Table 1.

The effect of OGT and OGA on DDR pathways

DDR pathways	OGT/OGA localization, protein abundance, and overproduction/knockdown studies	References
HR and single-strand annealing (SSA)	OGT deletion or inhibition analysis shows that OGT is essential for Rad52 IRIF formation. OGT is not required for chromosomal break end joining or Rad51 IRIF formation	(85)
DSB repair	In MCF7 human mammary carcinoma cells and xenograft tumors, upregulating of O-GlcNAc protected tumor xenografts against radiation. Downregulating O-GlcNAc delayed DSB repair, reduced cell proliferation, and increased cell senescence	(110)
DDR	In fly stem/progenitor cells, in mouse embryonic stem cells (ESCs) and mouse embryonic fibroblasts (MEFs), CHK1/2 stabilize OGT, augmenting O-GlcNAcylation and further promoting DDR	(81)
NHEJ	OGA is recruited to DNA lesions by its C-terminal pseudo-HAT domain. OGA suppression impaired NHEJ	(76)
HR	OGT is recruited to DNA damage sites	(73)
DDR-related pathways	Ataxia telangiectasia mutated (ATM) inhibition in the ovarian cancer cell line SKOV3 abnormally elevated OGT and OGA levels	(111)
UV damage	Chromatin binding of OGT was enhanced after UV treatment. OGT affects cellular response to UV radiation	(75)