Dr Michael Cahill

BSc (hons 1), UNSW 1987; PhD, UNSW 1996
Honorary Senior Lecturer
ANU College of Health and Medicine

Areas of expertise

  • Biochemistry And Cell Biology 3101
  • Receptors And Membrane Biology 310110
  • Cell Metabolism 310103
  • Signal Transduction 310111
  • Protein Trafficking 310108
  • Cancer Cell Biology 321101
  • Oncology And Carcinogenesis 3211
  • Neurosciences 3209
  • Proteomics And Intermolecular Interactions (Excl. Medical Proteomics) 310109
  • Medical Biochemistry Proteins And Peptides (Incl. Medical Proteomics) 320506
  • Evolutionary Biology 3104

Research interests

I have used a multidisciplinary suite of methods to characterise the cell and organism biology of the protein Progesterone Receptor Membrane Component 1 (PGRMC1) and related proteins. These range from Omics platforms (proteomics, metabolomics, genomics, methylomics in recent publications) to phylogenetic studies to identify which amino acids are the most functionally conserved in evolution, which is a surrogate for identifying residues involved in important cellular functions.

PGRMC1 is involved in diverse cell and organism processes, ranging from metabolism and migration to membrane trafficking and steroid biology. In 2022 I published a unifying model which proposes that PGRMC-like proteins were critical for both the regulation of mitochondrial metabolism during the endosymbiotic origin of eukaryotes, and also for the origin of the eumetazoan animal gastrulation organiser and its subsequent mechanism of defining new differentiated tissue types. The last common eumetazoan ancestor (LEUMCA) was the first organism to develop cells specialised for as nerves, muscle, insulogenic secretion, or photoreception. These were accompanied in evolution by the concomitant acquisition of a novel PGRMC C-terminus and new phosphorylated tyrosines. Mutation of PGRMC phosphorylated amino acids exerts profound effects over the epigenetic landscape, in patterns resembling those of early embryogenesis and tissue differentiation. Therefore PGRMC phosphorylated tyrosines were acquired in evolution just before complex body plans began to be specified by the gastrulation organiser, and may be a part of the mechanism by which differentiated cell identity is specified and/or maintained. See my recent publications for details.

PGRMC1 may also be centrally involved in the mechanism of Alzheimer's disease, being directly involved in the mechanism of action of novel synaptorestorative anti-Alzheimer's therapeutics that improve cognition in animal studies and are currently undergoing human Phase 2 trials. See my 2022 'Quo vadis' publication for details.


I obtained a BSc in Zoology and Biochemistry with the University of New South Wales, and moved to Germany for a PhD in the group of Alfred Nordheim at the Medizinische Hochschule Hannover (MHH). I remained in Germany for a total of almost the first 18 years of my postgraduate career, during which time I followed a career path through signal transduction and transcriptional regulation during my PhD and Postdoctoral time, into developing proteomics technologies, and applying those new technologies to biological conditions - especially cancer - at ProteoSys AG (Mainz), a German Biotechnology company that I co-founded (2000 - 2007) as a spin-off from the University of Tübingen Institute for Molecular Biology. During this time I successfully acquired >3.5 million Euros in grants from German national and European international agencies through the University of Tübingen and ProteoSys AG.

Among the many hundreds of proteomics discoveries at ProteoSys was the observation that the then obscure protein Progesterone Receptor Membrane Component 1 (PGRMC1) was differentially phosphorylated in breast cancers of differing morbidity. Perplexingly, it was attested to have a wide range of seemingly unrelated functions under different pseudonyms from different animals (see my 2007 review). Because the company chose not to pursue PGRMC1, I decided to relocate back to my native Australia to pursue what I considered to be this crown jewel of the company proteomics portfolio in the research dynamics of an academic environment.

In 2008 I moved back to Australia to Charles Sturt University at Wagga Wagga, NSW, as an academic with teaching and research responsibilities. I taught biochemistry and cell biology and pursued my research into PGRMC1 until I left by my own choice in January 2021 because, despite a successful European track record and a vigorous series of grant applications (30 grants between 2008 and 2020), I was never awarded a dollar in national competitive grant funds. This was despite hindsight showing that PGRMC1 was indeed an important protein in different ways for eukaryotic and animal biology, especially in metabolism, cancer biology, and neuronal differentiation status: e.g., it is probably a key point in the mechanism of Alzheimer's disease (see my 2022 reviews, especially the 'Quo Vadis" publication). That has led to my role as scientific advisor for Cognition Therapeutics Inc. (Pittsburgh, PA, USA) in 2013.They developed a novel synaptorestorative molecule to clear Alzheimer's neuronal synapses of oligomeric amyloid beta, which improves cognition in animal models and is currently in Phase 2 clinical trials. The mechanism involves a membrane trafficking function of PGRMC1.

I have been an Honorary academic associated with the Hannan Laboratory at The John Curtin School of Medical Research since 7 January 2019.




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Updated:  08 December 2023 / Responsible Officer:  Director (Research Services Division) / Page Contact:  Researchers