Abstract
Jun N-terminal kinase (JNK1) is a member of a family of stress-activated protein kinases which are activated by many forms of stress including UV radiation, resulting in the phosphorylation of c-Jun, ATF-2, Elk-1 and p53. As UV-B radiation is mainly responsible for ultraviolet (UV)-induced skin cancers, we chose to elucidate JNK1 activation in keratinocytes which represent a UV-relevant cell system. We have demonstrated rapid activation of JNK1 in a keratinocyte cell line, C50, in response to multiple doses of UV-B irradiation. JNK1 activation occurred within 1 min, peaked by 10 min and returned to near basal levels within 2 h following the UV-B treatments. Our data provide the first evidence to show that keratinocytes do respond to multiple doses of the physiologically relevant UV-B radiation through rapid activation of the JNK1 pathway.
This is a preview of subscription content, access via your institution
Access options
Subscribe to this journal
Receive 50 print issues and online access
$259.00 per year
only $5.18 per issue
Buy this article
- Purchase on SpringerLink
- Instant access to the full article PDF.
USD 39.95
Prices may be subject to local taxes which are calculated during checkout
Similar content being viewed by others
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Ramaswamy, N., Ronai, Z. & Pelling, J. Rapid activation of JNK1 in UV-B irradiated epidermal keratinocytes. Oncogene 16, 1501–1505 (1998). https://doi.org/10.1038/sj.onc.1201628
Received:
Revised:
Accepted:
Published:
Issue date:
DOI: https://doi.org/10.1038/sj.onc.1201628
Keywords
This article is cited by
-
Integrative transcriptomic analysis for linking acute stress responses to squamous cell carcinoma development
Scientific Reports (2020)
-
Function and regulation of AP-1 subunits in skin physiology and pathology
Oncogene (2001)
-
Inhibition of Bcl-xL expression sensitizes normal human keratinocytes and epithelial cells to apoptotic stimuli
Oncogene (1999)


