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KMID : 0578320100300020121
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Molecules and Cells
2010 Volume.30 No. 2 p.121 ~ p.125
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Control of TrkA-Induced Cell Death by JNK Activation and Differential Expression of TrkA upon DNA Damage
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Jung Eun-Joo
Kim Deok-Ryong
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Abstract
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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 (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.
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KEYWORD
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camptothecin, cell death, DNA damage, JNK, TrkA
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