Prof Mike Rogers
Research Level
Biography
Mike graduated from the University of Sheffield, UK, in 1989 with a first class honours in Biochemistry and in 1994 with a PhD in bone pharmacology. He remained in Sheffield as a postdoctoral fellow and moved to the University of Aberdeen, Scotland, as a Lecturer in 1997, becoming Senior Lecturer in 1999. He was promoted to Professor of Musculoskeletal Pharmacology in 2003. From 2005-2010 Mike led the multi-disciplinary Musculoskeletal Research Programme at the University of Aberdeen, recognised as a Centre of Excellence by the European League Against Rheumatism. He has strong links with the pharmaceutical industry and served on several Editorial Boards and Grant and Fellowship Committees. He was a member of the Board of Directors of the International Bone & Mineral Society and the committee of the UK Bone Research Society.
Mike relocated to the Garvan Institute in 2012 to establish a new Bone Therapeutics Group and, since 2021, co-leads the Skeletal Diseases Program. His previous, ground-breaking work elucidated the mechanisms of action and cause of adverse effects of bisphosphonates, a blockbuster class of drugs used worldwide in the treatment of bone diseases such as osteoporosis and cancer-associated bone disease. He has also made important contributions in the field of bone cell biology and human bone diseases. Mike's research is currently focused on the actions of bisphosphonate drugs on the mevalonate pathway in cells outside the skeleton, and the role of the mevalonate pathway and protein prenylation in health and disease. In particular, Mike's lab is developing new approaches for the diagnosis and treatment of the autoinflammatory disease mevalonate kinase deficiency.
Mike has published 89 peer-reviewed papers, 22 invited first/last author reviews and 11 first/last author book chapters. His publications have >24,000 citations (h index 68; Google Scholar, Aug 2020) and are cited in 278 patent applications.
Mike graduated from the University of Sheffield, UK, in 1989 with a first class honours in Biochemistry and in 1994 with a PhD in bone pharmacology. He remained in Sheffield as a postdoctoral fellow and moved to the University of Aberdeen, Scotland, as a Lecturer in 1997, becoming Senior Lecturer in 1999. He was promoted to Professor of Musculoskeletal Pharmacology in 2003. From 2005-2010 Mike led the multi-disciplinary Musculoskeletal Research Programme at the University of Aberdeen, recognised as a Centre of Excellence by the European League Against Rheumatism. He has strong links with the pharmaceutical industry and served on several Editorial Boards and Grant and Fellowship Committees. He was a member of the Board of Directors of the International Bone & Mineral Society and the committee of the UK Bone Research Society.
Mike relocated to the Garvan Institute in 2012 to establish a new Bone Therapeutics Group and, since 2021, co-leads the Skeletal Diseases Program. His previous, ground-breaking work elucidated the mechanisms of action and cause of adverse effects of bisphosphonates, a blockbuster class of drugs used worldwide in the treatment of bone diseases such as osteoporosis and cancer-associated bone disease. He has also made important contributions in the field of bone cell biology and human bone diseases. Mike's research is currently focused on the actions of bisphosphonate drugs on the mevalonate pathway in cells outside the skeleton, and the role of the mevalonate pathway and protein prenylation in health and disease. In particular, Mike's lab is developing new approaches for the diagnosis and treatment of the autoinflammatory disease mevalonate kinase deficiency.
Mike has published 89 peer-reviewed papers, 22 invited first/last author reviews and 11 first/last author book chapters. His publications have >24,000 citations (h index 68; Google Scholar, Aug 2020) and are cited in 278 patent applications.
Awards and Honours
2009 - First recipient of the Herbert A. Fleisch Award, International Bone & Mineral Society.
Education
1994 - PhD, University of Sheffield - UK
Selected Publications
Munoz, M.A., Skinner, O.P., Masle-Farquhar, E., Jurczyluk, J., Xiao, Y., Fletcher, E.K., Kristianto, E., Hodson, M.P., O’Donoghue, S.I., Kaur, S., Brink, R., Zahra, D., Deenick, E.K., Perry, K., Robertson, A.A.B., Mehr, S., Hissaria, P., Mulders-Manders, C.M., Simon, A. & Rogers, M.J. Increased core body temperature exacerbates defective protein prenylation in mouse models of mevalonate kinase deficiency. J Clin Invest 2022, 132(19):e160929. doi: 1172/JCI160929.
Munoz, M.A., Fletcher, E.K., Skinner, O.P., Jurczyluk, J., Kristianto, E., Hodson, M.P., Sun, S., Ebetino, F.H., Croucher, D.R., Hansbro, P.M., Center, J.R. & Rogers, M.J. Bisphosphonates have actions in the lung and inhibit the mevalonate pathway in alveolar macrophages. eLife 2021, 10.7554/eLife.72430.
Munoz, M.A., Jurczyluk, J., Simon, A., Hissaria, P., Arts, R.J.W., Coman, D.J., Boros, C., Mehr, S.S. & Rogers, M.J. Defective protein prenylation in a spectrum of patients with mevalonate kinase deficiency. Frontiers in Immunology 2019; 10, 1900. doi: 10.3389/fimmu.2019.01900.
Skinner, O.P., Jurczyluk, J., Baker, P.J., Masters, S.L., Rios Wilks, A., Clearwater, M.S., Robertson, A.A.B., Schroder, K., Mehr, S., *Munoz, M.A. & *Rogers, M.J. Lack of protein prenylation promotes NLRP3 inflammasome assembly in human monocytes. J Allergy Clin Immunol 2019; 143, 2315-2317. doi: 10.1016/j.jaci.2019.02.013.
Lee, N.J., Ali, N., Zhang, L., Qi, Y., Clarke, I., Enriquez, R.F., Brzozowska, M., Lee, I.C., Rogers, M.J., Laybutt, D.R., Center, J.R., Baldock, P.A., Herzog, H. Osteoglycin, a novel coordinator of bone and glucose homeostasis. Mol. Metab. 2018; 13, 30-44. doi: 10.1016/j.molmet.2018.05.004.
*Munoz, M.A., *Jurczyluk, J., Mehr, S., Chai, R.C., Arts, R.J.W., Sheu, A., McMahon, C., Center, J.R., Singh-Grewal, D., Chaitow, J., Campbell, D.E., Quinn, J.M.W., Alexandrov, K., Tnimov, Z., Tangye, S.G., Simon, A., Phan, T.G. & Rogers, M.J. Defective protein prenylation is a diagnostic biomarker of mevalonate kinase deficiency. J Allergy Clin Immunol 2017; 140:873-875. doi: 10.1016/j.jaci.2017.02.033.
*Jurczyluk, J., *Munoz, M., Skinner, O.P., Chai, R.C., Ali, N., Palendira, U., Quinn, J.M.W., Preston, A., Tangye, S.G., Brown, A.J., Argent, E., Ziegler, J.B., Mehr, S. & Rogers, M.J. Mevalonate kinase deficiency leads to decreased prenylation of Rab GTPases. Immunology & Cell Biology 2016; 94:994-999.
Lawson, M., McDonald, M., Kovacic, N., Khoo, W.H., Terry, R., Down, J., Kaplan, W., Paton-Hough, J., Fellows, C., Pettitt, J., Dear, T., Van Valckenborgh, E., Baldock, P., Rogers, M.J., Eaton, C., Vanderkerken, K., Pettit, A., Quinn, J., Zannettino, A., Phan, T.G. & Croucher, P.I. Osteoclasts Control Re-activation of Dormant Myeloma Cells by Remodeling the Endosteal Niche. Nature Communications 2015; 6:8983. doi: 10.1038/ncomms9983.
Ali, N., Jurczyluk, J., Shay, G., Tnimov, Z., Alexandrov, K., Munoz, M.A., Skinner, O.P., Pavlos, N.J. & Rogers, M.J. A highly sensitive prenylation assay reveals in vivo effects of bisphosphonate drug on the Rab prenylome of macrophages outside the skeleton. Small GTPases 2015; 6:202-211.
Junankar, S., Shay, G., Jurczyluk, J., Ali, N., Down, J., Pocock, N., Parker, A., Nguyen, A., Sun, S., Kashemirov, B., McKenna, C.E., Croucher, P.I., Swarbrick, A., Weilbaecher, K. Phan, T.G. & Rogers, M.J. Real-time intravital imaging establishes tumour-associated macrophages as the extraskeletal target of bisphosphonate action in cancer. Cancer Discovery 2015; 5:35-42.
Croucher, P.I., Parker, B.S., Corcoran, N. & Rogers, M.J. Bone turnover markers and prostate cancer: not just a measure of bone disease? Eur. Urol. 2015; 68:51-52.
Das, S., Edwards, P.A. Crockett, J.C. & Rogers, M.J. Upregulation of endogenous farnesyl diphosphate synthase overcomes the inhibitory effect of bisphosphonate on protein prenylation in HeLa cells. Biochim. Biophys. Acta 2014; 1841:569-573.
Rumpler, M., Würger, T., Roschger, P., Zwettler, E., Sturmlechner, I., Altmann, P., Fratzl, P., Rogers, M.J., Klaushofer, K. Osteoclasts on Bone and Dentin In Vitro: Mechanism of Trail Formation and Comparison of Resorption Behavior. Calcif Tiss Int 2013; 93:526-539.
Naylor AJ, Azzam E, Smith S, Croft A, Poyser C, Duffield JS, Huso DL, Gay S, Ospelt C, Cooper MS, Isacke C, Goodyear S, Rogers MJ & Buckley CD (2012). The MSC marker CD248 (Endosialin) is a negative regulator of bone formation. Arth Rheum 64, 3334-3343.
Su, X., Floyd, D.H., Hughes, D., Xiang, J., Schneider, J.G., Uluckan, O., Heller, E., Deng, H., Zou, W., Craft, C.S., Wu, K., Hirbe, A.C., Grabowska, D., Eagleton, M.C., Townsley, S., Collins, L., Piwmica-Worms, D., Steinberg, T.H., Novack, D.V., Conley, P.B., Hurchla, M.A., Rogers, M. & Weilbaecher, K.N. (2012). The ADP receptor P2RY12 regulates osteoclast function and pathologic bone remodelling. J. Clin. Invest. 122, 3579-3592.
Crockett, J.C., Mellis, D.J., Shennan, K.I.J., Duthie, A., Greenhorn, J., Wilkinson, D.I., Ralston, S.H., Helfrich, M.H. & Rogers, M.J. (2011). Signal peptide mutations in RANK prevent downstream activation of NK-kappa beta. J. Bone Miner. Res. 26, 1926-1938.
Rogers, M.J., Crockett, J.C., Coxon, F.P., Monkkonen, J. (2011). Biochemical and molecular mechanisms of action of bisphosphonates. Bone 49 (S1), 34-41.
Itzstein C, Coxon FP, Rogers MJ. (2011). The regulation of osteoclast function and bone resorption by small GTPases. Small GTPases 2, 117-130.
Hocking, L.J., Mellis, D.J., McCabe, P.S., Helfrich, M.H. & Rogers, M.J. (2010). Functional interaction between Sequestosome-1/p62 and Autophagy-Linked FYVE-containing protein WDFY3 in human osteoclasts. Biochem Biophys Res Commun 402, 543-548.
Roelofs, A.J., Coxon, F.P.; Ebetino, F.H., Lundy, M.W., Henneman, Z.J., Nancollas, G.H., Sun, S., Blazewska, K.M., Bala, J.L.F., Kashemirov, B.A., Khalid, A.B., McKenna, C.E. & Rogers, M.J. (2010). Fluorescent risedronate analogs reveal bisphosphonate uptake by bone marrow monocytes and localization around osteocytes in vivo. J Bone Miner Res 25, 606-616. 71
Whyte, L.S., Ryberg, E., Sims, N.A., Ridge, S., Mackie, K., Greasley P.J., Ross, R.A. & Rogers, M.J. (2009). The putative cannabinoid receptor GPR55 affects osteoclast function in vitro and bone mass in vivo. Proc Natl Acad Sci USA 106, 16511-16516.
Dunford, J.E., Thompson, K., Coxon, F.P., Luckman, S.P., Hahn, F.P., Poulter, C.D., Ebetino, F.H. & Rogers, M.J. (2001). Structure-activity relationships for inhibition of farnesyl diphosphate synthase in vitro and inhibition of bone resorption in vivo by nitrogen-containing bisphosphonates. J Pharmacol Exp Ther 296, 235-242.
Russell, R.G.G., Watts, N.B., Ebetino, F.H., Rogers, M.J. (2008). Mechanisms of action of bisphosphonates: similarities and differences and their potential influence on clinical efficacy. Osteoporos Int. 19, 733-759.
Sobacchi, C., Frattini, A., Guerrini, M.M., Abinun, M., Pangrazio, A., Susani, L., Bredius, R., Mancini, G., Cant, A., Bishop, N., Grabowski, P., Del Fattore, A., Messina, C., Errigo, G., Coxon, F.P., Scott, D.I., Teti, A., Rogers, M.J., Vezzoni, P., Villa, A. & Helfrich, M.H. (2007). Osteoclast-poor human osteopetrosis due to mutations in the gene encoding RANKL. Nature Genetics 39, 960-962.
Thompson, K., Rojas, J. & Rogers, M.J. (2006). Alkylamines cause Vg9Vd2-T cell activation and proliferation by inhibiting the mevalonate pathway. Blood 107, 651-654.
Frith, J.C., Monkkonen, J., Auriola, S. & Rogers, M.J. (2001). The molecular mechanism of action of the antiresorptive and antiinflammatory drug clodronate: evidence for the formation in vivo of a metabolite that inhibits bone resorption and causes osteoclast and macrophage apoptosis. Arth. Rheum. 44, 2201-2211.
Fisher, J.E., Rogers, M.J., Halasy, J.M., Luckman, S.P., Hughes, D.E., Masarachia, P.J., Wesolowski, G., Russell, R.G.G., Rodan, G.A. & Reszka, A.A. (1999). Mechanism of action of alendronate: geranylgeraniol, an intermediate of the mevalonate pathway, prevents inhibition of osteoclast formation, bone resorption and kinase activation in vitro. Proc. Natl. Acad. Sci. 96, 133-138.
Luckman, S.P., Hughes, D.E., Coxon, F.P., Russell, R.G.G. & Rogers, M.J. (1998). Nitrogen-containing bisphosphonates inhibit the mevalonate pathway and prevent post-translational prenylation of GTP-binding proteins, including Ras. J. Bone Miner. Res. 13, 581-589.
