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URMC / Labs / Rahman Lab / Projects / Mechanisms of Cigarette Smoke-induced Lung Cellular Senescence


Mechanisms of Cigarette Smoke-induced Lung Cellular Senescence

HistoneThe major goal of this proposal is to understand the mechanisms of cigarette smoke-induced cellular senescence and inflammation in p16-HDAC2 Stress-induced Premature Senescence in the pathogenesis of COPD.

Pictured Right: Ribbon model of histone H3 and H4 showing a comparison of differentially modified residues identified by mass spectrometry. Histone H3 and H4 modifications identified in air and CS-exposed mouse lung. Several amino acids showed multiple posttranslational histone modifications, though not all of them were observed simultaneously on the same peptide. The identified posttranslational histone modifications shown in ribbon model are indicated based on the following color code: Ac (acetylation) = yellow spheres; me1 (mono-methylation) = cyan spheres; me2 (di-methylation) = olive spheres; ac + me2 (acetylations and di-methylations) = red spheres; me1 + me2 (mono- and di-methylation) = orange spheres; and ac + me1 + me2 (acetylation, mono- and di-methylation) = grey spheres.

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