The kinase defective EPHB6 receptor tyrosine kinase activates MAP kinase signaling in lung adenocarcinoma.
Yu J, Bulk E, Ji P, Hascher A, Koschmieder S, Berdel WE, Müller-Tidow C
Forschungsartikel (Zeitschrift)Zusammenfassung
Decreased expression levels of EPHB6, a member of the receptor tyrosine kinases (RTKs), are associated with an increased risk of metastasis development in early stage non-small cell lung cancer (NSCLC). However, the signaling properties of the kinase-defective EPHB6 receptor are not well-understood. Here, we show that expression of EPHB6 in A549 lung adenocarcinoma cells led to phosphorylation of the MAP kinase ERK. Conversely, siRNA based knockdown of EPHB6 reversed ERK phosphorylation. Intriguingly, EPHB6-induced phosphorylation of ERK was uncoupled by activation of the Elk-1 transcriptional factor. These analyses suggest that kinase defective EPHB6 can lead to MAPK activation.
Details zur Publikation
Autor*innen der Universität Münster
| Berdel, Wolfgang Eduard | Medizinische Klinik A (Med A) |
| Bulk, Emma Etmar | Medizinische Klinik A (Med A) |
| Hascher, Antje | Medizinische Klinik A (Med A) |
| Koschmieder, Steffen | Medizinische Klinik A (Med A) |
| Müller-Tidow, Carsten | Medizinische Klinik A (Med A) |