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As telomeres shorten as a natural consequence of repeated cell division or due to other factors, such as oxidative stress, [19] shelterin proteins lose the ability to bind to telomeric DNA. When telomeres reach a critically short length, sufficient shelterin proteins to inhibit checkpoint activation are not available, although NHEJ and HR ...
Critically short telomeres trigger a DNA damage response and cellular senescence. [32] Mice have much longer telomeres, but a greatly accelerated telomere shortening-rate and greatly reduced lifespan compared to humans and elephants. [33] Telomere shortening is associated with aging, mortality, and aging-related diseases in experimental animals.
Telomere dysfunction during cellular aging (a state in which cells do not divide but are metabolically active) affects the health of the body. [2] Preventing telomere shortening without clearing old cells may lead to the accumulation of these cells in the body and contribute to age-related diseases and tissue dysfunction. [29]
The authors argued this could be because it reduces the number of carcinogens people ingest and lengthens telomeres, which are the DNA sequences at the ends of chromosomes that shorten over time ...
This enzyme extends telomeres, preventing the telomeres of cancer cells from shortening and giving them infinite replicative potential. [14] A proposed treatment for cancer is the usage of telomerase inhibitors that would prevent the restoration of the telomere, allowing the cell to die like other body cells. [15]
Shelterin (also called telosome) is a protein complex known to protect telomeres in many eukaryotes from DNA repair mechanisms, as well as to regulate telomerase activity. In mammals and other vertebrates, telomeric DNA consists of repeating double-stranded 5'-TTAGGG-3' (G-strand) sequences (2-15 kilobases in humans) along with the 3'-AATCCC-5' (C-strand) complement, ending with a 50-400 ...
When the cell does this due to telomere-shortening, the ends of different chromosomes can be attached to each other. This solves the problem of lacking telomeres, but during cell division anaphase, the fused chromosomes are randomly ripped apart, causing many mutations and chromosomal abnormalities. As this process continues, the cell's genome ...
The successive shortening of the chromosomal telomeres with each cell cycle is also believed to limit the number of divisions of the cell, contributing to aging. After sufficient shortening, proteins responsible for maintaining telomere structure, such as TRF2, are displaced, resulting in the telomere being recognized as a site of a double ...
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