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Dr John W Scott

Research Unit

Protein chemistry & metabolism

Information

Neurometabolism Team Leader
Email: [email protected]

Staff
Mr Luke McAloon
Mr Tiego Diniz

Professional Experience

1997     BSc (Hons) Biochemistry, University of Glasgow, UK
2002     PhD Biochemistry, University of Dundee, UK
2006     Senior Research Officer, Protein Chemistry and Metabolism Unit, SVI

Achievements

1996     Nuffield Foundation Scholarship
1997     Wellcome Trust Prize Scholarship (1997-2002)
2018     Honorary Research Fellowship, Florey Institute of Neuroscience and Mental Health
2018     Senior Research Academic, Mary MacKillop Institute of Health Research, ACU
2018     Scientific Advisory Board, Siragen Pharmaceuticals, USA

Research Interests

My team is primarily interested in understanding the molecular pathways that regulate mood and complex behaviour in response to hormones and metabolites that signal changes in energy availability. Our research is specifically focused on the control of the CaMKK2 signalling pathway, which is a major regulator of complex behaviour and whole-body energy metabolism.  CaMKK2 loss-of-function is linked with psychiatric illness in humans, especially mood disorders.  We collaborate with a range of academic and industrial partners to unleash the potential of targeting CaMKK2 with new drugs to treat mental illness.

Selected Publications

  1. Asquith CRM, Godoi PH, Couñago RM, Laitinen T, Scott JW, Langendorf CG, Oakhill JS, Drewry DH, Zuercher WJ, Koutentis PA, Willson TM and Kalogirou AS (2018). 1,2,6-Thiadiazinones as novel narrow spectrum Ca2+-calmodulin-dependent protein kinase kinase-2 (CaMKK2) inhibitors. Molecules. 23, E1221.
  2. O’Brien MT, Oakhill JS, Ling NXY, Langendorf CG, Hoque A, Dite TA, Means AR, Kemp BE, Scott JW (2017). Impact of genetic variation on human CaMKK2 regulation by Ca2+-calmodulin and multisite phosphorylation. Scientific Reports. 7, 43264.
  3. Scott JW, Park E, Rodriguiz RM, Oakhill JS, Issa SMA, O’Brien MT, Dite TA, Langendorf CG, Wetsel WC, Means AR, Kemp BE (2015). Autophosphorylation of CaMKK2 generates autonomous activity that is disrupted by a T85S mutation linked to anxiety and bipolar disorder. Scientific Reports. 5, 14436.
  4. Scott JW, Galic S, Graham KL, Foitzik R, Ling NXY, Dite TA, Issa SMA, Langendorf CG, Weng QP, Thomas HE, Kay TW, Birnberg NC, Steinberg GR, Kemp BE, Oakhill JS (2015). Inhibition of AMP-activated protein kinase at the allosteric drug-binding site promotes islet insulin resistance. Chemistry and Biology. 22, 705-711.
  5. Scott JW, Ling NXY, Issa SMA, Dite TA, O’Brien MT, Chen ZP, Galic S, Langendorf CG, Steinberg GR, Kemp BE, Oakhill JS (2014). Small-molecule drug A-769662 and AMP synergistically activate naïve AMPK independent of upstream kinase signaling. Chemistry and Biology. 21, 619-27.
  6. Green MF, Scott JW, Steel R, Oakhill JS, Kemp BE, Means AR (2011). Ca2+/calmodulin-dependent protein kinase kinase b is regulated by multi-site phosphorylation. Journal of Biological Chemistry. 286, 28066-28079.
  7. Oakhill JS, Steel R, Chen ZP, Scott JW, Ling NXY, Tam S, Kemp BE (2011).  AMPK is a direct adenylate-charged regulated protein kinase. Science. 332, 1433-1435.
  8. Oakhill JS, Chen ZP, Scott JW, Steel R, Castelli LA, Macaulay SL, Kemp BE (2010). b-subunit myristoylation is the gatekeeper for initiating metabolic stress sensing by AMPK. Proceedings of the National Academy of Sciences. 107, 19237-19241.
  9. Scott JW, van Denderen BJW, Jorgensen SB, Honeyman J, Steinberg GR, Iseli TJ, Oakhill JS, Koay A, Gooley PR, Stapleton D, Kemp BE (2008). Thienopyridone drugs are selective activators of AMP-activated protein kinase b1-containing complexes. Chemistry and Biology. 15, 1220-1230.
  10. Scott JW, Ross FA, Liu JKD, Hardie DG (2007). Regulation of AMP-activated protein kinase by a pseudosubstrate sequence on the g subunit. EMBO Journal. 26, 806-815.
  11. Scott JW, Hawley SA, Green KA, Anis M, Stewart G, Scullion GA, Norman DG & Hardie DG (2004). CBS domains form energy-sensing modules whose binding of adenosine ligands is disrupted by disease mutations. Journal of Clinical Investigation. 113, 274-284.