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. 2014 May 15;25(10):1641–1652. doi: 10.1091/mbc.E13-12-0717

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© 2014 Poletto et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 2: — NPM1 knockdown positively modulates BER proteins independently of p53 status. (A) Representative Western blotting analysis on HeLa whole-cell extracts (50 μg) from scrambled siRNA (siScr)– or NPM1 siRNA (siNPM1)–treated cells (left). An increased amount of a subset of BER proteins is visible upon NPM1 down-regulation. Antibodies used are indicated on the right-hand side. Right, histogram reporting the quantitative increment of different BER proteins in HeLa cells upon NPM1 down-regulation. Values reported are expressed as mean ± SD of the fold of induction relative to siScr-treated cells in at least three independent replicates. (B) Representative Western blotting analysis on HepG2 whole-cell extracts (50 μg) obtained from siScr or siNPM1 cells (left). NPM1 depletion leads to accumulation of different BER proteins. Antibodies used are indicated on the right-hand side. *Unspecific band. Right, histogram reporting the increase of BER protein levels in HepG2 cells upon NPM1 down-regulation. Values reported are expressed as mean ± SD of the fold of induction relative to siScr-treated cells in at least three independent replicates.