ArticleCell death and differentiation2013
Loss of PIDD limits NF-κB activation and cytokine production but not cell survival or transformation after DNA damage.
Article in Cell death and differentiation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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Who cites it
22 citing papers in PubMed, 26 citations in OpenAlex.
- PIDDosome deficiency impairs bone remodeling by increasing osteoclast ploidy and function.Cell death and differentiation · 2026Article
- Linking Environmental Hazards to Osteosarcoma Development: A Comprehensive Review.Cancer management and research · 2025Review
- Extra centrosomes delay DNA damage-driven tumorigenesis.Science advances · 2024Article
- A noncanonical IRAK4-IRAK1 pathway counters DNA damage-induced apoptosis independently of TLR/IL-1R signaling.Science signaling · 2023Article
- Extra centrosomes induce PIDD1-mediated inflammation and immunosurveillance.The EMBO journal · 2023Article
- When cell death goes wrong: inflammatory outcomes of failed apoptosis and mitotic cell death.Cell death and differentiation · 2023Review
- Gene expression profile associated with Asmt knockout-induced depression-like behaviors and exercise effects in mouse hypothalamus.Bioscience reports · 2022Article
- PIDD1 in cell cycle control, sterile inflammation and cell death.Biochemical Society transactions · 2022Review
- The functions of fluoxetine and identification of fluoxetine-mediated circular RNAs and messenger RNAs in cerebral ischemic stroke.Bioengineered · 2021Article
- Apoptotic stress-induced FGF signalling promotes non-cell autonomous resistance to cell death.Nature communications · 2021Article
- Phenome-wide and expression quantitative trait locus associations of coronavirus disease 2019 genetic risk loci.iScience · 2021Article
- Biallelic mutations in the death domain of PIDD1 impair caspase-2 activation and are associated with intellectual disability.Translational psychiatry · 2021Article
- The Role of Caspase-2 in Regulating Cell Fate.Cells · 2020Review
- Adverse outcome pathways for ionizing radiation and breast cancer involve direct and indirect DNA damage, oxidative stress, inflammation, genomic instability, and interaction with hormonal regulation of the breast.Archives of toxicology · 2020Review
- The Many Roles of Ubiquitin in NF-κB Signaling.Biomedicines · 2018Review
- Perturbing mitosis for anti-cancer therapy: is cell death the only answer?EMBO reports · 2018Review
- Inhibition of NF-κB by deoxycholic acid induces miR-21/PDCD4-dependent hepatocellular apoptosis.Scientific reports · 2015Article
- The p53 binding protein PDCD5 is not rate-limiting in DNA damage induced cell death.Scientific reports · 2015Article
- NF-κB signaling and vesicle transport are correlated with the reactivation of the memory trace of morphine dependence.Diagnostic pathology · 2014Article
- Death of p53-defective cells triggered by forced mitotic entry in the presence of DNA damage is not uniquely dependent on Caspase-2 or the PIDDosome.Cell death & disease · 2013Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Activation of NF-κB (nuclear factor of kappa light chain gene enhancer in B cells) in response to DNA damage is considered to contribute to repair of genetic lesions, increased cell survival and cytokine release. The molecular mechanisms orchestrating this cytoplasmic event involve core components of the nuclear DNA damage response machinery, including ATM-kinase (ataxia telangiectasia mutated kinase) and PARP-1 (poly (ADP-ribose) polymerase 1). The physiological consequences of defective NF-κB activation in this context, however, remain poorly investigated. Here we report on the role of the 'p53-induced protein with a death domain', PIDD, which appears rate limiting in this process, as is PARP-1. Despite impaired NF-κB activation, DNA damage did not increase cell death or reduce clonal survival of various cell types lacking PIDD, such as mouse embryonic fibroblasts or stem and progenitor cells of the hematopoietic system. Furthermore, lymphomagenesis induced by γ-irradiation (IR) was unaffected by deficiency for PIDD or PARP-1, indicating that loss of DNA damage-triggered NF-κB signalling does not affect IR-driven tumorigenesis. However, loss of either gene compromised cytokine release after acute IR injury. Hence, we propose that NF-κB's most notable function after DNA damage in primary cells is related to the release of cytokines, thereby contributing to sterile inflammation.
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