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Diseases
Themes / Divisions

About

Our work is focused on understanding how proteins within cells interact, and how genetic mutations that perturb these interactions can cause disease.

We are particularly interested in interactions between proteins involved in cell signalling. The network of signalling proteins within cells can be likened to an electronic circuit. Our research is identifying the missing components in these ‘circuits’ and explaining how diseases are caused by defects in the circuit components.

By understanding how defective signalling causes disease, we aim to develop drugs to control the actions of defective components. In particular we are seeking to understand how signalling defects can lead to a range of diseases, including ischemia-reperfusion injuries, such as stroke and kidney injury, inflammatory bowel disease, muscular dystrophy and cancers.

Publications

Selected publications from Prof James Murphy

Davies KA, Czabotar PE, Murphy JM. Death at a funeral: Activation of the dead enzyme, MLKL, to kill cells by necroptosis. Current Opinion in Structural Biology. 2024;88:10.1016/j.sbi.2024.102891

Chiou S, Al-Ani AH, Pan Y, Patel KM, Kong IY, Whitehead LW, Light A, Young SN, Barrios M, Sargeant C, Rajasekhar P, Zhu L, Hempel A, Lin A, Rickard JA, Hall C, Gangatirkar P, Yip RK, Cawthorne W, Jacobsen AV, Horne CR, Martin KR, Ioannidis LJ, Hansen DS, Day J, Wicks IP, Law C, Ritchie ME, Bowden R, Hildebrand JM, O’Reilly LA, Silke J, Giulino-Roth L, Tsui E, Rogers KL, Hawkins ED, Christensen B, Murphy JM, Samson AL. An immunohistochemical atlas of necroptotic pathway expression. EMBO Molecular Medicine. 2024;16(7):10.1038/s44321-024-00074-6

Samson AL, Murphy JM. Mapping where and when necroptotic cell death occurs in disease. Cell Death & Differentiation. 2024;31(7):10.1038/s41418-024-01318-1

Diplock N, Baudin M, Xiang X, Liang L-Y, Dai W, Murphy JM, Lucet IS, Hassan JA, Lewis JD. Molecular dissection of the pseudokinase ZED1 expands effector recognition to the tomato immune receptor ZAR1. Plant Physiology. 2024;:10.1093/plphys/kiae268

Liang L-Y, Geoghegan ND, Mlodzianoski M, Leis A, Whitehead LW, Surudoi MG, Young SN, Janes P, Shepherd D, Ghosal D, Rogers KL, Murphy JM, Lucet IS. Co-clustering of EphB6 and ephrinB1 in trans restrains cancer cell invasion. Communications Biology. 2024;7(1):10.1038/s42003-024-06118-4

Lawlor KE, Murphy JM, Vince JE. Gasdermin and MLKL necrotic cell death effectors: Signaling and diseases. Immunity. 2024;57(3):10.1016/j.immuni.2024.02.011

M. Bader S, Cooney JP, Bhandari R, Mackiewicz L, Dayton M, Sheerin D, Georgy SR, Murphy JM, Davidson KC, Allison CC, Pellegrini M, Doerflinger M. Necroptosis does not drive disease pathogenesis in a mouse infective model of SARS-CoV-2 in vivo. Cell Death & Disease. 2024;15(1):10.1038/s41419-024-06471-6

Kaiser J, Nay K, Horne CR, McAloon LM, Fuller OK, Muller AG, Whyte DG, Means AR, Walder K, Berk M, Hannan AJ, Murphy JM, Febbraio MA, Gundlach AL, Scott JW. CaMKK2 as an emerging treatment target for bipolar disorder. Molecular Psychiatry. 2023;28(11):10.1038/s41380-023-02260-3

Meng Y, Garnish SE, Davies KA, Black KA, Leis AP, Horne CR, Hildebrand JM, Hoblos H, Fitzgibbon C, Young SN, Dite T, Dagley LF, Venkat A, Kannan N, Koide A, Koide S, Glukhova A, Czabotar PE, Murphy JM. Phosphorylation-dependent pseudokinase domain dimerization drives full-length MLKL oligomerization. Nature Communications. 2023;14(1):10.1038/s41467-023-42255-w

Garnish SE, Martin KR, Kauppi M, Jackson VE, Ambrose R, Eng VV, Chiou S, Meng Y, Frank D, Tovey Crutchfield EC, Patel KM, Jacobsen AV, Atkin-Smith GK, Di Rago L, Doerflinger M, Horne CR, Hall C, Young SN, Cook M, Athanasopoulos V, Vinuesa CG, Lawlor KE, Wicks IP, Ebert G, Ng AP, Slade CA, Pearson JS, Samson AL, Silke J, Murphy JM, Hildebrand JM. A common human MLKL polymorphism confers resistance to negative regulation by phosphorylation. Nature Communications. 2023;14(1):10.1038/s41467-023-41724-6

Lab research projects

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