Alex Bullock trained at the University of Cambridge in biochemistry. His PhD research under the mentorship of Sir Alan Fersht characterised the folding and stability of mutant p53 and stimulated efforts to identify chemical chaperones that rescued mutant p53 activity in cancer cells. He was subsequently awarded a Wellcome Trust International Prize Travelling Research Fellowship, which he began in the group of David Baker at the University of Washington, Seattle. There he established methods to redesign protein-protein interaction specificity using the computer algorithm Rosetta. Alex concluded his fellowship with Sir Peter Ratcliffe at the University of Oxford. He demonstrated the oxygen dependence of the HIF-asparagine hydroxylase that regulates HIF-p300 interaction and performed proteomic studies with the VHL ubiquitin ligase. Alex helped to launch the SGC in 2004 working initially as a team leader on protein kinases with Stefan Knapp. He established the Growth Factor Signalling group in 2008.
The Growth Factor Signalling group is interested in the signalling pathways that control cell growth and differentiation and how these might be targeted by small molecule inhibitors to address devastating diseases such as cancer and inflammation. Our work is particularly focussed on the cross talk that regulates protein phosphorylation and ubiquitylation. We aim to understand the molecular structure and function of protein kinases and E3 ubiquitin ligases and to characterize their binding to substrates, regulatory partners and chemical inhibitors. This work involves a multidisciplinary approach using structural, chemical and cell biology as well as many collaborative studies with colleagues across industry and academia. Recent interests include the BMP/TGFβ receptor kinases which control the differentiation of stem cells and tissue morphogenesis. Dysregulation of these pathways is a common event in cancer as well as in many rare developmental disorders. In particular, we are working with FOP Action UK to develop BMP inhibitors for the treatment of fibrodysplasia ossificans progressiva (FOP). We are also interested in Cullin-RING E3 ligases such as KEAP1, which is a potential drug target in neurodegenerative conditions including Huntington’s disease.