| Project/Area Number |
22790294
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
General medical chemistry
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| Research Institution | Kagawa University |
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Principal Investigator |
UYAMA Toru 香川大学, 医学部, 助教 (30457337)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | PLA/ ATファミリー / HRASLSファミリー / 脂質代謝酵素 / ホスホリパーゼA1/ A2 / アシル転移酵素 / ペルオキシソーム / エーテル型脂質 / リン脂質 / PLA/ATファミリー / ホスホリパーゼA_1/A_2 / ホスホリパーゼA1 / ホスホリパーゼA2 / N-アシルトランスフェラーゼ / 癌抑制遺伝子 / グリセロリン脂質 / O-アシルトランスフェラーゼ |
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| Research Abstract |
We investigated possible lipid-metabolizing activities of HRASLS family members which were originally identified as tumor suppressor genes. We found that all of HRASLS family members possess lipid-metabolizing activities using glycerophospholipids as substrate. Thus, we termed the products of HRASLS1-5 genes as phospholipase A/ acyltransferase(PLA/ AT)-1-5, respectively. To analyze the biological functions of PLA/ AT-3 in living cells, we generated HEK293 cells stably expressing PLA/ AT-3. The examination of the cells revealed dysfunction of peroxisomes and a drastic decrease in the levels of ether-type lipids caused by the peroxisomal dysfunction. The results suggest that PLA/ AT-3 regulates intracellular content of peroxisomes by functioning as a phospholipid-metabolizing enzyme.
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