Top

Research Article

Split Viewer

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
Aug 31, 2022 Vol.45 No.8, pp. 513~602
COVER PICTURE
Cryo-EM structure of human porphyrin transporter ABCB6 (main figure) shows that binding of hemin (inset, magenta) in concert with two glutathione molecules (cyan) primes ABCB6 for high ATP turnover (Kim et al., pp. 575-587).

Share this article on

  • line
  • mail

Molecules and Cells

eISSN 0219-1032
qr-code Download