Molecules and Cells

, Volume 30, Issue 2, pp 121–125

Control of TrkA-induced cell death by JNK activation and differential expression of TrkA upon DNA damage

Article

DOI: 10.1007/s10059-010-0096-x

Cite this article as:
Jung, E.J. & Kim, D.R. Mol Cells (2010) 30: 121. doi:10.1007/s10059-010-0096-x

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

camptothecincell deathDNA damageJNKTrkA

Copyright information

© The Korean Society for Molecular and Cellular Biology and Springer Netherlands 2010

Authors and Affiliations

  1. 1.Department of Biochemistry and Institute of Health SciencesGyeongsang National University School of MedicineJinJuKorea