Implication of the small GTPase Rac1 in the apoptosis induced by UV in Rat-2 fibroblasts

Young Woo Eom; Min Hyuk Yoo; Chang Hoon Woo; Ki Chul Hwang; Woo Keun Song; Yung Joon Yoo; Jang Soo Chun; Jae Hong Kim

doi:10.1006/bbrc.2001.5233

Implication of the small GTPase Rac1 in the apoptosis induced by UV in Rat-2 fibroblasts

Young Woo Eom
, Min Hyuk Yoo
, Chang Hoon Woo
, Ki Chul Hwang
, Woo Keun Song
, Yung Joon Yoo
, Jang Soo Chun
, Jae Hong Kim^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

26 Citations (Scopus)

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-Rac^N17 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
Pages (from-to)	825-829
Number of pages	5
Journal	Biochemical and biophysical research communications
Volume	285
Issue number	3
DOIs	https://doi.org/10.1006/bbrc.2001.5233
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

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10.1006/bbrc.2001.5233

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title = "Implication of the small GTPase Rac1 in the apoptosis induced by UV in Rat-2 fibroblasts",

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.",

keywords = "Apoptosis, Rac, UV, p38 kinase",

author = "Eom, \{Young Woo\} and Yoo, \{Min Hyuk\} and Woo, \{Chang Hoon\} and Hwang, \{Ki Chul\} and Song, \{Woo Keun\} and Yoo, \{Yung Joon\} and Chun, \{Jang Soo\} and Kim, \{Jae Hong\}",

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.",

year = "2001",

doi = "10.1006/bbrc.2001.5233",

language = "English",

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journal = "Biochemical and biophysical research communications",

issn = "0006-291X",

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T1 - Implication of the small GTPase Rac1 in the apoptosis induced by UV in Rat-2 fibroblasts

AU - Eom, Young Woo

AU - Yoo, Min Hyuk

AU - Woo, Chang Hoon

AU - Hwang, Ki Chul

AU - Song, Woo Keun

AU - Yoo, Yung Joon

AU - Chun, Jang Soo

AU - Kim, Jae Hong

N1 - 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.

PY - 2001

Y1 - 2001

N2 - 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.

AB - 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.

KW - Apoptosis

KW - Rac

KW - UV

KW - p38 kinase

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DO - 10.1006/bbrc.2001.5233

M3 - Article

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AN - SCOPUS:0034810415

SN - 0006-291X

VL - 285

SP - 825

EP - 829

JO - Biochemical and biophysical research communications

JF - Biochemical and biophysical research communications

IS - 3

ER -

Implication of the small GTPase Rac1 in the apoptosis induced by UV in Rat-2 fibroblasts

Abstract

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Keywords

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