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Guo, X., Deng, Y., Lin, Y., Cosme-Blanco, W., Chan, S., He, H., Yuan, G., Brown, J.E. and Chang, S. (2007) Dysfunctional Telomeres Activate an ATM-ATR-Dependent DNA Damage Response to Suppress Tumorigenesis. The EMBO Journal, 26, 4709-4719.
https://doi.org/10.1038/sj.emboj.7601893

has been cited by the following article:

• TITLE: Telomeres and Telomerase: Molecular Views and Perspectives

  AUTHORS: Kumar Arvind, Tony Grace

  KEYWORDS: Telomere, Telomerase, Aging, Tumorigenesis, TMM, Shelterin

  JOURNAL NAME: Advances in Aging Research, Vol.7 No.5, September 20, 2018

  ABSTRACT: Telomere, the nucleoprotein structure at the end of eukaryotic linear chromosomes is indispensable for maintaining the genome stability. Telomeric DNA loss is apparent with each cell division, which marks an endpoint to the indefinite replication of the cell by causing replicative senescence that may lead to the programmed cell death. The loss of telomere is normal in cell division and as such after 20 - 40 divisions, telomere becomes too short to facilitate the capping function. Telomere uncapping or chromosomal free end causes a potential threat to the genomic stability and thus leads to the accumulation of chromosomal abnormalities that have been known to play a role in aging and cancer. Telomerase, the ribonucleoprotein complex, and its accessory proteins are required to maintain the telomere sequence. Telomerase plays a key role in maintaining the length of telomere by adding G-rich repeat sequences. Its activity has been found to be quite high in the gametes, stem cells and most importantly tumor cells. Almost 85% of tumor cells compensate for telomere loss aided by telomerase-associated protein complex and shelter in complex or telosome. However, 5% - 10% of the cells undergo telomerase-independent mechanism. This review presents the molecular view of the telomere and telomerase along with its associated complex structures. It also discusses its contrasting role in causing cellular senescence and promoting tumorigenesis.