RS-1

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Background

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].

[1]. Jayathilaka K, Sheridan S D, Bold T D, et al. A chemical compound that stimulates the human homologous recombination protein RAD51[J]. Proceedings of the National Academy of Sciences, 2008, 105(41): 15848-15853.
[2]. Baumann P, Benson F E, West S C. Human Rad51 protein promotes ATP-dependent homologous pairing and strand transfer reactions in vitro[J]. Cell, 1996, 87(4): 757-766.
[3]. Sonoda E, Sasaki M S, Buerstedde J M, et al. Rad51‐deficient vertebrate cells accumulate chromosomal breaks prior to cell death[J]. The EMBO journal, 1998, 17(2): 598-608.
[4]. Mason J M, Logan H L, Budke B, et al. The RAD51-stimulatory compound RS-1 can exploit the RAD51 overexpression that exists in cancer cells and tumors[J]. Cancer research, 2014, 74(13): 3546-3555.
[5]. Song J, Yang D, Xu J, et al. RS-1 enhances CRISPR/Cas9-and TALEN-mediated knock-in efficiency[J]. Nature communications, 2016, 7.