Telomeres are specialized nucleoprotein structures at the ends of linear chromosomes that
prevent the activation of DNA damage response and repair pathways. Numerous factors …

The replication of the ends of linear chromosomes, or telomeres, poses unique problems,
which must be solved to maintain genome integrity and to allow cell division to occur. Here …

The mechanism by which telomeres prevent end-to-end fusion has remained elusive. Here,
we show that the human telomeric protein TRF2 plays a key role in the protective activity of …

In normal human cells, telomeres shorten with successive rounds of cell division, and
immortalization correlates with stabilization of telomere length. These observations suggest …

Telomere shortening triggers replicative senescence in human fibroblasts. The inability of
DNA polymerases to replicate a linear DNA molecule completely (the end replication …

During the evolution of linear genomes, it became essential to protect the natural
chromosome ends to prevent triggering of the DNA-damage repair machinery and …

We have demonstrated recently that chronic hyperoxic treatment accelerates the rate of
aging of fibroblasts and the rate of telomere shortening in parallel. It was hypothesized that …

In virtually all eukaryotic organisms, telomeric DNA is composed of a variable number of
short direct repeats. While the primary sequence of telomeric repeats has been determined …

During telomere replication in yeast, chromosome ends acquire an S-phase–specific
overhang of the guanosine-rich strand. Here it is shown that in cells lacking Ku, a …

Telomeres protect chromosome ends from being detected as lesions and from triggering
DNA damage checkpoints. Paradoxically, telomere function depends on checkpoint proteins …