GSE24.2 reduces DNA damage and oxidative stress in dyskeratosis congenita cells

What is it about?

We are working with a dyskerin-derived peptide, GSE24.2, that improves some of the deficiencies observed in cells derived for dyskeratosis congenita patients. Cells from other telomerophaties, such as aplastic anemia, also respond to GSE24.2 treatment. We had previously shown that GSE24.2 increases telomerase activity. In this article we shown that GSE24.2 decreases DNA damage and oxidatibe stress in these cells. All these effects result in increased proliferation capacity of the cells.

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Why is it important?

The results obtained in this and previous publications indicate that GSE24.2 has a good potential as a possible drug for the treatment of dyskeratosis congenita patients and related diseases that involve the biology of the telomeres, or telomeropathies. Actualy, GSE24.2 has been recently aproved as an orphan drug for treatment of this disease.