ArticleOncotarget2016
S-nitrosation on zinc finger motif of PARP-1 as a mechanism of DNA repair inhibition by arsenite.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- The first and second zinc finger domains from Poly-ADP-ribose polymerase 1 (PARP1) are modified by hydrogen sulfide.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2026Article
- Persulfidation of the zinc finger protein ZRANB2 modulates its RNA binding and alternative splicing function.Journal of inorganic biochemistry · 2026Article
- Liquid‒liquid phase separation and poly(ADP‒ribosyl)ation in the context of ultraviolet radiation-induced stress in mammalian cells.Biophysical reviews · 2025Review
- Mechanisms of genotoxicity and proteotoxicity induced by the metalloids arsenic and antimony.Cellular and molecular life sciences : CMLS · 2023Review
- Neuronal Zinc Transporter ZnT3 Modulates Cerebral Ischemia-Induced Blood-Brain Barrier Disruption.Aging and disease · 2023Article
- Arsenic causing gallbladder cancer disease in Bihar.Scientific reports · 2023Article
- Arsenic co-carcinogenesis: Inhibition of DNA repair and interaction with zinc finger proteins.Seminars in cancer biology · 2021Review
- Modulation of PARP activity by Monomethylarsonous (MMAToxicology and applied pharmacology · 2021Article
- Arsenic Exposure and Compromised Protein Quality Control.Chemical research in toxicology · 2020Review
- Molecular Mechanisms of Arsenic-Induced Disruption of DNA Repair.Chemical research in toxicology · 2020Review
- Zinc deficiency alters the susceptibility of pancreatic beta cells (INS-1) to arsenic exposure.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2019Article
- Peroxynitrite contributes to arsenic-induced PARP-1 inhibition through ROS/RNS generation.Toxicology and applied pharmacology · 2019Article
- The interaction of zinc and the blood-brain barrier under physiological and ischemic conditions.Toxicology and applied pharmacology · 2019Review
- Marginal Zinc Deficiency and Environmentally Relevant Concentrations of Arsenic Elicit Combined Effects on the Gut Microbiome.mSphere · 2018Article
- Differential sensitivities of cellular XPA and PARP-1 to arsenite inhibition and zinc rescue.Toxicology and applied pharmacology · 2017Article
- Pathophysiological role of zinc in ischemic brain injury.Oncotarget · 2017Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Arsenic, a widely distributed carcinogen, is known to significantly amplify the impact of other carcinogens through inhibition of DNA repair. Our recent work suggests that reactive oxygen/nitrogen species (ROS/RNS) induced by arsenite (AsIII) play an important role in the inhibition of the DNA repair protein Poly(ADP-ribose) polymerase 1 (PARP-1). AsIII-induced ROS lead to oxidation of cysteine residues within the PARP-1 zinc finger DNA binding domain. However, the mechanism underlying RNS-mediated PARP inhibition by arsenic remains unknown. In this work, we demonstrate that AsIII treatment of normal human keratinocyte (HEKn) cells induced S-nitrosation on cysteine residues of PARP-1 protein, in a similar manner to a nitric oxide donor. S-nitrosation of PARP-1 could be reduced by 1400W (inducible nitric oxide synthase inhibitor) or c-PTIO (a nitric oxide scavenger). Furthermore, AsIII treatment of HEKn cells leads to zinc loss and inhibition of PARP-1 enzymatic activity. AsIII and 1400W/c-PTIO co-treatment demonstrate that these effects occur in an iNOS- and NO-dependent manner. Importantly, we confirmed S-nitrosation on the zinc finger DNA binding domain of PARP-1 protein. Taken together, AsIII induces S-nitrosation on PARP-1 zinc finger DNA binding domain by generating NO through iNOS activation, leading to zinc loss and inhibition of PARP-1 activity, thereby increasing retention of damaged DNA. These findings identify S-nitrosation as an important component of the molecular mechanism underlying AsIII inhibition of DNA repair, which may benefit the development of preventive and intervention strategies against AsIII co-carcinogenesis.
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