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. Author manuscript; available in PMC: 2012 Jul 15.
Published in final edited form as: J Immunol. 2011 Jun 20;187(2):987–998. doi: 10.4049/jimmunol.1001861

FIGURE 8. Deficiency of FoxO3 leads to augmented NF-κB-DNA binding activity due to loss of its interaction with RelA/p65 in lungs of mouse exposed to CS.

FIGURE 8

A, NF-κB-DNA binding was measured by the Trans-AM transcription factor RelA/p65 ELISA kit in nuclear proteins from CS-exposed mice lung for 3 days. Data are shown as mean ± SEM (n= 3 to 4 per group). *P < 0.05, **P < 0.01, significant compared to corresponding air-exposed mice. +P < 0.05, significant compared with CS-exposed WT mice. B, Nuclear fraction from mouse lung exposed to CS for 3 days were immunoprecipitated (IP) with anti-RelA/p65 antibodies. C, Reciprocal IP of nuclear fraction from mouse lung exposed to CS 3 days was performed with anti-FoxO3 antibodies, followed by immunoblot analysis. D, H292 epithelial cells were treated with CSE (1%), and nuclear fractions from cell lysates were used for IP with anti-RelA/p65 antibody. IgG was used as an isotype control. Immunoprecipitates were subjected to immunoblot analysis and probed with anti-FoxO3 or anti-RelA/p65 antibody.