We are looking for a PostDoc who wants to figure out with us how human cells use a-arrestin ubiquitin ligase complexes to selectively adjust their nutrient transporter repertoire during entry and exit from quiescence. Mutations in one a-arrestin cause defects in the selective lysosomal degradation of an essential amino acid transporter, and are linked with a novel rare metabolic disease. The key questions of this research project are: (1) How do a-arrestins work together with ubiquitin ligases to selectively target nutrient transports for degradation? (2) How are a-arrestins controlled? (3) How does the a-arrestin mediated downregulation of nutrient transporters curb cell growth?
If you are interested, please send an email + CV to david.teis(at)i-med.ac.at