Ian HicksonCenter for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, Denmark F1000 Faculty Member (since 13 December 2010)
Professor, Department of Cellular and Molecular Medicine
Fellow of the Royal Society
The chromosomes in all living organisms are under constant attack from mechanical stress and reactive chemical species that can damage the structural integrity of the DNA. All cells, therefore, devote considerable energy to both preventing and repairing DNA structural abnormalities. Despite this, thousands of DNA lesions still arise daily in each human cell. The majority of these lesions pose no threat to cell viability, but their cumulative effect in a long-lived species influences lifespan and the incidence of age-related diseases such as cancer and neurodegeneration.
Our laboratory investigates the biochemical, molecular and cell biological functions of DNA repair factors in eukaryotic cells and how these factors act to maintain chromosome stability. In particular, we focus on those genes that, when defective, give rise to disorders in humans associated with the premature onset of aging and/or age-associated diseases such as cancer.
In recent years, a major focus has been on characterization of BLM, the protein defective in Bloom's syndrome, a disorder associated with an elevated incidence of cancers of all types. The BLM gene encodes a DNA helicase of the RecQ family, which has important roles in DNA replication and repair via the homologous recombination pathway. We combine analysis of the biochemical properties of BLM with both studies in human cells lacking BLM and studies of SGS1, the budding yeast ortholog of BLM.
Following our recent move from the University of Oxford to the Center for Healthy Aging in the Department of Cellular and Molecular Medicine (ICMM), we have re-aligned many of our studies to focus on the aging process in humans. Fortunately, chromosome maintenance pathways, including those involving RecQ helicases, are known to impact directly on the rate of human aging. This can be seen most strikingly in human disorders associated with accelerated aging, such as Werner's syndrome (WS). In WS, loss of the RecQ helicase encoded by the WRN gene leads to early onset, multi-organ aging.
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