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. Author manuscript; available in PMC: 2012 Nov 4.
Published in final edited form as: Mol Cell. 2011 Nov 4;44(3):476–490. doi: 10.1016/j.molcel.2011.08.033

Figure 2. Inhibition of Proteasomal Degradation and PHD Activity Restores the HIF-1α-Mediated Hypoxic Response in p75NTR−/− Cells.

Figure 2

(A) Western blot for HIF-1α stabilization in WT and p75NTR−/− MEFs treated with MG132 for 1 hour before hypoxia (1% O2). β-Actin loading controls were performed on the same membrane. The HIF1-α/β-actin ratio is normalized to the hypoxic WT cells. Representative image from n=3 independent experiments is shown.

(B) Western blot for HIF-1α stabilization in WT and p75NTR−/− MEFs treated with DFO for 1 hour before hypoxia (1% O2). β-Actin loading controls were performed on the same membrane. The HIF1-α/β-actin ratio is normalized to hypoxic WT cells. Representative image from n=3 independent experiments is shown.

(C) Immunocytochemistry for HIF-1α nuclear accumulation in WT and p75NTR−/− MEFs treated with DFO for 5 hours (1% O2) (WT hypoxia, n=163; p75NTR−/− hypoxia, n=240; WT hypoxia, n=114; p75NTR−/− hypoxia, n=189). Values are mean ± SD of the HIF1-α/β-actin ratio (n=2 independent experiments, *P<0.05 by unpaired Student's t test).

(D) Real-time PCR analysis of GLUT1 and PHD3 gene expression in WT and p75NTR−/− MEFs treated with DFO for 5 hours (200 μM). Values are mean ± SEM (n=3 independent experiments, *P<0.05; by one-way ANOVA).