{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chang SC"],"funding":["NCRR NIH HHS","Howard Hughes Medical Institute","NIEHS NIH HHS","NCI NIH HHS","NIGMS NIH HHS"],"pagination":["5489-500"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4477646"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["43(11)"],"pubmed_abstract":["Etheno DNA adducts are a prevalent type of DNA damage caused by vinyl chloride (VC) exposure and oxidative stress. Etheno adducts are mutagenic and may contribute to the initiation of several pathologies; thus, elucidating the pathways by which they induce cellular transformation is critical. Although N(2),3-ethenoguanine (N(2),3-εG) is the most abundant etheno adduct, its biological consequences have not been well characterized in cells due to its labile glycosidic bond. Here, a stabilized 2'-fluoro-2'-deoxyribose analog of N(2),3-εG was used to quantify directly its genotoxicity and mutagenicity. A multiplex method involving next-generation sequencing enabled a large-scale in vivo analysis, in which both N(2),3-εG and its isomer 1,N(2)-ethenoguanine (1,N(2)-εG) were evaluated in various "],"journal":["Nucleic acids research"],"pubmed_title":["Next-generation sequencing reveals the biological significance of the N(2),3-ethenoguanine lesion in vivo."],"pmcid":["PMC4477646"],"funding_grant_id":["S10 RR019022","P01 CA160032","P30 ES000267","P01 ES005355","P01 CA026731","P30 ES002109","R01 CA080024","R01 ES010546","T32 ES007020","R01 GM069857","R37 CA080024","P30 CA068485","P01 ES05355"],"pubmed_authors":["Marnett LJ","Chang SC","Wu J","Yau E","Fedeles BI","Li D","Rizzo CJ","Christov PP","Jost M","Levine SS","Zhao L","Delaney JC","Essigmann JM","Drennan CL","Guengerich FP","Singh V"],"additional_accession":[]},"is_claimable":false,"name":"Next-generation sequencing reveals the biological significance of the N(2),3-ethenoguanine lesion in vivo.","description":"Etheno DNA adducts are a prevalent type of DNA damage caused by vinyl chloride (VC) exposure and oxidative stress. Etheno adducts are mutagenic and may contribute to the initiation of several pathologies; thus, elucidating the pathways by which they induce cellular transformation is critical. Although N(2),3-ethenoguanine (N(2),3-εG) is the most abundant etheno adduct, its biological consequences have not been well characterized in cells due to its labile glycosidic bond. Here, a stabilized 2'-fluoro-2'-deoxyribose analog of N(2),3-εG was used to quantify directly its genotoxicity and mutagenicity. A multiplex method involving next-generation sequencing enabled a large-scale in vivo analysis, in which both N(2),3-εG and its isomer 1,N(2)-ethenoguanine (1,N(2)-εG) were evaluated in various ","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Jun","modification":"2026-04-12T19:56:55.571Z","creation":"2019-03-27T01:53:54Z"},"accession":"S-EPMC4477646","cross_references":{"pubmed":["25837992"],"doi":["10.1093/nar/gkv243"]}}