The human uracil-DNA glycosylase (UNG) gene encodes both mitochondrial (UNG1) and nuclear (UNG2) forms through differentially regulated promotes and alternative splicing. While UNG2 is the major enzyme in the base excision repair pathway that removes uracil residues from nuclear DNA that arise through either misincorporation during replication or cytosine deamination, inhibition of UNG1 by uracil glycosylase inhibitor did not lead to increased levels of spontaneous or induced mitochondrial DNA mutations. However, decreased levels of UNG activity and increased oxidative damage to mitochondrial DNA were seen in older mice, suggesting that mitochondrial DNA repair mechanisms may be involved in various neurodegenerative disorders in an age-dependent manner. This UNG1 antibody will not cross-react with UNG2.
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