Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
1947709 | Biochimica et Biophysica Acta (BBA) - General Subjects | 2012 | 6 Pages |
Abstract
âºNO/RNS can directly or indirectly cause DNA mutation. âºKey DNA repair proteins AGT, Ogg1, APE1, and DNA-PKcs are targets of S-nitrosylation. âºS-nitrosylation modulates DNA repair protein activity, stability, and localization. âºS-nitrosylation levels depend on NO synthesis by NOS and denitrosylation by GSNOR. âºGSNOR deficiency leads to nitrosative inactivation of AGT and hepatocarcinogenesis.
Keywords
S-nitrosoglutathioneGSNO reductaseO6-alkylguanine-DNA-alkyltransferaseDNA repair proteinsAP endonuclease 1GSNORS-nitrosylationAPE1DNA-PKcsOGG18-oxoGS-nitrosothiolSNOGSNONO synthaseDenDSBLPSRNSNOSDTTBERGAPDH8-oxoguanineNERHCCNitrosative stressinflammationnucleotide excision repairbase excision repairdiethylnitrosaminedithiothreitolCarcinogenesisdouble-strand breakZinclipopolysaccharideNitric oxideAGTDNA-dependent protein kinase catalytic subunitHepatocellular carcinomaglyceraldehyde-3-phosphate dehydrogenasereactive nitrogen species
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Authors
Chi-Hui Tang, Wei Wei, Limin Liu,