Andrei Seluanov

CLK-1 protein has DNA binding activity specific to O(L) region of mitochondrial DNA.

Expression of human telomerase (hTERT) does not prevent stress-induced senescence in normal human fibroblasts but protects the cells from stress-induced apoptosis and necrosis.

Evidence that high telomerase activity may induce a senescent-like growth arrest in human fibroblasts.

Selectable system for monitoring the instability of CTG/CAG triplet repeats in mammalian cells.

Telomerase as a growth-promoting factor.

DNA end joining becomes less efficient and more error-prone during cellular senescence.

Genome-wide demethylation destabilizes CTG.CAG trinucleotide repeats in mammalian cells.

Making ends meet in old age: DSB repair and aging.

Cell divisions are required for L1 retrotransposition.

Telomerase activity coevolves with body mass not lifespan.

TRF2 is required for repair of nontelomeric DNA double-strand breaks by homologous recombination.

Changes in the level and distribution of Ku proteins during cellular senescence.

Changes in DNA repair during aging.

Genome-wide demethylation promotes triplet repeat instability independently of homologous recombination.

Coevolution of telomerase activity and body mass in mammals: from mice to beavers.

Comparison of nonhomologous end joining and homologous recombination in human cells.

DNA repair by nonhomologous end joining and homologous recombination during cell cycle in human cells.

Distinct tumor suppressor mechanisms evolve in rodent species that differ in size and lifespan.

Use of the Rad51 promoter for targeted anti-cancer therapy.

Rodents for comparative aging studies: from mice to beavers.

DNA repair by homologous recombination, but not by nonhomologous end joining, is elevated in breast cancer cells.

Hypersensitivity to contact inhibition provides a clue to cancer resistance of naked mole-rat.

SIRT6 promotes DNA repair under stress by activating PARP1.

SIRT6 overexpression induces massive apoptosis in cancer cells but not in normal cells.

Repairing split ends: SIRT6, mono-ADP ribosylation and DNA repair.

Rad51 promoter-targeted gene therapy is effective for in vivo visualization and treatment of cancer.

Adenoviral vector driven by a minimal Rad51 promoter is selective for p53-deficient tumor cells.