Title : Alkyladenine DNA glycosylase deficiency uncouples alkylation-induced strand break generation from PARP-1 activation and glycolysis inhibition.

Pub. Date : 2020 Feb 10

PMID : 32042007






5 Functional Relationships(s)
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1 To address this question, we temporally profiled repair and metabolism in wild-type and Aag-/- cells treated with the alkylating agent methyl methanesulfonate (MMS). Methyl Methanesulfonate N-methylpurine DNA glycosylase Homo sapiens
2 To address this question, we temporally profiled repair and metabolism in wild-type and Aag-/- cells treated with the alkylating agent methyl methanesulfonate (MMS). Methyl Methanesulfonate N-methylpurine DNA glycosylase Homo sapiens
3 Accordingly, Aag-/- cells are protected from MMS-induced NAD+ depletion and glycolysis inhibition. Methyl Methanesulfonate N-methylpurine DNA glycosylase Homo sapiens
4 MMS-induced mitochondrial dysfunction, however, is AAG-independent. Methyl Methanesulfonate N-methylpurine DNA glycosylase Homo sapiens
5 Furthermore, treatment with FK866, a selective inhibitor of the NAD+ salvage pathway enzyme nicotinamide phosphoribosyltransferase (NAMPT), synergizes with MMS to induce cytotoxicity and Aag-/- cells are resistant to this combination FK866 and MMS treatment. Methyl Methanesulfonate N-methylpurine DNA glycosylase Homo sapiens