Mechanisms of Dok2 signaling during TGF beta-induced EMT

• Antragstellerin: Dr. Elena Zimina
• Fachliche Zuordnung: Dermatologie
• Förderung: Förderung von 2008 bis 2012
• Projektkennung: Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 92177455

Epithelial-mesenchymal transition (EMT) normally occurs during embryonic morphogenesis, but it is also involved in the progression of primary tumors towards metastases. EMT is a process of disaggregation of the structured epithelial units to enable cell movement and morphogenesis. EMT involves the remodeling of cell-extracellular matrix (ECM) interactions. Recent advances have provided a more detailed understanding of the molecular mechanisms governing EMT in tumor progression and have underlined the key mediating role of TGF beta (TGFβ) in this process. The laboratory of Dr. Attisano recently identified the adaptor protein Dok2, a member of Dok-protein family, to be essential for TGFβ−induced ΕΜΤ. Observations by Dr. Attisano s laboratory suggest an important role for Dok2 in the reorganization of cell- ECM interactions. The intended research aims to examine the molecular mechanisms whereby Dok2 functions in TGFβ−induced EMT. We plan to determine how Dok2 influences cell-ECM adhesion and associated signaling upon TGFβ−dependent EMT. Understanding of Dok2 function upon TGFβ− induced EMT is especially relevant for cancer cell invasion and metastasis.

• DFG-Verfahren: Forschungsstipendien
• Internationaler Bezug: Kanada
• Gastgeberinnen / Gastgeber: Professorin Dr. Liliana Attisano; Professor Boris Hinz, Ph.D.