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- 郡山 恵樹
- 金沢大学医薬保健研究域医学系脳情報分子学
書誌事項
- タイトル別名
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- Role of Protein <i>S</i>-nitrosylation in Central Nervous System Survival and Regeneration
- 中枢神経修復・再生におけるタンパク質のS-ニトロシル化の役割
- チュウスウ シンケイ シュウフク ・ サイセイ ニ オケル タンパクシツ ノ S-ニトロシルカ ノ ヤクワリ
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The retina has been regarded as 'an approachable part of the brain' for investigating central nervous system (CNS). The optic nerve injury is a well-accepted model to study the mechanisms of neural degeneration and/or axonal regeneration after trauma in the CNS. Nitric oxide (NO) is a gaseous messenger molecule biosynthesized from L-arginine and molecular oxygen by NO synthase. Many reports suggest that excess production of NO plays a crucial role in neuronal cell death including in death of retinal ganglion cells (RGCs). In contrast, several lines of evidence indicate that NO can prevent neuronal death. In general, NO mediates neuroprotection through two main signaling pathways: the NO/cyclic guanosine monophosphate (cGMP) pathway and the S-nitrosylation pathway. Especially, whether S-nitrosylation of proteins promotes RGCs survival and its axonal regeneration after injury is unclear. Thus, we focused on the S-nitrosylation-dependent mechanism of RGCs survival and axonal regeneration by NO after nerve injury.<br>
収録刊行物
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- 薬学雑誌
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薬学雑誌 133 (8), 843-848, 2013
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390001206128912000
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- NII論文ID
- 130003361977
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- NII書誌ID
- AN00284903
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- COI
- 1:STN:280:DC%2BC3sflsleisw%3D%3D
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- ISSN
- 13475231
- 00316903
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- NDL書誌ID
- 024827432
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- PubMed
- 23903223
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- 本文言語コード
- ja
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- データソース種別
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- JaLC
- IRDB
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可