{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,5]],"date-time":"2026-03-05T23:49:24Z","timestamp":1772754564682,"version":"3.50.1"},"reference-count":50,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2006,7,19]],"date-time":"2006-07-19T00:00:00Z","timestamp":1153267200000},"content-version":"vor","delay-in-days":5313,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Carcinogenesis"],"published-print":{"date-parts":[[1992,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We used a shuttle vector based on the Epstein\u2010Barr virus origin of plasmid replication (oriP) to determine the types of mutations induced by depurination in human cells. Plasmid DNA was incubated at pH 2 at 40\u00b0C for various times to induce up to 20 apurinic (AP) sites per 9.7\u2010kb plasmid and electroporated into lymphoblastoid cells derived from either a normal individual or an ataxia telangiectasia patient. After replication of the vector in the human cells, plasmid DNA was isolated and analyzed for mutations induced in the plasmid\u2010encoded herpes simplex virus type 1\u2010thymidine kinase gene. Both the frequencies and types of mutations induced by depurination were essentially identical for normal and ataxia telangiectasia cells. The mutant frequency at 20 AP sites\/plasmid was 10\u2010fold to 13\u2010fold greater than that observed for untreated DNA. Deletion and frameshift events accounted for 46\u201355% of the mutants induced by depurination. The induced deletions were relatively small (median size, 100\u2013150 bp) and characterized by short (1\u20135 bp) regions of sequence homology at the end\u2010points. These mutations and the frameshifts, a majority of which occurred in runs of identical nucleotides, are consistent with a model involving AP\u2010site\u2010induced template dislocation during DNA synthesis. A broad spectrum of base\u2010substitution mutations, which accounted for 19\u201336% of the induced mutants, was observed. The apparent preference for insertion opposite AP sites in human cells was G (43\u201355%) &gt; A\u00b0C (18\u201321%) &gt; T (9\u201314%). Our results in human cells contrast markedly with those published previously for the mutational specificity of AP sites in Escherichia coli, in which a large majority of the mutants resulted from insertion of an A opposite the abasic site.\u00a9 1992 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/mc.2940060107","type":"journal-article","created":{"date-parts":[[2007,2,21]],"date-time":"2007-02-21T20:11:34Z","timestamp":1172088694000},"page":"32-42","source":"Crossref","is-referenced-by-count":43,"title":["Mutagenesis by apurinic sites in normal and ataxia telangiectasia human lymphoblastoid cells"],"prefix":"10.1002","volume":"6","author":[{"given":"Donna K.","family":"Klinedinst","sequence":"first","affiliation":[]},{"given":"Norman 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