was mediated by the PLC/IP3R/Ca(2+)/PKCα signaling axis. Mechanistically, H2O2-induced PAR formation correlated with Ca(2+)-dependent DNA damage, which, however, was PKCα-independent. In contrast, PAR formation was completely lost upon knockdown of PKCα, suggesting that DNA damage alone was not sufficient for inducing PAR formation, but required a PKCα-dependent process. Intriguingly, the loss of PAR formation observed upon PKCα depletion was overcome when the chromatin structure-modifying protein HMGB1 was co-depleted with PKCα, suggesting that activation and nuclear translocation of PKCα releases the inhibitory effect of HMGB1 on PAR formation. Together, these results identify PKCα and HMGB1 as important co-regulators involved in H2O2-induced PAR formation, a finding that may have important relevance for oxidative stress-associated pathophysiological conditions.
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