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. 2010 May 14;299(2):L192–L203. doi: 10.1152/ajplung.00426.2009

Fig. 7.

Fig. 7.

Deficiency of Glrx1 led to increased histone modification in mouse lungs in response to CS exposure. A: histone modifications were assessed by measuring phosphorylation (Ser10) and acetylation (Lys9) of histone H3, and acetylation of histone H4 (Lys12) in lung by immunoblotting using acid-extracted nuclear histone fraction (i). B: acetylated histone H3 and H4 on the IL-6 gene promoter in mouse lung were analyzed by ChIP assay. Lung homogenates were immunoprecipitated with anti-acetylated histone H3 and H4 antibodies, and chromatin modification on the promoter region of proinflammatory cytokine was detected by PCR using the primers for IL-6. Gel pictures shown are representative of at least 3 separate experiments.*P < 0.05, **P < 0.01, significant compared with respective air-exposed mice. #P < 0.05, ##P < 0.01, significant compared with CS-exposed WT mice. +P < 0.05 significant compared with air-exposed WT mice.