ArticleLife science alliance2021
NF-κB inhibition in keratinocytes causes RIPK1-mediated necroptosis and skin inflammation.
Article in Life science alliance, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Epithelial-Dermal Immune Memory: TrackingInternational journal of molecular sciences · 2026Review
- RIPK1 autophosphorylation at S161 mediates cell death and inflammation.The Journal of experimental medicine · 2025Article
- PIEZO1 promotes psoriasis-like skin inflammation in mice via NF-κB/IL-17 signaling pathway activation.Molecular medicine (Cambridge, Mass.) · 2025Article
- The role of hydrogen sulfide in the regulation of necroptosis across various pathological processes.Molecular and cellular biochemistry · 2025Review
- Innate Immune Sensors and Cell Death-Frontiers Coordinating Homeostasis, Immunity, and Inflammation in Skin.Viruses · 2025Review
- CARD14 signalosome formation is associated with its endosomal relocation and mTORC1-induced keratinocyte proliferation.The Biochemical journal · 2024Article
- Functions of the RIP kinase family members in the skin.Cellular and molecular life sciences : CMLS · 2023Review
- The therapeutic potential of targeting regulated non-apoptotic cell death.Nature reviews. Drug discovery · 2023Review
- Repressive Control of Keratinocyte Cytoplasmic Inflammatory Signaling.International journal of molecular sciences · 2023Review
- SHARPIN Enhances Ferroptosis in Synovial Sarcoma Cells via NF-κB- and PRMT5-Mediated PGC1α Reduction.Cancers · 2023Article
- IKK-mediated TRAF6 and RIPK1 interaction stifles cell death complex assembly leading to the suppression of TNF-α-induced cell death.Cell death and differentiation · 2023Article
- Death by TNF: a road to inflammation.Nature reviews. Immunology · 2023Review
- Unfolded protein response inhibits KAT2B/MLKL-mediated necroptosis of hepatocytes by promoting BMI1 level to ubiquitinate KAT2B.Open medicine (Warsaw, Poland) · 2023Article
- Primary cilia suppress Ripk3-mediated necroptosis.Cell death discovery · 2022Article
- Macrophages in Skin Wounds: Functions and Therapeutic Potential.Biomolecules · 2022Review
- Cell death in skin function, inflammation, and disease.The Biochemical journal · 2022Review
- Antidepressant Mechanism of Traditional Chinese Medicine Formula Xiaoyaosan in CUMS-Induced Depressed Mouse Model via RIPK1-RIPK3-MLKL Mediated Necroptosis Based on Network Pharmacology Analysis.Frontiers in pharmacology · 2021Article
- Pharmacological SIRT2 Inhibition by AGK2 Attenuates Hapten-Induced Keratinocyte Inflammation via NF-κB/NLRP3 Suppression and Nrf2 Reactivation.Iranian journal of pharmaceutical research : IJPRArticle
Corrections and comments
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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
Tumor necrosis factor receptor 1 (TNFR1) activates NF-κB-dependent pro-inflammatory gene expression, but also induces cell death by triggering apoptosis and necroptosis. Inhibition of inhibitor of NF-κB kinase (IKK)/NF-κB signaling in keratinocytes paradoxically unleashed spontaneous TNFR1-mediated skin inflammation in mice, but the underlying mechanisms remain poorly understood. Here, we show that TNFR1 causes skin inflammation in mice with epidermis-specific knockout of IKK2 by inducing receptor interacting protein kinase 1 (RIPK1)-dependent necroptosis, and to a lesser extent also apoptosis, of keratinocytes. Combined epidermis-specific ablation of the NF-κB subunits RelA and c-Rel also caused skin inflammation by inducing TNFR1-mediated keratinocyte necroptosis. Contrary to the currently established model that inhibition of NF-κB-dependent gene transcription causes RIPK1-independent cell death, keratinocyte necroptosis, and skin inflammation in mice with epidermis-specific RelA and c-Rel deficiency also depended on RIPK1 kinase activity. These results advance our understanding of the mechanisms regulating TNFR1-induced cell death and identify RIPK1-mediated necroptosis as a potent driver of skin inflammation.
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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.