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. Author manuscript; available in PMC: 2014 Aug 7.
Published in final edited form as: Sci Signal. 2013 Feb 12;6(262):ra10. doi: 10.1126/scisignal.2003417

Fig. 7.

Fig. 7

HIF-1α inhibits Cdc7-mediated phosphorylation and activation of the MCM helicase. (A) The chromatin fraction and whole-cell lysates of HCT116 cells exposed to 20 or 1% O2 were isolated and analyzed with anti-Cdc7, HIF-1α, or histone H3 antibodies. (B and C) NIH-3T3 cells were untreated or treated with DFX (B) or DMOG (C) for 24 hours, after which the chromatin fraction was isolated. (D) HCT116 cells were left untreated, treated with DMOG, or exposed to 1% O2 for 24 hours, and cell lysates were probed with the indicated antibodies. (E) The chromatin fraction from HCT116 cells exposed to 20 or 1% O2 was probed with indicated antibodies. (F) HeLa cells were processed as in (D). (G) Lysates from HeLa, HCT116, and WT8 cells exposed to either 20 or 1% O2 were probed with the indicated antibodies. (H) The chromatin fraction from HCT116 cells exposed to 20 or 1% O2 was probed with indicated antibodies. (I and J) HCT116 cells were transfected with either empty shRNA vector or vector encoding shRNA against HIF-1α and exposed to DMOG (I) or 1% O2 (J). The chromatin fraction was analyzed with the indicated antibodies. Data in (I) and (J) represent two independent experiments. Western blot data from three independent replicates were quantified for (A) to (H). Results are shown as means ± SEM. *P < 0.05.