Abstract
Exposure of mammalian cells to ultraviolet (UV) light elicits a cellular response and also lead to apoptotic cell death. However, the role of Rac, a member of Rho family GTPases, in the UV-induced apoptosis has never been examined. In UV-irradiated Rat-2 fibroblasts, nuclear fragmentation began to be observed within 2 h and the total viability of Rat-2 cells were only about 15% at 6 h following by UV irradiation, whereas the total viability in Rat2-RacN17 cells stably expressing RacN17, a dominant negative Rac1 mutant, was almost close to 67%. Pretreatment with SB203580, a specific inhibitor of p38 kinase, likewise attenuated UV-induced cell death, but PD98059, a MEK inhibitor, did not. Thus, Rac1 and p38 kinase appear to be components in the apoptotic signaling pathway induced by UV irradiation in Rat-2 fibroblasts. In addition, our results show that p38 kinase stimulation by UV is dramatically inhibited by RacN17, suggesting that p38 kinase is situated downstream of Rac1 in the UV signaling to apoptosis.
Original language | English |
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Pages (from-to) | 825-829 |
Number of pages | 5 |
Journal | Biochemical and biophysical research communications |
Volume | 285 |
Issue number | 3 |
DOIs | |
Publication status | Published - 2001 |
Externally published | Yes |
Bibliographical note
Funding Information:This work was supported by grants from the National Research Laboratory (NRL), Life Phenomena and Function Research Group Program-2000 from the Ministry of Science and Technology, and the Brain Korea 21 (BK21) program.
Keywords
- Apoptosis
- Rac
- UV
- p38 kinase
ASJC Scopus subject areas
- Biophysics
- Biochemistry
- Molecular Biology
- Cell Biology