Simon Ellington

Keywords synthetic lethality PARP inhibitor sensitivity transcription-replication conflicts Okazaki fragment maturation replication stress single-stranded DNA gaps Get full text access Log in, subscribe or purchase for full access. References 1. O'Neil, N.J. ∙ Bailey, M.L. ∙ Hieter, P. Synthetic lethality and cancer Nat. Rev. Genet. 2017; 18:613-623 2. Setton, J. ∙ Zinda, M. ∙ Riaz, N. ... Synthetic lethality in cancer therapeutics: The next generation Cancer Discov. 2021; 11:1626-1635 3. Huang, A.

Abstract Oncogene-induced replication stress generates endogenous DNA damage that activates cGAS–STING-mediated signalling and tumour suppression1,2,3. However, the precise mechanism of cGAS activation by endogenous DNA damage remains enigmatic, particularly given that high-affinity histone acidic patch (AP) binding constitutively inhibits cGAS by sterically hindering its activation by double-stranded DNA (dsDNA)4,5,6,7,8,9,10.