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Upregulation of the Rac1/JNK signaling pathway in primary human schwannoma cells. Human Molecular Genetics (2003)
| Citations: | 6 - 0 self |
BibTeX
@MISC{Kaempchen03upregulationof,
author = {Katherine Kaempchen and Kirsten Mielke and Tamara Utermark and Sonja Langmesser and C. Oliver Hanemann},
title = {Upregulation of the Rac1/JNK signaling pathway in primary human schwannoma cells. Human Molecular Genetics},
year = {2003}
}
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Abstract
Schwann cells lacking the tumor-suppressor-protein merlin tend in man to build benign tumors (schwannoma). We observed that characteristic features of these cells which are relevant to tumorigenicity resemble those described in cells with high Rac activity. Moreover this small GTPase also phosphorylates merlin via PAK activation. We hypothesized that merlin deficiency might cause an activation of Rac and its dependent signaling pathways, in particular the pro-tumorigenic JNK pathway. We show an enhanced activation of Rac1 in primary human schwannoma cells, find both Rac and its effector PAK at the membrane where they colocalize, and describe increased levels of phosphorylated JNK in the nucleus of these cells. Further we describe regulation at post-transcriptional level with upregulated protein, but not mRNA levels for Rac1, and JNK1/2. We conclude that merlin regulates Rac activation, and suggest that this is important for human schwannoma cell dedifferentiation.
Keyphrases
primary human schwannoma cell human molecular genetics rac1 jnk dependent signaling pathway merlin deficiency post-transcriptional level pak activation pro-tumorigenic jnk pathway effector pak schwann cell high rac activity upregulated protein enhanced activation mrna level small gtpase characteristic feature benign tumor rac activation human schwannoma cell dedifferentiation tumor-suppressor-protein merlin tend
