After measuring protein turnover in cultured cells from skin biopsies of both progeria sufferers and healthy people, she found that it wasn't just lamin A that was affected in the disease. Initially, Salk Staff Scientist Abigail Buchwalter, first author of the paper, was interested in whether the mutation was making the lamin A protein less stable and shorter lived. The rare mutation occurs in one of the structural proteins in the cell nucleus, lamin A, but it has been unclear how a single defective protein in the nucleus causes the myriad rapid-aging features seen in the disease. Hutchinson-Gilford progeria is a very rare genetic disease causing people to age 8 to 10 times faster than the rest of us and leading to an early death. ![]() Our work suggests that one driver of both abnormal and normal aging could be accelerated protein turnover." "When a cell devotes valuable resources to producing protein, other important functions may be neglected. "The production of proteins is an extremely energy-intensive process for cells ," says Martin Hetzer, vice president and chief science officer of the Salk Institute and senior author of the paper. The work, described in Nature Communications on August 30, 2017, adds to a growing body of evidence that reducing protein synthesis can extend lifespan - and thus may offer a useful therapeutic target to counter both premature and normal aging. ![]() Scientists at the Salk Institute found that protein synthesis is overactive in people with progeria.
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