Dr Andrew Brooks
Dr Andrew Brooks

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Dr Andrew Brooks' interests are in understanding the molecular nature of cell communication and transmission of signals from the outside of cells to the nucleus of cells to regulate gene expression, cell growth, and cell differentiation. Understanding these fundamental mechanisms will lead to a greater understanding of disease states and will ultimately lead to vastly improved therapeutics and outcomes for patients.

Dr Brooks utilises a large range of technologies and research collaborations. He focuses on how cytokines and hormones activate their receptors on cells to transmit their signals to the inside of cells. The cytokine receptors his research focuses on activate the JAK and SRC kinases. These kinases activate important cell signalling pathways and mechanisms, such as gene mutations, that result in these signals being left “on” and unable to be turned off are responsible for many diseases including many cancers.

Dr Andrew Brooks is the Group Leader of the Cytokine Receptor Signalling Group at the University of Queensland Diamantina Institute (Australia) partner in the Translational Research Institute.

Andrew completed his Honours research on Flaviviruses in 1996 at the Department of Microbiology and Immunology at James Cook University and then moved to the Department of Biochemistry to study Dengue Virus where he completed his PhD in 2002.

He then moved to St Jude Children’s Research Hospital in Memphis, TN, USA where he researched the role of Epstein-Barr Virus in B-cell lymphomagenesis. He then joined the research group headed by Prof Michael Waters in 2006.

Andrew’s research interests are in cytokine receptors, cell signalling, and oncogenesis. His current research focus is on the molecular mechanisms of class I cytokine receptor activation including the growth hormone receptor (GHR), erythropoietin receptor (EpoR), thrombopoietin receptor (TpoR/MPL), granulocyte-macrophage colony-stimulating factor receptor (GM-CSFR), and IL-6 receptor (IL-6R). This research has led to publications in journals including Science, Nature Cell Biology, PNAS, and Molecular Endocrinology.

He has been the recipient of over $2.4 million in research grant funding (over $900 000 as CIA) and has a number of national and international collaborations.

Andrew is an Editorial Board member for the Journal JAK-STAT and has been a committee member of Australian Early-Mid Career Researchers Forum (AEMCRF) launched by the Australian Academy of Science. 

Email: a.brooks@uq.edu.au

Telephone: +61 7 3443 7071


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Selected Publications

Brooks, A. J., Dai, W., O'Mara, M. L., Abankwa, D., Chhabra, Y., Pelekanos, R. A., Gardon, O., Tunny, K. A., Blucher, K. M., Morton, C. J., Parker, M. W., Sierecki, E., Gambin, Y., Gomez, G. A., Alexandrov, K., Wilson, I. A., Doxastakis, M., Mark, A. E. and Waters, M. J. (2014).Mechanism of Activation of Protein Kinase JAK2 by the Growth Hormone Receptor. Science. 334. 124978-1-12.

Waters, M. J., Brooks A. J., & Chhabra, Y. (2014). A new mechanism for GH receptor activation of JAK2, and implications for related cytokine receptors. JAK-STAT 3 (1), e29569. 

Fernández-Rojo, M. A., Gongora, M., Fitzsimmons, R., Pearen, M., Martel, N., Martin, S. D., Nixon, S. J., Brooks, A. J., Ikonomopoulou, M., Martin, S., Lo H., Myers, S., Restall, C., Ferguson, C., Pilch, P., McGee, S., Anderson, R. L., Waters, M. J., Hancock, J. F., Grimmond, S. M., Muscat, G. E. O., & Parton, R. G. (2013) Caveolin-1 maintains hepatocyte oxidative lipid metabolism, ketogenesis and liver mitochondrial biogenesis. Cell Reports 4, 1-10.

Waters, M. J. & Brooks A. J. (2012) Growth Hormone and Cell Growth. Endocr Dev 23, 86-95.

Duell B. L., Carey A. J., Tan C. K., Cui X., Webb R. I., Totsika M., Schembri M. A., Derrington P., Irving-Rodgers H., Brooks A. J., Cripps A. W., Crowley M. & Ulett G. C. (2012). Innate transcriptional networks activated in bladder in response to uropathogenic Escherichia coli drive diverse biological pathways and rapid synthesis of IL-10 for defense against bacterial urinary tract infection. J Immunol 188, 781-792.

Chhabra Y., Waters M. J. & Brooks A. J. (2011). Role of the growth hormone–IGF-1 axis in cancer. Expert Review of Endocrinology & Metabolism 6, 71-84.

Waters M.J. & Brooks A. J. (2011) Growth Hormone Receptor: structure function relationships. Horm Res Paediatr 76 Suppl 1, 12-16.

Brooks A. J. and Waters M. J. (2010) The Growth Hormone Receptor: Mechanism of Activation and Clinical Implications. Nature Reviews Endocrinology 6, 515-525.

Conway-Campbell B. L. Brooks A. J., Robinson P. J., Perani M. & Waters M. J. (2008). The extracellular domain of the growth hormone receptor interacts with coactivator activator to promote cell proliferation. Mol Endocrinol 22, 2190-2202.

Rowlinson S. W., Yoshizato H., Barclay J. L., Brooks A. J., Behncken S. N., Kerr L. M., Millard K., Palethorpe K., Nielsen K., Clyde-Smith J., Hancock J. F., Waters M. J. (2008) An agonist-induced conformational change in the Growth Hormone Receptor determines choice of signalling pathway. Nature Cell Biology 10 (6), 740-747.

Brooks, A. J., Wooh, J. W., Tunny, K. A. & Waters, M. J. (2008). Growth hormone receptor; mechanism of action. Int J Biochem Cell Biol 40 (10), 1984-1989.

Conway-Campbell, B. L., Wooh, J. W., Brooks, A. J., Gordon, D., Brown, R. J., Lichanska, A. M., Chin, H. S., Barton, C. L., Boyle, G. M., Parsons, P. G., Jans, D. A. & Waters, M. J. (2007). Nuclear targeting of the growth hormone receptor results in dysregulation of cell proliferation and tumorigenesis. Proc Natl Acad Sci U S A 104, 13331-13336.

Jimenez-Ramirez, C., Brooks, A. J., Plym Forshell, L., Yakimchuk, K., Zhao, Fulgham, T., Sample, C. E. (2006).Epstein-Barr virus EBNA-3C is targeted to and regulates expression from the bidirectional LMP-1/2B promoter. Journal of Virology 80, 11200-11208.

Brooks, A. J., Johansson, M., John, A. V., Xu, Y., Jans, D. A., & Vasudevan, S. G. (2002). The interdomain region of dengue NS5 protein that binds to the viral helicase NS3 contains independently functional importin beta 1 and importin alpha/beta-recognized nuclear localization signals. Journal of Biological Chemistry

Johansson, M., Brooks, A. J, Jans, D. J., & Vasudevan, S. G. (2001). A small region of the dengue virus-encoded RNA-dependent RNA polymerase, NS5, confers interaction with both the nuclear transport receptor importin-beta and the viral helicase, NS3. Journal of General Virology 82, 735-45.

Class I cytokine receptors.  

Members of the class 1 cytokine receptor family are important therapeutic targets in cancers, inflammatory bowel disease, osteoporosis, multiple sclerosis, and disorders related to blood cell formation, postnatal growth, obesity, lactation, and neural function. Loss or gain of function mutations in these receptors are known to lead to a wide variety of clinically important disorders. Class I cytokine receptors regulate a wide range of clinically relevant and cellular processes. This family contains around 30 members including receptors for erythropoietin (EPO), prolactin (PRL), growth hormone (GH), thrombopoietin (TPO), granulocyte-macrophage colony-stimulating factor (GM-CSF), leukaemia inhibitory factor (LIF), interleukin-3 (IL-3), IL-5, and IL-6. Despite great progress in elucidating the structural details of ligand binding to the extracellular domain of receptors for several members of this family, the means by which these receptors activate their associated JAK kinases to initiate signalling has remained elusive. Recently we elucidated the mechanism of action of the archetypal class I cytokine receptor, the GH receptor (GHR), in unprecedented detail (published in Science 2014). Next we plan to determine if the same or similar mechanism exist for the related homodimeric and heterodimeric cytokine receptors. By utilising this new molecular understanding we will develop potential therapeutic molecules by targeting a novel region of these cytokine receptors. 

  • Understanding the mechanism of cytokine receptor activation
  • Understanding the mechanism of the JAK2 kinase activation
  • How mutations in cytokine receptor signalling pathways contribute to cancer
  • Defining the molecular mechanism of JAK2 activation by the EPO receptor
  • Molecular mechanism for activation of Src by the Growth Hormone receptor.
  • Defining the molecular mechanism of JAK2 activation by the Prolactin receptor
  • Defining the molecular mechanism of JAK2 activation by the GM-CSF receptor
  • Defining the molecular mechanism of JAK2 activation by the IL-6 receptor