Natural chromosome ends resemble double-stranded DNA breaks, but they do not activate
a damage response in healthy cells. Telomeres therefore have evolved to solve the'end …

Telomeres shorten during each cellular division, with cumulative attrition resulting in
telomeric damage and replicative senescence. Bypass of replicative senescence …

Simple Summary Cells undergoing malignant transformation must circumvent replicative
senescence and eventual cell death associated with progressive telomere shortening that …

Alternative lengthening of telomeres (ALT) involves homology-directed telomere synthesis.
This multistep process is facilitated by loss of the ATRX or DAXX chromatin-remodeling …

Abstract Structure-specific endonucleases (SSEs) have key roles in DNA replication,
recombination and repair, and emerging roles in transcription. These enzymes have …

Alternative lengthening of telomeres (ALT) is a telomere lengthening pathway that
predominates in aggressive tumors of mesenchymal origin; however, the underlying …

The shelterin proteins protect telomeres against activation of the DNA damage checkpoints
and recombinational repair. We show here that a dimer of the shelterin subunit TRF2 …

Abstract Repressor/activator protein 1 (RAP1) is a highly conserved telomere-interacting
protein. Yeast Rap1 protects telomeres from non-homologous end joining (NHEJ), plays …

Cancer cells rely on the activation of telomerase or the alternative lengthening of telomeres
(ALT) pathways for telomere maintenance and survival. ALT involves homologous …

The SLX4 Fanconi anemia protein is a tumor suppressor that may act as a key regulator that
engages the cell into specific genome maintenance pathways. Here, we show that the SLX4 …