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硫化水素に依存するヒト硫化キノン酸化還元酵素の活性化
Joseph V Roman1, Yashvi Shukla1, David A Hanna1
1Department of Biological Chemistry, University of Michigan, Ann Arbor, MI 48109.
The Journal of biological chemistry
|September 5, 2025
まとめ
硫化水素 (H2S) 曝露は,トランスレーション後のメカニズムを通じてミトコンドリア硫化キノン酸化還元酶 (SQOR) を活性化させる. この研究は,H2SがSQORの活動を調節し,細胞呼吸と解毒に影響を与える方法を示しています.
科学分野:
- 生物化学
- 細胞の代謝
- 酵素の規制
背景:
- 硫化水素 (H2S) は有毒なガスであり,代謝副産物である.
- ミトコンドリアの硫化キノン酸化還元酵素 (SQOR) は,H2Sを酸化し,コエンザイムQを還元することによって解毒する.
- SQORは,他のフラビン二硫化還元酵素と異なるユニークなシステイン三硫化共因子を持っています.
研究 の 目的:
- H2SによるSQOR活性化のメカニズムを調査する.
- H2Sの曝露がSQORの活動に影響するかどうかを判断する.
- SQOR 規制における翻訳後の変更の役割を明らかにする.
主な方法:
- 人間の結腸腺癌 (HT-29) と内皮細胞 (EA.hy926) をH2Sにさらす.
- SQORの活性とタンパク質のレベルを測定する.
- CRISPRのノックダウンを用いて硫黄トランスフェラーゼ (MPST,TST) を検出する.
- 薬学的な抑制とシスティン補給を用いる.
主要な成果:
- H2Sの曝露はHT-29細胞でSQORの活性を5倍,EA.hy926細胞で2倍に増加させた.
- SQORの増加はタンパク質濃度の上昇と関連せず,これは翻訳後の調節を示唆している.
- CRISPRのノックダウンは,SQORの活性化から硫黄トランスファーゼを除外した.
- H2Sは低分子量パーソルフィードではなく,SQORの活性を調節する.
結論:
- H2SによるSQORの活性化には,翻訳後のメカニズムが含まれています.
- システイン酸化と硫化物添加による三硫化物設置と活性化のモデルが提案されています.
- H2SはSQORの活動を自己調節し 細胞の保護反応を示唆する.
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