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. 2016 Oct 27;45(1):509–511. doi: 10.1093/nar/gkw1091

FANCJ is essential to maintain microsatellite structure genome-wide during replication stress

Joanna Barthelemy 1, Helmut Hanenberg 2,3, Michael Leffak 1,*
PMCID: PMC5224479  PMID: 27794046

Nucl. Acids Res. (2016) 44 (14): 6803–6816. doi: 10.1093/nar/gkw433

The authors wish to make the following correction to their article:

Figure 2B: an error was introduced in the reagent labelling. The + signs for siControl should be above lanes 1, 3; the + signs for siFANCJ should be above lanes 2, 4; the + signs for APH should be above lanes 3, 4.

Figure 2.

Figure 2.

FANCJ knockdown leads to loss of ectopic CTG/CAG microsatellite signals in (CTG/CAG)12 cells under replication stress (APH). (A) Maps of the ectopic loci. (B) Western blots. Whole cell extracts were isolated after treatment of cells with siControl or siFANCJ for a total of five transfections and 0.2 μM aphidicolin, or parallel untreated cultures and immunoblotted for FANCJ. (C) Duplex spPCR with primers spanning the ectopic (CAG/CTG)12 repeats and primers for a non-repeat internal PCR control site.

Figure 4K: the bands labeled “internal control” and “TP53 poly T repeat” have been switched compared to the other figures.

Figure 4.

Figure 4.

FANCJ−/− patient cells treated with aphidicolin are prone to microsatellite signal loss at multiple endogenous sites. (A–L) Duplex spPCR across endogenous repeated sequences in DNA from FANCJ−/− patient fibroblasts with or without aphidicolin (0.5 μM) treatment.

New Figures 2 and 4 are provided below.

The Authors apologise to the Readers for the inconvenience caused.


Articles from Nucleic Acids Research are provided here courtesy of Oxford University Press

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