Kelvin J. A. Davies, Ph.D., D.Sc.
James E. Birren Professor of Gerontology,
and Professor of Molecular & Computational Biology.
Regulation of gene expression in oxidative stress; degradation of oxidatively damaged proteins by the Proteasome and the mitochondrial Lon protease; adaptive responses to oxidative stress; apoptosis, necrosis, and mitoptosis in oxidative stress; role of oxidative stress, and stress resistance, in the aging process.

Kelvin J. A. Davies, Ph.D., D.Sc. is the James E. Birren Chair of Gerontology. Professor Davies was born and raised in London, England and is a dual citizen of Great Britain and the U.S.A. Educated at London University, the University of Wisconsin, and the University of California at Berkeley, he was previously a faculty member at Harvard University and Harvard Medical School. Before moving to USC’s Andrus Gerontology Center in 1996, Professor Davies was Chairman of the Department of Biochemistry & Molecular Biology at the Albany Medical College, where he was also professor of Molecular Medicine.

Deeply involved in research into oxidative stress and free radicals, Professor Davies is the (founding) Editor-in-Chief of the premier scientific journal in the field, Free Radical Biology & Medicine and President of the International Society for Free Radical Research. Professor Davies is a Fellow of the Society for Free Radical Biology & Medicine; a Fellow of the Gerontological Society of America; a Fellow of the American Association for the Advancement of Science; winner of the Harwood S. Belding award of the American Physiological Society; and holder of various medals, honorary degrees, and fellowships from several universities and foreign scientific societies. Professor Davies is past President of the Oxygen Society and, In 1996, he was named the National Parkinson Foundation Scholar.

Professor Davies' research centers on the role of free radicals and oxidative stress in biology. In particular he is interested in genes that repair oxidatively damaged proteins, lipids, RNA, and DNA, and his laboratory has made major contributions to our understanding of this subject over the past twenty years. At the Andrus Gerontology Center, Professor Davies is focusing his research on the regulation of oxidative stress repair genes during aging. His laboratory is involved in biochemical, molecular biology, and genetic studies of both normal aging processes, and aging pathologies such as Parkinson and Alzheimer's diseases.

During aging, and in several age-related disease processes, vital cellular proteins are damaged by free radicals produced by metabolism, chronic inflammation, radiation, smoke, and by many foods and drugs. These oxidized and non-functional proteins must be removed before they aggregate, cross-link, and become permanent cellular inclusion bodies that propagate damage. Professor Davies’ research group has discovered that the Proteasome (cytoplasm, nucleus, endoplasmic reticulum) and the Lon Protease (mitochondria) recognize and selectively degrade such damaged proteins, thus minimizing aggregate formation, and allowing the synthesis of replacement proteins. The Davies group has also discovered that, unfortunately, both the Proteasome and the Lon Protease decline in aging, making older individuals more prone to deterioration and diseases associated with the accumulation of damaged protein aggregates. The mechanisms by which such damaged protein aggregates, and the Proteasome and Lon Protease, contribute to age-related diseases is now a major topic of interest.

While one half of the Davies laboratory works on proteins, the other half is studying the genetic basis of adaptation to oxidative stress, and has discovered seven new genes that contribute to stress resistance. One of these genes, called DSCR1(Adapt78), unfortunately seems to have a dual nature; a Jeckyll and Hyde gene? The DSCR1(Adapt78) gene consists of seven exons that undergo differential splicing to encode a family of proteins, called the Calcipressin1 proteins, that inhibit the serine/threonine phosphatase, Calcineurin. When expressed transiently, Calcipressins seem to promote a strong and protective adaptive response to stress by preventing calcineurin from turning the stress response off. When DSCR1(Adapt78) is expressed chronically, however, it seems to promote hyperphosphorylation of the tau protein and the formation of neurofibrillary tangles, which are common features of both Down syndrome and Alzheimer disease. In postmortem studies, the Davies group has found very high levels of DSCR1(Adapt78) expression in the brains of Alzheimer and Down patients. The group is now trying to determine whether or not DSCR1(Adapt78) is actually a causal factor in the progression of neurodegenerative diseases.

As the Founder of the Los Angeles County School District/USC S.T.A.R. program (a science/medical magnet program), a scout leader, a high school football boosters club director, a former Board of Trustees member of the Albany Academy for Boys, and a former high school teacher and youth club director, Professor Davies is vitally interested in the education of our children. Kelvin Davies lives in San Marino, California with his wife, Joanna M.S. Davies, M.D., a fellow faculty member at USC's Andrus Gerontology Center, medical specialist in Rheumatology and Osteoporosis, and Director of the Osteoporosis Center of Los Angeles, and their two children, Sebastian and Alexander. Outside of the University, Professor Davies is a fan of cricket and soccer, and has coached both of his sons' soccer teams. He is a devotee of opera and classical music and was founding President of the California Philharmonic Orchestra Foundation.

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