ArticleMolecular cell2024
The ribotoxic stress response drives acute inflammation, cell death, and epidermal thickening in UV-irradiated skin in vivo.
Article in Molecular cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer.Molecular oncology · 2026Review
- The integrated stress response kinase GCN2 prevents ZAKα-Dependent inflammatory hyperactivation in macrophages.The Journal of biological chemistry · 2026Article
- Article
- From crown to cosmetics: Exploring the efficacy of an upcycled pineapple biopolymer in sustainable skincare, suncare and hair care applications.International journal of cosmetic science · 2026Article
- Effect of organic collagen peptide-chelated zinc on skin quality of meat ducks during 22∼42 days of old.Poultry science · 2026Article
- Mechanism of RACK1-dependent ZAKα activation at stalled and collided ribosomes.Molecular cell · 2026Article
- An inhibitor of GCN2 and the integrated stress response directly targets ZAK protein kinase to limit cytotoxicity.The Journal of biological chemistry · 2026Article
- Kaempferol-modified mesenchymal stem cell extracellular vesicle-mimetics promote photoaging repair by suppressing ADAM10.Cell communication and signaling : CCS · 2026Article
- Article
- Hesperidin from Chenpi Ameliorates Skin Photoaging by Targeting HSPA1L to Stabilize GPX4 and Suppress Ferroptosis.Antioxidants (Basel, Switzerland) · 2026Article
- Rapid photo-crosslinking in living cells reveals protein-nucleic acid dynamics on a timescale of minutes.Nucleic acids research · 2026Article
- NDRG2 deficiency exacerbates UVB-induced photodamage in human keratinocytes via impaired Nrf2-mediated antioxidant defense.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026Article
- tRNA synthetase activity is required for stress granule and P-body assembly.Genes & development · 2026Article
- 5-Azacytidine incorporation into mRNAs disrupts translation and induces ribosome collisions.bioRxiv : the preprint server for biology · 2026Article
- Multimodality Molecular Profiling Nominates Targetable Mechanisms in Progressive RV Dysfunction.bioRxiv : the preprint server for biology · 2026Article
- M2 Macrophage-Derived Exosomes Ameliorate BPD by Inhibiting Ferroptosis via Suppression of the ZAKα-p38 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2026Article
- A MIF-p38-GSDMD inflammatory loop in keratinocytes underlies UVB-induced cutaneous lupus.Cell death & disease · 2026Article
- TKI-mediated inhibition of NLRP1 inflammasome restores erythropoiesis in DBA syndrome.EMBO molecular medicine · 2026Article
- ZAK activation at the collided ribosome.Nature · 2026Article
- ZAK kinase at the crossroads of cellular stress: functional plasticity, human pathobiology, and precision therapeutics.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Solar UVB light causes damage to the outermost layer of skin. This insult induces rapid local responses, such as dermal inflammation, keratinocyte cell death, and epidermal thickening, all of which have traditionally been associated with DNA damage response signaling. Another stress response that is activated by UVB light is the ribotoxic stress response (RSR), which depends on the ribosome-associated mitogen-activated protein 3 kinases (MAP3K) ZAKα and culminates in p38 and JNK activation. Using ZAK knockout mice, we here show that it is the RSR that is responsible for the early manifestation of UVB-induced skin inflammation and keratinocyte death and subsequent proliferation in vivo. We also show that the RSR controls both p38-mediated pyroptotic and JNK-mediated apoptotic programmed cell death of human keratinocytes in vitro. In sum, our work highlights that skin cells rely on a cytoplasmic and ribosomal stress signal rather than a nuclear and DNA-templated signal for rapid inflammatory responses to UV exposure.
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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.