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Assoc. Prof. Michael P. Gantier

Scientific Advisor

MEng (Biol), PhD.

Associate Professor Michael Gantier leads the Nucleic Acids and Innate Immunity laboratory in the Centre for Innate Immunity and Infectious Disease at the Hudson Institute of Medical Research. The central theme of his research is to define how nucleic acids (RNA and DNA) modulate immune responses. He was trained as a biological engineer in Compiegne, France, prior to undertaking his PhD in Medicine and Therapeutics in University College Dublin with Prof. Seamas Donnelly, working on the then emerging RNA interference technology. 

Following on his PhD studies he joined the laboratory of Prof Bryan Williams in 2006, to define the interaction of RNAs with the innate immune system. This led to the discoveries of structural determinants of RNAs which underlie their capacity to activate or inhibit immune responses by Toll Like Receptors, a theme he has developed further in his independent laboratory since 2015. 

More recently, his laboratory discovered how immune responses could be engaged in damaged cells, with implications in infection, immunity, and cancer - through the engagement of the cGAS-STING pathway.

In 2015, following the award of an ARC Future Fellowship and several NHMRC project grants, he was promoted to lead his own research group in the Hudson Institute of Medical Research and in 2020 was promoted to Associate Professor.

He received the prestigious Milstein Young Investigator award from the International Cytokine and Interferon Society (2010), and Oligonucleotide Therapeutics Society Young Investigator award (2014) among several other international and national awards. He has published over 70 peer-reviewed publications, and is an inventor on 5 PCT patents. He currently serves as Associate Editor for the prestigious Molecular Therapy-Nucleic Acids journal and Journal of Interferon and Cytokine Research. 

Associate Professor Gantier’s team made the ground-breaking discovery that idronoxil was a potent inhibitor of TBK1, effectively blocking STING and MAVS signalling, at the root of the NOXCOVID trial.