Senescence Induced by Altered Telomere State, Not Telomere Loss

By J. Karlseder, A. Smogorzewska, T. de Lange. Science, 2002

841 citations recorded by the source corpus.

Subfields: Aging, Physiology, Pollution

View Paper: https://www.semanticscholar.org/paper/843a45413bc274646101d13a6aeb59dbcf4f86d1

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Aging

1. T. de Lange
2. S. Chan
3. Elizabeth H Blackburn
4. D. Loayza
5. G. Celli
6. J. Shay
7. W. Wright
8. Roderick J. O’Sullivan

In Physiology

1. T. de Lange
2. J. Karlseder
3. Elizabeth H Blackburn
4. S. Chan
5. Roderick J. O’Sullivan
6. J. Shay
7. W. Wright
8. G. Celli

In Pollution

1. T. de Lange
2. G. Celli
3. Elizabeth H Blackburn
4. D. Loayza
5. S. Chan

Citations in the corpus

• Telomeres and telomerase. (2002, positive): “Such overexpression in these cells, in which telomerase was not active, allowed telomere length to decline to a much shorter average length before senescence occurred than in control cells without such TRF2 overexpression (Karlseder et al. 2002).”
• Human Telomerase and Its Regulation (2002, background): “Overexpression of a dominant negative TRF1, which removes endogenous TRF1 from telomeres, results in telomere lengthening in telomerase-positive cells but not in telomerase-negative cells (118, 236).”
• DNA processing is not required for ATM-mediated telomere damage response after TRF2 deletion (2005, methodology): “In-gel hybridization with a 32 P-γATP end-labelled (CCCTAA) 4 oligonucleotide and subsequent denaturation and hybridization steps were performed as describe”
• Cellular senescence and its effector programs (2014, background): “In addition, the TRF2-dependent suppression of DNA repair within telomeres can yield DDR signaling from telomere-associated damage resulting from causes other than telomere shortening (Karlseder et al. 2002; Fumagalli et al. 2012).”
• Telomeres: protecting chromosomes against genome instability (2010, background): “, and the bulk of telomeres, as determined by southern analysis, seem to be around 4 k”
• POT1 as a terminal transducer of TRF1 telomere length control (2003, methodology): “Myc-tagged POT1 and POT1(ΔOB) were retrovirally expressed in HTC75 cells as describe”
• Senescence impairs successful reprogramming to pluripotent stem cells. (2009, background): “This idea is supported by studies that demonstrate that telomere structure, rather than telomere length, is the main determinant of functional telomeres (Karlseder et al., 2002).”
• Telomerase maintains telomere structure in normal human cells. (2003, neutral): “telomere length activates replicative senescence (Blackburn, 2001; Karlseder et al., 2002).”