What governs how fast we age? Why do some biological processes stop working earlier than others? And what is happening at the molecular and cellular level as some organisms age while others continue to thrive?
Although seemingly philosophical in nature, these questions address one of the major mysteries of biology, the process of aging. With recent developments in genetics, molecular biology, and genomics, we now have the possibility of addressing these questions at the molecular level. Because our ultimate goal is not simply to extend lifespan, but to improve overall health, we must identify the genes associated with biological functions that we typically associate with quality of life. The goal of our laboratory's work is to understand the molecular mechanisms governing longevity and maintenance of the biological processes that exhibit age-related decline.
Recent Publications
Ageing is marked by physical decline. Caenorhabditis elegans is a valuable model for identifying genetic regulatory mechanisms of ageing and longevity. Here we report a simple method to assess C. elegans' maximum physical ability based on the worms' maximum movement velocity. We show maximum velocity declines with age, correlates well with…
Protein turnover of FOXO family transcription factors is regulated by the ubiquitin-proteasome system. A complex interplay of factors that covalently attach certain types of ubiquitin chains (E3-ubiquitin ligases), and enzymes that are able to remove ubiquitin conjugates (deubiquitylases), regulate the degradation of FOXO proteins by the…
The Caenorhabditis elegans transcription factor HSF-1, which regulates the heat-shock response, also influences aging. Reducing hsf-1 activity accelerates tissue aging and shortens life-span, and we show that hsf-1 overexpression extends lifespan. We find that HSF-1, like the transcription factor DAF-16, is required for daf-2-insulin/IGF-1…
Contact information
Carl Icahn Lab 140
Princeton University
Princeton NJ, 08540
Lab phone: 609-258–9505