Journal
MOLECULES AND CELLS
Volume 30, Issue 2, Pages 121-125Publisher
KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
DOI: 10.1007/s10059-010-0096-x
Keywords
camptothecin; cell death; DNA damage; JNK; TrkA
Categories
Funding
- MRC program [R13-2005-012-02002-0]
- National Research Foundation of Korea [2009-0071600, 2009-0072696]
- Ministry of Health and Welfare [A080403]
- National Research Foundation of Korea [2009-0072696, 2009-0071600] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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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 (JNK1 alpha 2) 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.
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