Project 2

Huntigton’s disease (HD) is one of the major neurodegenerative disorders caused by a polyglutamine tract expansion of mutant protein huntingtin. The mutant proteins accumulate in intraneuronal aggregates and impair the cell function mainly in the brain, but also at the periphery. Factors regulating the synthesis and clearance of these aggregate-prone proteins may be potential therapeutic targets. A major clearance pathway for the removal of these intracellular mutant proteins apart from the ubiquitin-proteasome system is represented by autophagy, as was previously shown by our lab. The aim of the project is to identify 2-3 novel autophagy modifiers (genes or drugs) and to elucidate the mechanisms through those regulate this degradation process.

The laboratory techniques used for this project are: transfection with overexpression, western-blotting, immunocytochemistry, microscopy, to live cell imaging and FACS analysis.