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RS-1 is a stimulatory compound of RAD51, a key player in the HR complex. RS-1 could increase the DNA binding activity of RAD51 and function in vivo to enhance the homologous recombination activity of hRAD51 by promoting the formation of active presynaptic filaments [1].

The hRAD51 protein could bind with single- and double-stranded DNA and exhibit DNA-dependent ATPase activity. Rad51 mediates homology recognition and initiates strand exchange [2]. Chromosome analysis revealed that Rad51‐deficient vertebrate cells accumulated chromosomal breaks in the G2/M phase of the cell cycle prior to cell death. Rad51 played an essential role in the repair of spontaneously occurring chromosome breaks in proliferating cells of higher eukaryotes [3].

RS-1 treatment promoted significant antitumor responses in a mouse mode. It can be used to kill human cancer cells, and that its toxicity is modulated by both RAD51 and RAD54 translocase expression levels [4]. RS-1 effectively improved the knock-in rates in the TALEN- and the Cas9-mediated genome-editing systems in rabbits. RS-1 showed little toxic effects on the overall animal health and reproduction. RS-1 enhanced Cas9- and TALEN-mediated knock-in efficiency in rabbit embryos both in vitro and in vivo. RS-1 treatment (15 μM) appeared to enhance the blastocyst development in embryos. Treating embryos with RS-1 at 7.5 μM resulted in 26.1% knock-in rate [5].

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