Fig. 8: MRE11 SUMOylation defects relate to cancer development. | Nature Communications

Fig. 8: MRE11 SUMOylation defects relate to cancer development.

From: Crosstalk between SUMOylation and ubiquitylation controls DNA end resection by maintaining MRE11 homeostasis on chromatin

Fig. 8

a Overlap between MRE11 SUMOylation sites and disease-related mutation sites. MRE11 mutation sites were collected from the ClinVar and cBioPortal databases. b The cancer-related MRE11 mutants showed a decrease in SUMOylation. c 255E384Q mutant was easier to degrade after the treatment of CPT (1 μM, 4 h). d HeLa cells expressing the cancer-related MRE11 mutants exhibited defects in RPA2 phosphorylation and the ATR-CHK1 pathway activation upon CPT treatment. e HeLa cells with K255E or K384Q mutant were sensitive to olaparib and cisplatin at the indicated doses (means ± SEM, n = 3 independent experiments). f Purified 255E384Q protein was analyzed by Coomassie blue staining. The nuclease assay in vitro was performed as in Fig. 5j, k (means ± SD, n = 3 independent experiments, ns = no significance).

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