Premature Aging Protein

A group of American scientists from the University of Illinois at Chicago has discovered a new function of the DDB2 protein (DNA damage-binding protein 2, "a protein that stitches DNA damage").

It was previously known that this protein is involved in DNA repair.  It turned out that this protein also contributes to the accumulation of reactive oxygen species (ROS) in cells, which leads to their premature aging. DDB2–deprived cells are not susceptible to premature aging caused in normal cells by various damaging effects - exogenous oxidative stress, culture shock, oncogenic stress, DNA damage. There is no accumulation of ROS in DDB2-deprived cells when DNA is damaged, this is the result of increased expression of antioxidants in such cells in vitro and in vivo. DDB2 suppresses antioxidant genes, and the expression of this protein is induced in the presence of ROS.

Thus, the results of the study showed that under oxidative stress, the DDB2 protein functions on the principle of positive feedback, suppressing the expression of antioxidant genes and contributing to the continuous accumulation of ROS, which causes premature aging of the cell, leading to apoptosis.

This discovery can be used in the clinic both to fight tumors when it is necessary to cause the death of cancer cells, and to prevent unwanted premature cell death in various pathological conditions (for example, in the penumbra area during a stroke), as well as to find ways to delay aging.

The research materials are presented in the article Roy N, et al. DDB2, an essential mediator of premature senescence. Mol Cell Biol. 2010 Jun;30(11):2681-92. Epub 2010 Mar 29.

Portal "Eternal youth" http://vechnayamolodost.ru according to the materials Stemcells.Ru15.06.2010