Ubiquitin-dependent degradation of Myc is frequently perturbed in cancers by mutations in the Myc protein itself or several targeting ubiquitin ligases. How exactly different degrading ligases act in concert to regulate Myc turnover is poorly understood. It is even less clear how ubiquitin contributes to Myc-dependent tumorigenesis in a non-proteolytic manner.
Our aim is to understand how ubiquitination, via degrading and non-degrading pathways, controls the ability of Myc and related proteins to promote tumor formation, and whether selective components of these pathways can be exploited as drug targets in cancer therapy. We use biochemistry and cell biology to establish molecular regulatory mechanisms and mouse genetics to validate our findings in relevant models of human disease.
To apply, please send a statement of research interests, CV, and recommendations to nikita.popov@ biozentrum. uni-wuerzburg. de
Methoden:
Mammalian cell culture, FACS, shRNA/siRNA library screening, biochemistry, mass spectrometry, deep sequencing, mouse genetics
Anfangsdatum: 5. Februar 2010
geschtzte Dauer: 3 years
Bezahlung: TVL-E13/2
Verffentlichu ngen:
Adhikary et al, Cell 2005
Popov et al, Nat Cell Biol 2007
Otto et al, Cancer Cell 2009
Homepage: http://www.pch2.biozentrum.uni-wuerzburg.de
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