HUMAN RAD51 RECOMBINASE: THE ROLE IN THE CELL CYCLE CHECKPOINT AND CELLULAR SURVIVAL
T. A. Shtam, E. Yu. Varfolomeeva, E. V. Semenova, M. V. Filatov 1
Petersburg B. P. Konstantinov Nuclear Physics Institute RAS, Gatchina;
1 e-mail: filatov@omrb.pnpi.spb.ru
The RAD51 protein, an eukaryotic homologue of Escherichia coli RecA, plays a central role in both mitotic and meiotic homologous recombination. Here,
we demonstrate that short-term silencing of Rad51 gene by specific small interfering (si) RNA induces cell death of the most part of investigated cancer cell
lines and normal fibroblasts. Disruption of the Rad51 gene in these cells results in S or(and) G2 cell cycle arrest leading to apoptosis. But some
human cancer cell lines demonstrate abolishment of pre-mitotic checkpoint and are not sensitive to siRNA silencing of RAD51 recombinase. Recent experiments
show that normal functioning of the recombination repair system is essential for maintenance of genome stability, proliferation of vertebrate cells and, finally, for
prevention of dramatic cell death.
Key words: homologous recombination, Rad51, cell cycle, DNA reparation
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