Mol. Cells 2010; 30(2): 121-125
Published online July 23, 2010
https://doi.org/10.1007/s10059-010-0096-x
© The Korean Society for Molecular and Cellular Biology
Correspondence to : *Correspondence: drkim@gsnu.ac.kr
TrkA, a receptor for nerve growth factor, plays a crucial role in neuronal cell growth and differentiation. However, overactivation of TrkA signaling leads to cell death in various cell types. TrkA-mediated cell death shows some similarities to DNA damage-induced cell death. In this study, we examined how TrkA-induced cell death is regulated upon DNA damage. Cytoplasmic expression of TrkA protein was differentially modulated during the camptothecin-induced DNA damage response in TrkA-expressing U2OS cells. TrkA-induced cell death was synergistically increased by DNA damage, but it was blocked in the presence of the JNK inhibitor SP600125. Overexpression of a 54-kDa JNK isoform (JNK1α2) aggravated TrkA-induced cell death and was associated with TrkA functional activation. These results suggest that TrkA shares a functional connection with other mediators in the DNA damage response via JNK signaling.
Keywords camptothecin, cell death, DNA damage, JNK, TrkA
Mol. Cells 2010; 30(2): 121-125
Published online August 31, 2010 https://doi.org/10.1007/s10059-010-0096-x
Copyright © The Korean Society for Molecular and Cellular Biology.
Eun Joo Jung, and Deok Ryong Kim*
Department of Biochemistry and Institute of Health Sciences, Gyeongsang National University School of Medicine, JinJu 660-751, Korea
Correspondence to:*Correspondence: drkim@gsnu.ac.kr
TrkA, a receptor for nerve growth factor, plays a crucial role in neuronal cell growth and differentiation. However, overactivation of TrkA signaling leads to cell death in various cell types. TrkA-mediated cell death shows some similarities to DNA damage-induced cell death. In this study, we examined how TrkA-induced cell death is regulated upon DNA damage. Cytoplasmic expression of TrkA protein was differentially modulated during the camptothecin-induced DNA damage response in TrkA-expressing U2OS cells. TrkA-induced cell death was synergistically increased by DNA damage, but it was blocked in the presence of the JNK inhibitor SP600125. Overexpression of a 54-kDa JNK isoform (JNK1α2) aggravated TrkA-induced cell death and was associated with TrkA functional activation. These results suggest that TrkA shares a functional connection with other mediators in the DNA damage response via JNK signaling.
Keywords: camptothecin, cell death, DNA damage, JNK, TrkA
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