ArticleMolecular and cellular biology2002
The UV (Ribotoxic) stress response of human keratinocytes involves the unexpected uncoupling of the Ras-extracellular signal-regulated kinase signaling cascade from the activated epidermal growth factor receptor.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 96 citations in OpenAlex.
- Protein Post-Translational Modifications in UV-Induced Skin Damage.Experimental dermatology · 2026Review
- Rhomboid protease RHBDL2 is a calcium-activated suppressor of EGFR signalling in keratinocytes.Cellular and molecular life sciences : CMLS · 2026Article
- Article
- Transcriptome-wide mapping of small ribosomal subunits elucidates scanning mechanisms of translation initiation in the mammalian brain.Communications biology · 2025Article
- Integration of RNA-seq and ATAC-seq analyzes the effect of low dose neutron-γ radiation on gene expression of lymphocytes from oilfield logging workers.Frontiers in chemistry · 2023Article
- Amentoflavone-EnrichedLife (Basel, Switzerland) · 2022Article
- Mucosal ribosomal stress-induced PRDM1 promotes chemoresistance via stemness regulation.Communications biology · 2021Article
- TRPV3 enhances skin keratinocyte proliferation through EGFR-dependent signaling pathways.Cell biology and toxicology · 2021Article
- Role of Small GTPase RhoA in DNA Damage Response.Biomolecules · 2021Review
- Frog Skin Derived Peptides With Potential Protective Effects on Ultraviolet B-Induced Cutaneous Photodamage.Frontiers in immunology · 2021Article
- Article
- Fibroblast growth factor receptor promotes progression of cutaneous squamous cell carcinoma.Molecular carcinogenesis · 2019Article
- JNK activation induced by ribotoxic stress is initiated from 80S monosomes but not polysomes.BMB reports · 2019Article
- A protective Langerhans cell-keratinocyte axis that is dysfunctional in photosensitivity.Science translational medicine · 2018Article
- BNIP3 upregulation via stimulation of ERK and JNK activity is required for the protection of keratinocytes from UVB-induced apoptosis.Cell death & disease · 2017Article
- Role of EGF receptor ligands in TCDD-induced EGFR down-regulation and cellular proliferation.Chemico-biological interactions · 2016Article
- Mechanism of Macrophage-Derived Chemokine/CCL22 Production by HaCaT Keratinocytes.Annals of dermatology · 2015Article
- Ribosomal alteration-derived signals for cytokine induction in mucosal and systemic inflammation: noncanonical pathways by ribosomal inactivation.Mediators of inflammation · 2014Review
- The role of AKT/mTOR pathway in stress response to UV-irradiation: implication in skin carcinogenesis by regulation of apoptosis, autophagy and senescence.International journal of molecular sciences · 2013Review
- Cellular functions regulated by phosphorylation of EGFR on Tyr845.International journal of molecular sciences · 2013Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
In mammals, UVB radiation is of biological relevance primarily for the cells of the epidermis. We report here the existence of a UVB response that is specific for proliferating human epidermal keratinocytes. Unlike other cell types that also display a UVB response, keratinocytes respond to UVB irradiation with a transient but potent downregulation of the Ras-extracellular signal-regulated kinase (ERK) signaling cascade. The downregulation of ERK precedes a profound decrease in the steady-state levels of cyclin D1, a mediator of the proliferative action of ERK. Keratinocytes exhibit high constitutive activity of the Ras-ERK signaling cascade even in culture medium lacking supplemental growth factors. The increased activity of Ras and phosphorylation of ERK in these cells are maintained by the autocrine production of secreted molecules that activate the epidermal growth factor receptor (EGFR). Irradiation of keratinocytes increases the phosphorylation of EGFR on tyrosine residues Y845, Y992, Y1045, Y1068, Y1086, Y1148, and Y1173 above the basal levels and leads to the increased recruitment of the adaptor proteins Grb2 and ShcA and of a p55 form of the regulatory subunit of the phosphatidylinositide 3-kinase to the UVB-activated EGFR. Paradoxically, however, UVB causes, at the same time, the inactivation of Ras and a subsequent dephosphorylation of ERK. By contrast, the signaling pathway leading from the activated EGFR to the phosphorylation of PKB/Akt1 is potentiated by UVB. The UVB response of keratinocytes appeared to be a manifestation of the more general ribotoxic stress response inasmuch as the transduction of the UVB-generated inhibitory signal to Ras and ERK required the presence of active ribosomes at the time of irradiation.
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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.