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. 2016 Apr 1;310(10):L964–L974. doi: 10.1152/ajplung.00054.2016

Fig. 7.

Fig. 7.

The Sirt-2 selective inhibitor, sirtinol, counters the 17-AAG effect and stabilizes Sirt-2 promoter binding in HLMVEC. We performed ChIP assays with HLMVEC treated with 17-AAG and LPS and increasing concentrations of sirtinol. A: a representative image of PCR products resolved on ethidium bromide agarose gel. B–E: the quantification of data from A (± SE, n = 3), expressed as fold changes in promoter binding of p65, Sirt-2, histone H3, and RNA Pol II, respectively. LPS induced p65 and RNA Pol II promoter binding but reduced Sirt-2 and histone H3 binding to the IKBα promoter. 17-AAG blocked the LPS effects and this was restored by sirtinol, in a concentration-dependent manner. F: total HLMVEC lysate was immunoprecipitated with anti-Sirt-2 antibody and immunoblotted with anti-histone H3 antibody. We observed coimmunoprecipitation of Sirt-2 and histone H3.