OGG1 and MUTYH repair activities promote telomeric 8-oxoguanine induced senescence in human fibroblasts

Abstract excerpt

Telomeres are hypersensitive to the formation of the common oxidative lesion 8-oxoguanine (8oxoG), which impacts telomere stability and function. OGG1 and MUTYH glycosylases initiate base excision repair (BER) to remove 8oxoG or prevent mutation. Here, we show OGG1 loss or inhibition, or MUTYH loss, partially rescues telomeric 8oxoG-induced premature senescence and associated proinflammatory responses, while loss...

Topics

Share this publication in a Topic to start or enrich a Post.

• Share to DNA Repair Mechanisms
• Share to PARP inhibition in cancer therapy
• Share to Telomeres, Telomerase, and Senescence