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. Author manuscript; available in PMC: 2020 Apr 15.
Published in final edited form as: Chem Res Toxicol. 2019 Feb 8;32(4):753–761. doi: 10.1021/acs.chemrestox.8b00411

Figure 5.

Figure 5.

The spiroiminodihydantoin lesions are substrates of BER and NER in intact cells. The 32P-internally labeled DNA hairpins harbouring Sp lesions were transfected either into fully BER/NER-competent HeLa cells (lanes 1–4), or into NEIL1−/− cells that lack the glycosylase NEIIL1 (lanes 5–8) that is known to excise Sp lesions in double-stranded DNA.19, 20 The incubation times (t) varied between 2 and 8 hours. Lanes M: oligonucleotide size markers (We note that the intensity of the synthetic maker Lane M only, was diminished separately from the rest of the gel because it was oversaturated). Lanes C: Control experiments; the hairpins were not transfected into the cells, but were subjected to the same treatment otherwise. The panel shown is a composite of autoradiographs of two gels.