Telomeres and their control.

By M. McEachern, A. Krauskopf, Elizabeth H Blackburn. Annual Review of Genetics, 2000

706 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/3c6d04b41e9bfa12dd9ac3007736c1b7369fd7fb

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In Molecular Biology

1. Ian D. Hickson
2. J. Campisi
3. Jan H. J. Hoeijmakers
4. M. Blasco
5. M. Demaria
6. Jesús Gil
7. Alan Ashworth
8. Adam Freund

In Physiology

1. Jan H. J. Hoeijmakers
2. J. Campisi
3. M. Blasco
4. M. Demaria
5. Jesús Gil
6. Adam Freund
7. J. Kirkland
8. T. Tchkonia

Citations in the corpus

• Biologic properties of mesenchymal stem cells derived from bone marrow and adipose tissue (2006, background): “The extent of telomere shortening and the levels of telomerase activity often correlatewith the stemcell characteristics [Greider and Blackburn, 1985; Morin, 1989; Prowse et al., 1993; Hirato et al., 1994; Bodnar et al., 1998; McEachern et al., 2000].”
• Genome maintenance mechanisms for preventing cancer (2001, background): “In the germ line and in some specific tissues, telomere length is maintained by a specialized reverse transcriptase, called telomerase, adding new repeats using a tightly associated RNA template to compensate for the loss (reviewed in ref”
• Telomerase in the human organism (2002, background): “For most of the cell cycle, telomeres are packaged into the chromatin structure responsible for end protection (reviewed by McEachern et al., 2000).”
• Telomeres and telomerase. (2002, neutral): “In dividing cells with active telomerase, telomeres are heterogeneous in length even within a single cell, but the population of telomeres is tightly controlled and kept within well-defined limits specific to that cell type (reviewed in McEachern et al. 2000).”
• RecQ helicases: caretakers of the genome (2003, background): “However, ∼10–15% of human cancers are thought to use a telomerase-independent mechanism termed ALT (alternative lengthening of telomeres) to extend their telomeres and thereby sustain proliferatio”
• From polyploidy to aneuploidy, genome instability and cancer (2004, background): “Telomeres shorten with each round of DNA replication but are renewed by the reverse transcriptase telomeras”
• Aging, Cellular Senescence, and Cancer (2012, background): “Telomere shortening does not occur in cells that express telomerase, the reverse transcriptase that can replenish the repetitive telomeric DNA de novo (15, 16).”