文化大學機構典藏 CCUR:Item 987654321/49513
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    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: https://irlib.pccu.edu.tw/handle/987654321/49513


    题名: The NF kappa B Antagonist CDGSH Iron-Sulfur Domain 2 Is a Promising Target for the Treatment of Neurodegenerative Diseases
    作者: Kung, WM (Kung, Woon-Man)
    Lin, MS (Lin, Muh-Shi)
    贡献者: 運健系
    关键词: neurodegenerative disease
    CISD2
    proinflammatory response
    mitochondrial dysfunction
    NF954
    B
    日期: 2021
    上传时间: 2021-04-24 14:26:23 (UTC+8)
    摘要: Proinflammatory response and mitochondrial dysfunction are related to the pathogenesis of neurodegenerative diseases (NDs). Nuclear factor kappa B (NF kappa B) activation has been shown to exaggerate proinflammation and mitochondrial dysfunction, which underlies NDs. CDGSH iron-sulfur domain 2 (CISD2) has been shown to be associated with peroxisome proliferator-activated receptor-beta (PPAR-beta) to compete for NF kappa B and antagonize the two aforementioned NF kappa B-provoked pathogeneses. Therefore, CISD2-based strategies hold promise in the treatment of NDs. CISD2 protein belongs to the human NEET protein family and is encoded by the CISD2 gene (located at 4q24 in humans). In CISD2, the [2Fe-2S] cluster, through coordinates of 3-cysteine-1-histidine on the CDGSH domain, acts as a homeostasis regulator under environmental stress through the transfer of electrons or iron-sulfur clusters. Here, we have summarized the features of CISD2 in genetics and clinics, briefly outlined the role of CISD2 as a key physiological regulator, and presented modalities to increase CISD2 activity, including biomedical engineering or pharmacological management. Strategies to increase CISD2 activity can be beneficial for the prevention of inflammation and mitochondrial dysfunction, and thus, they can be applied in the management of NDs.
    關聯: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES 卷冊: 22 期: 2 文獻號碼: 934
    显示于类别:[運動與健康促進學系] 期刊論文

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