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Mol. Cells 2010; 30(2): 121-125

Published online August 31, 2010

https://doi.org/10.1007/s10059-010-0096-x

© The Korean Society for Molecular and Cellular Biology

Control of TrkA-Induced Cell Death by JNK Activation and Differential Expression of TrkA upon DNA Damage

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

Received: February 5, 2010; Revised: April 20, 2010; Accepted: May 10, 2010

Abstract

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

Article

Research Article

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.

Control of TrkA-Induced Cell Death by JNK Activation and Differential Expression of TrkA upon DNA Damage

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

Received: February 5, 2010; Revised: April 20, 2010; Accepted: May 10, 2010

Abstract

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
Jun 30, 2022 Vol.45 No.6, pp. 353~434
COVER PICTURE
ERα is modified by UFM1 and this modification (ufmylation) plays a crucial role in promoting the stability of ERα and breast cancer development. However, when ERα is deufmylated and then ubiquitinated, it disappears by proteasome-mediated degradation (Yoo et al., pp. 425-434).

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