ArticlePloS one2011
NF-κB potentiates caspase independent hydrogen peroxide induced cell death.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Decoding signaling architectures: CAR versus TCR dynamics in solid tumor immunotherapy.Acta biochimica et biophysica Sinica · 2026Review
- Changes Within H3K4me3-Marked Histone Reveal Molecular Background of Neutrophil Functional Plasticity.Frontiers in immunology · 2022Article
- Burn injury induces elevated inflammatory traffic: the role of NF-κB.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Review
- NFκB promotes oxidative stress-induced necrosis and ischemia/reperfusion injury by inhibiting Nrf2-ARE pathway.Free radical biology & medicine · 2020Article
- Article
- Signaling via the NFκB system.Wiley interdisciplinary reviews. Systems biology and medicine · 2016Review
- IKK-β mediates hydrogen peroxide induced cell death through p85 S6K1.Cell death and differentiation · 2013Article
- Effect of silencing PARG in human colon carcinoma LoVo cells on the ability of HUVEC migration and proliferation.Cancer gene therapy · 2012Article
- The diverse and complex roles of NF-κB subunits in cancer.Nature reviews. Cancer · 2012Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe pro-survival activity of NF-κB in response to a variety of stimuli has been extensively characterized. Although there have been a few reports addressing the pro-cell death role of NF-κB, the precise mechanism of NF-κB's pro-cell death function still remains elusive. METHODOLOGY/PRINCIPAL
findingsIn the present study, we investigated the role of NF-κB in cell death induced by chronic insult with hydrogen peroxide (H(2)O(2)). Here, we show that NF-κB promotes H(2)O(2) induced caspase independent but PARP dependent fibroblast cell death. The pro-death activity of NF-κB is due to the DNA binding activity of RelA, which is induced through IKK- mediated IκBα degradation. NF-κB dependent pro-survival genes, Bcl-2 and XIAP, were significantly repressed, while NF-κB dependent pro-death genes, TNFα and Fas Ligand, were induced in response to H(2)O(2). CONCLUSIONS/SIGNIFICANCE: We discovered an unexpected function of NF-κB, in that it potentiates chronic H(2)O(2) exposure induced cell death, and suggest that NF-κB mediates cell death through the repression of pro-survival genes and induction of pro-death genes. Since unremitting exposure of tissues to H(2)O(2) and other reactive oxygen species can lead to several degenerative disorders and diseases, our results have important implications for the use of NF-κB inhibitors in therapeutic drug design.
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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.