AMPK is a serine/threonine protein kinase with central roles in cellular metabolism. AMPK becomes hyperactive in a wide range of prevalent human diseases and conditions including ischemic stroke, neurodegeneration, cancer and viral infection.  

In ischemic stroke, a life-threatening or debilitating event for many millions worldwide with no immediate therapeutic options, AMPK activation has been linked to excitotoxic shock that damages neurones surrounding the initial ischemic core. We are in a unique position to explore pharmacological AMPK inhibition as a strategy to reduce neuronal damage associated with ischemic stroke. Using cutting-edge phosphoproteomics and inducible mouse models of stroke, this project will assist in providing proof-of-concept on inhibiting AMPK in the brain to improve patient outcomes and rehabilitation, ultimately leading to a reduction in disease burden for stroke patients and their carers. See Dite et al, Journal of Biological Chemistry 293(23):8874–8885 (2018); Hoque et al, Cell Death and Disease 10(3):213 (2019). 

You will receive applicable training from experts in biochemistry, cell biology, mass spectrometry and animal models. The team strives to maintain a highly supportive and inclusive research environment and adopts a collaborative approach. Our studies are regularly published in high impact journals. 

 

Supervised by

Jon Oakhill
Jon Oakhill

Head, Metabolic Signalling

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[email protected]

+ 61 3 9231 2480

Available for Student Supervision

Ash Hoque
Ashfaqul Hoque

Postdoctoral Senior Research Officer, Metabolic signalling

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[email protected]

Available for Student Supervision