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John Hayes

John Hayes

John Hayes FRSE, FSB

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Prof Hayes initially trained between 1972 and 1976 in the School of Biological Sciences at the University of Edinburgh, with final year of studies in Molecular Biology.  He gained a PhD from the Medical School of the same university in 1980, awarded for investigation into bile acid-binding properties of hepatic glutathione S-transferases. In 1981, he was appointed a Lecturer within the Department of Clinical Chemistry at the University of Edinburgh. Here, he focused attention on the enzymology and protein chemistry of the glutathione S-transferase (GST) superfamily in rodents and human, and became particularly interested in the contribution of inducible class Alpha GST to chemoprevention against the liver carcinogen aflatoxin B1 and the contribution made by overexpressed GST in tumours to acquired resistance to anticancer drugs. In 1991, he took sabbatical leave from the University of Edinburgh to work in the laboratory of Dr Cecil B. Pickett, in the Department of Molecular Biology, Merck Frosst, Montreal, Canada, which was responsible for discovering the antioxidant response element (ARE) in the promoters of genes for inducible drug-metabolizing enzymes. Upon return from sabbatical, the University of Edinburgh promoted Dr Hayes to a Readership in Clinical Biochemistry.

In October 1992, Dr Hayes moved as a Reader to the University of Dundee to help Prof C. Roland Wolf set up the Biomedical Research Centre in the Medical School. In this environment, he focused more on the molecular biology and regulation of detoxication enzymes and identified a new family of inducible aldo-keto reductases (AKR7A1) that metabolise a dialdehydic form of aflatoxin B1. In January 1997, the University of Dundee promoted him to a personal chair. Since then, his interest in the role of the ARE in directing induction of antioxidant and detoxication genes has continued, and he has collaborated with Prof Masayuki Yamamoto (Tsukuba, Japan) to demonstrate that the Nrf2 transcription factor regulates both basal and inducible expression of GST, AKR, quinone reductase and glutathione biosynthetic enzymes. More recently, Prof Hayes’ lab has shown that control of the ARE-gene battery critically depends on the stability of Nrf2 protein, and inhibition of Keap1 blocks turn-over of the transcription factor. Workers in the Hayes laboratory were the first to show that Nrf2 stability is controlled by Keap1, and have more recently demonstrated the existence of three independent stress sensors in Keap1 that evolved separately.

The Hayes lab has published a total of 198 peer-reviewed papers, most of which can be viewed through ResearchGate (www.researchgate.net/profile/John_Hayes9/).

Prof Hayes was elected a Fellow of the Royal Society of Edinburgh in May 2008, and a Fellow of the Society of Biology in September 2008.

 

 

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