Not exact matches
When the protein is mutated in Werner syndrome it disrupts the replication and repair of DNA and the expression of
genes, which was thought to cause
premature aging.
Inflammation also erodes telomeres, the «caps» at the ends of chromosomes that protect
genes from degradation, which can lead to early cell death,
premature aging and even cancer.
A rare,
premature aging disease, Hutchinson - Gilford progeria is caused by a single point mutation in the
gene encoding lamin A, which forms a protein scaffold on the inner edge of the nucleus that helps maintain chromatin structure and organize nuclear processes such as RNA and DNA synthesis.
Lanza suspects that the
premature aging may be related to using viruses to carry the turn - back - the - calendar
genes into adult cells, which is what «induces» them to act (sort of) like embryonic cells.
This modification is of special interest to p53 - dependent anti-senescence and pro-longevity functions because genetically engineered mice with p53 serine18 mutated to alanine (p53S18A) show increased ROS levels, metabolic stress, tumor frequency,
premature aging symptoms and defects in regulation of a subset of p53 target
genes that include sestrins.
Thus, chronically increased p53 activity causes
premature aging in mice, whereas transgenic mice with extra copies of p53 and ARF
genes under normal regulation show tumor resistance and extended life span.