Presentation description

Degenerative diseases are partly driven my accumulation of senescent cells. This senescence can result from DNA damage accumulation. BLST, an under researched gene that has been a subject of study for the Bowles lab, has been shown to be a regulator of senescence through DNA damage repair. The mechanism by which BLST accomplishes this is unknown. This study shows the beginnings of characterizing the mechanism. Once this mechanism is more fully understood, it can't be applied therapeutically. Secondary Mentor: Jonah Holbrook Jonah.holbrook@utah.edu