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PKCε-mediated ERK1/2 activation involved in radiation-induced cell death in NIH3T3 cells

Title
PKCε-mediated ERK1/2 activation involved in radiation-induced cell death in NIH3T3 cells
Authors
Lee Y.-J.Soh J.-W.Jeoung D.-I.Cho C.-K.Jhon G.J.Lee S.-J.Lee Y.-S.
Ewha Authors
전길자
SCOPUS Author ID
전길자scopus
Issue Date
2003
Journal Title
Biochimica et Biophysica Acta - Molecular Cell Research
ISSN
0167-4889JCR Link
Citation
vol. 1593, no. 2-3, pp. 219 - 229
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Protein kinase C (PKC) isoforms play distinct roles in cellular functions. We have previously shown that ionizing radiation activates PKC isoforms (α, δ, ε, and ζ), however, isoform-specific sensitivities to radiation and its exact mechanisms in radiation mediated signal transduction are not fully understood. In this study, we showed that overexpression of PKC isoforms (α, δ, ε, and ζ) increased radiation-induced cell death in NIH3T3 cells and PKCε overexpression was predominantly responsible. In addition, PKCε overexpression increased ERK1/2 activation without altering other MAP-kinases such as p38 MAPK or JNK. Co-transfection of dominant negative PKCε (PKCε-KR) blocked both PKCε-mediated ERK1/2 activation and radiation-induced cell death, while catalytically active PKCε construction augmented these phenomena. When the PKCε overexpressed cells were pretreated with PD98059, MEK inhibitor, radiation-induced cell death was inhibited. Co-transfection of the cells with a mutant of ERK1 or -2 (ERK1-KR or ERK2-KR) also blocked these phenomena, and co-transfection with dominant negative Ras or Raf cDNA revealed that PKCε-mediated ERK1/2 activation was Ras-Raf-dependent. In conclusion, PKCε-mediated ERK1/2 activation was responsible for the radiation-induced cell death. © 2002 Elsevier Science B.V. All rights reserved.
DOI
10.1016/S0167-4889(02)00392-0
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자연과학대학 > 화학·나노과학전공 > Journal papers
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