Cancer cells establish replicative immortality by activating a telomere-maintenance
mechanism (TMM), be it telomerase or the alternative lengthening of telomeres (ALT) …

Activation of a telomere maintenance mechanism (TMM) is permissive for replicative
immortality and a hallmark of human cancer. While most cancers rely on reactivation of …

Mammalian telomeres consist of (TTAGGG) n repeats. Transcription of the C-rich strand
generates a G-rich RNA, termed TERRA, containing G-quadruplex structures. Recent …

To escape replicative senescence, cancer cells have to overcome telomere attrition during
DNA replication. Most of cancers rely on telomerase to extend and maintain telomeres, but 4 …

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

UV-DDB, consisting of subunits DDB1 and DDB2, recognizes UV-induced photoproducts
during global genome nucleotide excision repair (GG-NER). We recently demonstrated a …

ADAR1 is involved in adenosine-to-inosine RNA editing. The cytoplasmic ADAR1p150 edits
3'UTR double-stranded RNAs and thereby suppresses induction of interferons. Loss of this …

The mechanism of activation of the alternative lengthening of telomeres (ALT) pathway of
mammalian chromosome-end maintenance has been unclear. We have now discovered …

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

Mammalian cells have evolved specialized mechanisms to sense and repair double-strand
breaks (DSBs) to maintain genomic stability. However, in certain cases, the activity of these …