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DNA Ligase Inhibitor: SCR7 Pyrazine
Initially, it was believed that SCR7 could block non-homologous end joining (NHEJ) mediated DNA repair by inhibiting DNA ligase IV, resulting in the increase of the genome editing efficiency of CRISPR-Cas9.1-4) However, researchers found later that the major product which was formed from the initial synthetic method was SCR7 pyrazine, not SCR7, and SCR7 itself could not inhibit DNA ligase IV.5,6) After that, it has been reported that SCR7 cyclizes automatically due to its instability, and is autoxidized to give SCR7 pyrazine. The SCR7 pyrazine inhibits NHEJ in vitro although its selectivity to DNA ligase IV is not so high.7,8)
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References
- 1) CRISPR-Cas systems for editing, regulating and targeting genomes
- 2) Increasing the efficiency of precise genome editing with CRISPR-Cas9 by inhibition of nonhomologous end joining
- 3) Increasing the efficiency of homology-directed repair for CRISPR-Cas9-induced precise gene editing in mammalian cells
- 4) An Inhibitor of Nonhomologous End-Joining Abrogates Double-Strand Break Repair and Impedes Cancer Progression
- 5) SCR7 is neither a selective nor a potent inhibitor of human DNA ligase IV
- 6) Synthesis and structure determination of SCR7, a DNA ligase inhibitor
- 7) Autocyclized and oxidized forms of SCR7 induce cancer cell death by inhibiting nonhomologous DNA end joining in a Ligase IV dependent manner
- 8) Water-soluble version of SCR7-pyrazine inhibits DNA repair and abrogates tumor cell proliferation
