Stephen Helliwell, PhD
Chemical Biology & Therapeutics
Mitochondria are critical for life, but genetic and environmental factors cause dysfunction, leading to disease. We wish to improve mitochondrial function in cellular models of mitochondrial disorders. One pathway that we are currently studying in depth is the PINK-Parkin mitophagy pathway, the major pathway implicated in the clearance of damaged mitochondria. Using a genome-wide siRNA screen, we have isolated a large number of genes that alter Parkin recruitment to damaged mitochondria, and a major goal of our research is to elucidate the molecular role of these genes in mitophagy. In particular we would like to understand the behaviour of mitochondria in relation to the alteration of these genes in in vitro models of mitochondrial disorders.
An integrated approach for identification and target validation of antifungal compounds active against Erg11p.
Hoepfner, D., Karkare, S., Helliwell, S.B., Pfeifer, M., Trunzer, M., De Bonnechose, S., Zimmerlin, A., Tao, J., Richie, D., Hofmann, A., Reinker, S., Frederiksen, M., Movva, N.R., Porter, J., Ryder, N., and Parker, C.
Antimicrob Agents Chemother. 2012 Aug;56(8):4233-40.
Components of a ubiquitin ligase complex specify the intracellular trafficking of the general amino acid permease
Helliwell, S.B., Losko, S. and Kaiser, C.A.
J Cell Biol. 2001 May 14;153(4):649-62.
The RHO1 effector PKC1, but not BNI1, mediates signalling from TOR2 to the actin cytoskeleton
Helliwell, S.B., Schmidt, A., Ohya, Y., and Hall, M.N.
Curr Biol. 1998 Nov 5;8(22):1211-4.
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