TIRR: a potential front runner in HDR race-hypotheses and perspectives.

A A Anuchina, A V Lavrov, S A Smirnikhina

Molecular biology reports 2020 Mar

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The majority of CRISPR-Cas9 methods for mutations correction are oriented on gene editing through homologous recombination that is normally restrained by non-homologous end joining (NHEJ). A recently identified protein TIRR can bind a 53BP1 protein, a key effector of NHEJ, and inhibit its recruitment to double-strand break loci. Several studies elucidated the molecular mechanisms of TIRR-53BP1 binding and established bidirectional role of TIRR in 53BP1 functions and stability. It was proved that overexpression of TIRR promotes the double-strand break repair through homologous recombination. All findings, which were described in the review, allow assuming TIRR as a suitable target for enhancing efficacy of genome editing through homology directed repair.

Citation

A A Anuchina, A V Lavrov, S A Smirnikhina. TIRR: a potential front runner in HDR race-hypotheses and perspectives. Molecular biology reports. 2020 Mar;47(3):2371-2379