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Aging manifests at many levels, from single cell to whole animal. Normal human somatic cells lose their dividing potential and become senescent after about 50 to 60 divisions. Questions that are of interest: Why normal cells age whereas cancer cells are immortal? What is the clocking mechanism that causes the senescent cells lose dividing potential?
The hallmark of cell aging is the loss of dividing potential in normal cells during senescence. We have demonstrated that there is a global attenuation of G1/S gene expression during cell aging and proposed that such attenuation may account for the mortality of normal cells. Importantly, most of these G1/S genes are controlled by two transcription factors, NF-Y and E2F. Our current focuses are: (i) to investigate the role of NF-Y and E2F on this age-dependent attenuation of G1/S genes; (ii) to screen for small molecules that can modulate the lifespan of human cells in culture.
