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The average cell will divide between 50 and 70 times before cell death. As the cell divides the telomeres on the end of the chromosome get smaller. The Hayflick limit is the theoretical limit to the number of times a cell may divide until the telomere becomes so short that division is inhibited and the cell enters senescence.
The ability to maintain functional telomeres may be one mechanism that allows cancer cells to grow in vitro for decades. [54] Telomerase activity is necessary to preserve many cancer types and is inactive in somatic cells, creating the possibility that telomerase inhibition could selectively repress cancer cell growth with minimal side effects ...
In general, TERRA has been shown to be most abundant in cells with long telomeres, [2] [3] while cells with short telomeres express comparatively lower levels of transcript expression. There is also evidence that overexpression of TERRA in human cells can help promote telomere processing by inhibiting the 5'-3' exonuclease Exo1 through the Ku70 ...
This results in the two daughter cells receiving an uneven chromatid. [4] Since the two resulting chromatids lack telomeres, when they replicate the BFB cycle will repeat, and will continue every subsequent cell division until those chromatids receive a telomere, usually from a different chromatid through the process of translocation. [4]
They then used α factor to block cells with induced short telomeres in late G1 phase and measured the change in telomere length when the cells were released under a variety of conditions. They found that when the cells were released and concurrently treated with nocodazole , a G2/M phase cell cycle inhibitor, telomere length increased for the ...
Alternative Lengthening of Telomeres (also known as "ALT") is a telomerase-independent mechanism by which cancer cells avoid the degradation of telomeres.. At each end of the chromosomes of most eukaryotic cells, there is a telomere: a region of repetitive nucleotide sequences which protects the end of the chromosome from deterioration or from fusion with neighboring chromosomes.
The end replication problem is handled in eukaryotic cells by telomere regions and telomerase. Telomeres extend the 3' end of the parental chromosome beyond the 5' end of the daughter strand. This single-stranded DNA structure can act as an origin of replication that recruits telomerase.
hTERT is often up-regulated in cells that divide rapidly, including both embryonic stem cells and adult stem cells. [18] It elongates the telomeres of stem cells, which, as a consequence, increases the lifespan of the stem cells by allowing for indefinite division without shortening of telomeres. Therefore, it is responsible for the self ...