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Papers In Press, published online ahead of print January 10, 2005
Division of Molecular Radiobiology, School of Health Sciences, Purdue University, West Lafayette, Indiana 47907
Corresponding Author: jjli{at}purdue.edu
NF-
J. Biol. Chem, 10.1074/jbc.M410982200
Submitted on September 24, 2004
Revised on January 10, 2005
Accepted on January 10, 2005
Co-activation of ERK, NF-
B and GADD45
in response to ionizing radiation
B has been well-documented to play a critical role in signaling cell stress reactions. The extracellular-signal regulated kinase (ERK) regulates cell proliferation and survival. GADD45
is a primary cell cycle element responsive to NF-B activation in antiapoptotic responses. The present study provides evidence demonstrating that NF-B, ERK and GADD45 are co-activated by ionizing radiation (IR) in a pattern of mutually dependence to increase cell survival. Stress conditions generated in human breast cancer MCF-7 cells by the administration of a single exposure of 5 Gy IR resulted in the activation of ERK but not p38 or JNK, along with an enhancement of the NF-B transactivation and GADD45 expression. Overexpression of dominant negative Erk (DN-Erk) or pre-exposure to ERK inhibitor PD98059 inhibited NF-B. Transfection of dominant negative mutant IB that blocks NF-B nuclear translocation, inhibited ERK activity and GADD45 expression and increased cell radiosensitivity. Interaction of p65 and ERK was visualized in living MCF-7 cells by bimolecular fluorescence complementation analysis. Antisense inhibition of GADD45 strikingly blocked IR induced NF-B and ERK but not p38 and JNK. Overall, these results demonstrate a possibility that NF-B, ERK and GADD45 are able to coordinate in a loop-like signaling network to defend cells against the cytotoxicity induced by ionizing radiation.
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