| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Outline of Final Research Achievements |
The isomerization of aspartic acid and asparagine residues among several post-translational protein modifications is one of the damages by oxidative stress which occurs in the pathogenesis of chronic obstructive pulmonary disease (COPD). Its D-isoaspartyl (D-isoAsp) and D-aspartic acid (D-Asp) cause the protein structure alteration and functional impairment. This process is partially reversed by the protein carboxyl-isoaspartyl methyltransferase 1 (PCMT1) repair enzyme. We investigated PCMT1 expression in the pulmonary tissue from COPD patients and evaluated its significant reduction. The mitochondrial protein, Prohibitin1 (PHB1) is deeply associated with production of active oxygen species and oxidative stress. Under low PCMT1 condition、D-Asp content in PHB1 increased significantly. In this regard, deamidation of Asp residues in the mitochondrial protein, PHB1 is associated with aging via changes of cellular organelles.
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