Phylogenetic and biochemical approach for identifying the chronic proinflammatory proteins accumulated in protease-deficient species and individuals
| Project/Area Number |
24592836
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pathobiological dentistry/Dental radiology
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| Research Institution | Nagasaki University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SAKAI Eiko 長崎大学, 医歯薬学総合研究科(歯学系), 助教 (10176612)
OKAMOTO Kuniaki 長崎大学, 医歯薬学総合研究科(歯学系), 准教授 (10311846)
TSUKUBA Takayuki 長崎大学, 医歯薬学総合研究科(歯学系), 教授 (30264055)
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| Research Collaborator |
FUKUMA Yutaka
SUGAWARA Megumi
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | プロテアーゼ / 分子進化 / 偽遺伝子 / 細胞内プロテアーゼ / 免疫 / 感染 / 炎症 |
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| Outline of Final Research Achievements |
We investigated the evolution and gene organization of the aspartic proteases, including cathepsin D, cathepsin E, pepsins, renin and napsins. Cathepsin E gene appears to be absent in Ruminants and Platypus. Human napsin B has been annotated as a pseudogene because it lacks an in-frame stop codon. napsin B orthologs are primarily distributed in primates, while napsin A orthologs are the only napsin genes in other species. Napsin B was duplicated from napsin A during the early stages of primate evolution, and the subsequent loss of napsin B function reflected ongoing human-specific napsin B pseudogenization.
Cathepsin E deficiency causes autophagy impairment concomitantly with increased aberrant mitochondria as well as increased oxidative stress in macrophage. The impaired adipose tissue development in high fat diet-fed cathepsin E-deficient mice was probably due to reduced infiltration of macrophages and may lead to hepatomegaly accompanied by hepatic steatosis and hypercholesterolemia.
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Report
(4 results)
Research Products
(27 results)
