ERK mediates anti-apoptotic effect through phosphorylation and cytoplasmic localization of p21Waf1/Cip1/Sdi in response to DNA damage in normal human embryonic fibroblast (HEF) cells

Jee In Heo; Soo Jin Oh; Yoon Jung Kho; Jeong Hyeon Kim; Hong Joon Kang; Seong Hoon Park; Hyun Seok Kim; Jong Yeon Shin; Min Ju Kim; Sung Chan Kim; Jae Bong Park; Jaebong Kim; Jae Yong Lee

doi:10.1007/s11033-010-0423-5

ERK mediates anti-apoptotic effect through phosphorylation and cytoplasmic localization of p21^{Waf1/Cip1/Sdi} in response to DNA damage in normal human embryonic fibroblast (HEF) cells

Jee In Heo, Soo Jin Oh, Yoon Jung Kho, Jeong Hyeon Kim, Hong Joon Kang, Seong Hoon Park, Hyun Seok Kim, Jong Yeon Shin, Min Ju Kim, Sung Chan Kim, Jae Bong Park, Jaebong Kim, Jae Yong Lee

Department of Life Science

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

15 Scopus citations

Abstract

Since anti-apoptotic effect of ERK has not been elucidated clearly in DNA-damage-induced cell death, the role of ERK was examined in normal HEF cells treated with mild DNA damage using etoposide or camptothecin. ERK was activated by DNA damage in HEF cells. PD98059 increased apoptosis and reduced DNA-damageinduced p21^{Waf1/Cip1/Sdi} level. Depletion of p21 ^{Waf1/Cip1/Sdi} induced cell death and PD98059 induced additional cell death. DNA-damage-induced increase in cytoplasmic localization and phosphorylation of threonine residues of p21^{Waf1/Cip1/Sdi} was reversed by PD98059. Thus, the results suggest that ERK pathway mediates anti-apoptotic effects through phosphorylation and cytoplasmic localization of p21^{Waf1/Cip1/Sdi} in response to mild DNA damage.

Original language	English
Pages (from-to)	2785-2791
Number of pages	7
Journal	Molecular Biology Reports
Volume	38
Issue number	4
DOIs	https://doi.org/10.1007/s11033-010-0423-5
State	Published - Apr 2011

Bibliographical note

Funding Information:
Acknowledgment This work was supported by Priority Research Centers Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2009-0094074).

Keywords

Apoptosis
Camptothecin
ERK
Etoposide
HEF
P21

Access to Document

10.1007/s11033-010-0423-5

Cite this

Heo, J. I., Oh, S. J., Kho, Y. J., Kim, J. H., Kang, H. J., Park, S. H., Kim, H. S., Shin, J. Y., Kim, M. J., Kim, S. C., Park, J. B., Kim, J., & Lee, J. Y. (2011). ERK mediates anti-apoptotic effect through phosphorylation and cytoplasmic localization of p21^{Waf1/Cip1/Sdi} in response to DNA damage in normal human embryonic fibroblast (HEF) cells. Molecular Biology Reports, 38(4), 2785-2791. https://doi.org/10.1007/s11033-010-0423-5

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title = "ERK mediates anti-apoptotic effect through phosphorylation and cytoplasmic localization of p21Waf1/Cip1/Sdi in response to DNA damage in normal human embryonic fibroblast (HEF) cells",

abstract = "Since anti-apoptotic effect of ERK has not been elucidated clearly in DNA-damage-induced cell death, the role of ERK was examined in normal HEF cells treated with mild DNA damage using etoposide or camptothecin. ERK was activated by DNA damage in HEF cells. PD98059 increased apoptosis and reduced DNA-damageinduced p21Waf1/Cip1/Sdi level. Depletion of p21 Waf1/Cip1/Sdi induced cell death and PD98059 induced additional cell death. DNA-damage-induced increase in cytoplasmic localization and phosphorylation of threonine residues of p21Waf1/Cip1/Sdi was reversed by PD98059. Thus, the results suggest that ERK pathway mediates anti-apoptotic effects through phosphorylation and cytoplasmic localization of p21Waf1/Cip1/Sdi in response to mild DNA damage.",

keywords = "Apoptosis, Camptothecin, ERK, Etoposide, HEF, P21",

author = "Heo, {Jee In} and Oh, {Soo Jin} and Kho, {Yoon Jung} and Kim, {Jeong Hyeon} and Kang, {Hong Joon} and Park, {Seong Hoon} and Kim, {Hyun Seok} and Shin, {Jong Yeon} and Kim, {Min Ju} and Kim, {Sung Chan} and Park, {Jae Bong} and Jaebong Kim and Lee, {Jae Yong}",

note = "Funding Information: Acknowledgment This work was supported by Priority Research Centers Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2009-0094074).",

year = "2011",

month = apr,

doi = "10.1007/s11033-010-0423-5",

language = "English",

volume = "38",

pages = "2785--2791",

journal = "Molecular Biology Reports",

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Heo, JI, Oh, SJ, Kho, YJ, Kim, JH, Kang, HJ, Park, SH, Kim, HS, Shin, JY, Kim, MJ, Kim, SC, Park, JB, Kim, J & Lee, JY 2011, 'ERK mediates anti-apoptotic effect through phosphorylation and cytoplasmic localization of p21^{Waf1/Cip1/Sdi} in response to DNA damage in normal human embryonic fibroblast (HEF) cells', Molecular Biology Reports, vol. 38, no. 4, pp. 2785-2791. https://doi.org/10.1007/s11033-010-0423-5

ERK mediates anti-apoptotic effect through phosphorylation and cytoplasmic localization of p21^{Waf1/Cip1/Sdi} in response to DNA damage in normal human embryonic fibroblast (HEF) cells. / Heo, Jee In; Oh, Soo Jin; Kho, Yoon Jung et al.
In: Molecular Biology Reports, Vol. 38, No. 4, 04.2011, p. 2785-2791.

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

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AU - Kho, Yoon Jung

AU - Kim, Jeong Hyeon

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AU - Kim, Hyun Seok

AU - Shin, Jong Yeon

AU - Kim, Min Ju

AU - Kim, Sung Chan

AU - Park, Jae Bong

AU - Kim, Jaebong

AU - Lee, Jae Yong

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