2012 Fiscal Year Final Research Report
Explication of the regulatory mechanism of S-nitrosylation signaling
| Project Area | Signaling functions of reactive oxygen species |
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| Project/Area Number |
20117008
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| Research Category |
Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | Chiba University (2009-2012)
Osaka University (2008) |
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Principal Investigator |
MATSUMOTO Akio 千葉大学, 大学院・医学研究院, 准教授 (60437308)
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| Co-Investigator(Kenkyū-buntansha) |
OZAWA Kentaro 奈良県立医科大学, 医学部, 講師 (80507393)
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| Co-Investigator(Renkei-kenkyūsha) |
MATSUMOTO Ayako 東邦大学, 理学部・生物学科, 講師 (60444519)
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| Research Collaborator |
SHIMIZU Takeshi 千葉大学, 大学院・医学研究院, 准教授 (70312840)
ENDO Hidemi 千葉大学, 大学院・医学研究院, 博士前期課程
NAKAYA Haruaki 千葉大学, 大学院・医学研究院, 教授 (60113594)
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| Project Period (FY) |
2008 – 2012
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| Keywords | 一酸化窒素 / S-ニトロシル化 / S-ニトロソシステイン / シグナル伝達 / 細胞間情報伝達 / ニトロソシステイン代謝酵素 / ニトロソストレス / 神経変性疾患 |
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| Research Abstract |
The major focus of this project is to elucidate the effects of NO, particularly through S-nitrosylation of the target protein, transmitted through the plasma membrane of juxtaposed cells. NO reacts with cysteine to convert itself to membrane transferrable molecule, CysNO, which in tern can travel through the amino acid transporter to the juxtaposed cells. The intracellular decomposition enzyme for CysNO works to prevent excess influx of NO signal into the cell resulting in the formation of pathophysiological conditions.
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[Remarks] (1)朝日新聞夕刊一面「O157 に「猛毒型」千葉大チーム,識別方法も解明」
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[Remarks] (2)フジテレビニュース「「O157」に猛毒型が存在千葉大学研究グループが発見」
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[Remarks] (3)NHK テレビおはよう日本「病原性大腸菌の毒性検査法開発」
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[Remarks] (4)毎日新聞「O157 の重症化NO 還元酵素が要因」
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[Remarks] (5)共同通信「O157,酵素あれば重症化」
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