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. Author manuscript; available in PMC: 2013 Sep 11.
Published in final edited form as: Cancer Genet. 2012 Jan-Feb;205(0):25–33. doi: 10.1016/j.cancergen.2012.01.005

Figure 1.

Figure 1

ChIP followed by PCR and Sanger sequencing for rs67491583. (A) In HeLa cells, ectopically over-expressed GFI1B favors binding to the wild-type allele of rs67491583. Sanger-sequencing of anti-GFI1B precipitated DNA (αGFI1B) reveals that the wild-type allele (TC) is enriched by the GFI1B precipitation when compared with the input DNA (Input). (B) In the GM19240 lymphoblast, endogenous GFI1 (αGFI1) and GFI1B (αGFI1B) both prefer to bind to the wild-type allele (TC). (C) In HeLa cells over-expressing GFI1B, Sanger-sequencing of anti-histone H3 monomethyl Lysine 4 precipitated DNA (αH3K4me1) reveals that the risk-allele (TG) is enriched by the H3K4me1 precipitation when compared with the input DNA (Input).