Biography

Present Positions:
1996-present Head, Cell Signalling Unit, Children's Medical Research Institute, Sydney.
1998-2022 Senior Principal Research Fellow, Nat Health & Med Research Council (NHMRC)
1996-present Professor, Faculty of Medicine, The University of Sydney, NSW.
1996-present Conjoint Professor, Chemistry Department, University Of Newcastle.
2022-present Honorary Doctorate, The University of Southern Denmark
Qualifications:
BSc (Hons) 1980 University of Sydney, NSW Australia, Biochemistry
PhD 1984 University of Newcastle, NSW Australia , Medical Biochemistry
Previous Employment:
1984-1985 Visiting Fellow, National Institutes of Health, MD, USA.
1985-1987 Postdoctoral Fellow - University of Cincinnati, Ohio.
1988 NHMRC Australian Postdoctoral Fellow. University of Melbourne.
1989-1991 QEII Fellow, St. Vincent's Institute of Medical Research, Melbourne.
1991-1996 Principal Hospital Scientist, John Hunter Hospital, Newcastle N.S.W.
1996-2003 Clinical Senior Lecturer, Faculty of Medicine, University of Newcastle.

Prof. Robinson is a lab-based scientist and world leader in protein function, proteomics and drug discovery. His achievements focus on proteins within the both neuroscience and cancer, which are among the top drug therapy target groups worldwide. He generates seminal fundamental science contributions with strong translation and commercialization programs. Overall, he has molecularly characterised dynamin function, identified new cellular roles, and created a rationally-designed drug discovery program to modulate its activity.

He has made seminal discoveries of proteins and protein kinases that regulate endocytosis and synaptic transmission and understanding their molecular mechanisms of action in cells. He has defined the paradigm that synaptic vesicle recycling in nerve terminals is a regulated neuronal event triggered by dephosphorylation of dynamin and this controls the sustainability of synaptic transmission. He continues to uncover the molecular mechanisms and regulation of proteins and kinases in multiple modes of endocytosis: clathrin-mediated endocytosis (CME), bulk endocytosis, and other newly recognised forms. He was co-first to clone dynII and co-identified its role in actin-mediated fusion pore dynamics in exocytosis and HIV virus fusion. He found that dynamin exists in 4 splice variants, and is uncovering the different functions of each. This work has had enormous impact on the field and is foundational for the translational outcomes he is pioneering.

In collaboration with Professor Adam McCluskey, they developed the world's only comprehensive endocytosis pharmacology. They are designing and engineering targeted endocytosis modulators. They identified ~40 diverse series of inhibitors or activators of dynamin and clathrin. Regulating endocytosis has pleiotropic cellular impacts, and their teams show they modulate synaptic transmission, exocytosis, cancer cell cycle, viral infection and infectious disease. These tools are now widely used to microdissect the cellular roles of dynamin and clathrin. Compounds from different chemical classes target different sites within either dynamin or clathrin. This leads to important cell biology uses, but also improves the ability to demonstrate the cellular roles of these proteins. For example, the use of chemically distinct modulators targeting different sites on the same protein, along with their inactive analogues, provides the ability to acquire more definitive evidence of on-target drug action in cells.

Using repurposed clinically approved drugs their team obtained the first evidence for on-target endocytosis inhibition in humans and that such an approach is safe. This opens the gates to endocytosis-based human therapies as mono- or combination therapies. Working with a large group of disease model experts they showed how endocytosis inhibitors are a platform approach to: i) reduce synaptic vesicle recycling for epilepsy; ii) alter receptor signal transduction pathways for neuropathic pain and leukemia drug resistance; iii) inhibit cytokinesis for glioblastoma; iv) reduce initial entry and infection by multiple viruses. This is due to the pleiotropic cellular impacts in different tissues.

Prof. Robinson has world leadership in proteomics and phosphoproteomics. This includes building the largest cancer proteome-mapping project ever undertaken, ProCan (the ACRF Centre for the Proteome of Human Cancer). This industrial scale proteome map is beginning to allow rapid diagnosis and will ultimately provide new personalised cancer treatment options for individual patients.