ArticleThe Biochemical journal2002
UVB-mediated activation of p38 mitogen-activated protein kinase enhances resistance of normal human keratinocytes to apoptosis by stabilizing cytoplasmic p53.
Article in The Biochemical journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 126 citations in OpenAlex.
- In vivo identification of solar radiation-responsive gene network: role of the p38 stress-dependent kinase.PloS one · 2010Trial
- Differential Effects of Biomimetic Thymine Dimers and Corresponding Photo-Adducts in Primary Human Keratinocytes and Fibroblasts.Biomolecules · 2024Article
- Emerging role and therapeutic implications of p53 in intervertebral disc degeneration.Cell death discovery · 2023Review
- Plant Extracts as Skin Care and Therapeutic Agents.International journal of molecular sciences · 2023Review
- Photoprotective Effects ofInternational journal of molecular sciences · 2023Article
- Amentoflavone-EnrichedLife (Basel, Switzerland) · 2022Article
- Photo-Protective and Anti-Inflammatory Effects ofMolecules (Basel, Switzerland) · 2022Article
- UVB-mediated DNA damage induces matrix metalloproteinases to promote photoaging in an AhR- and SP1-dependent manner.JCI insight · 2022Article
- Hyperoside and Quercitrin inAntioxidants (Basel, Switzerland) · 2022Article
- A carbazole compound, 9-ethyl-9H-carbazole-3-carbaldehyde, plays an antitumor function through reactivation of the p53 pathway in human melanoma cells.Cell death & disease · 2021Article
- In Vitro Antitumor Potential of Sulfated Polysaccharides from Seaweed Caulerpa cupressoides var. flabellata.Marine biotechnology (New York, N.Y.) · 2021Article
- Nonylphenol Induces Apoptosis through ROS/JNK Signaling in a Spermatogonia Cell Line.International journal of molecular sciences · 2020Article
- Review
- Voriconazole enhances UV-induced DNA damage by inhibiting catalase and promoting oxidative stress.Experimental dermatology · 2020Article
- Article
- BMAL1 and CLOCK proteins in regulating UVB-induced apoptosis and DNA damage responses in human keratinocytes.Journal of cellular physiology · 2018Article
- Involvement of NADPH oxidase 1 in UVB-induced cell signaling and cytotoxicity in human keratinocytes.Biochemistry and biophysics reports · 2018Article
- ADA-07 Suppresses Solar Ultraviolet-Induced Skin Carcinogenesis by Directly Inhibiting TOPK.Molecular cancer therapeutics · 2017Article
- Up-regulation of Siah1 by ethanol triggers apoptosis in neural crest cells through p38 MAPK-mediated activation of p53 signaling pathway.Archives of toxicology · 2017Article
- ROCK inhibitor reduces Myc-induced apoptosis and mediates immortalization of human keratinocytes.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human keratinocytes respond to UV rays by developing a fast adaptive response that contributes to maintaining their functions and survival. We investigated the role of the mitogen-activated protein kinase pathways in transducing the UV signals in normal human keratinocytes. We found that UVA, UVB or UVC induced a marked and persistent activation of p38, whereas c-Jun N-terminal kinase or extracellular signal-regulated kinase were less or not activated respectively. Inhibition of p38 activity by expression of a dominant-negative mutant of p38 or with SB203580 impaired cell viability and led to an increase in UVB-induced apoptosis. This sensitization to apoptosis was independent of caspase activities. Inhibition of p38 did not sensitize transformed HaCaT keratinocytes to UVB-induced apoptosis. In normal keratinocytes, expression of a dominant-negative mutant of p53 increased UVB-induced cell death, pointing to a role for p53. In these cells, UVB triggered a p38-dependent phosphorylation of p53 on Ser-15. This phosphorylation was associated with an SB203580-sensitive accumulation of p53, even in the presence of a serine phosphatase inhibitor. Accumulated p53 was localized mainly in the cytoplasm, independently of CRM1 nuclear export. In HaCaT cells, p53 was localized exclusively in the nucleus and its distribution and level were not affected by UVB or p38 inhibition. However, UVB induced an SB203580-insensitive phosphorylation on Ser-15 of mutated p53. Overall, our results suggest that, in normal human keratinocytes, protection against UVB depends on p38-mediated phosphorylation and stabilization of p53 and is tightly associated with the cytoplasmic sequestration of wild-type p53. We conclude that the p38/p53 pathway plays a key role in the adaptive response of normal human keratinocytes against UV stress.
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