De novo Mutation Enables NOTCH3ECD Aggregation and Mitochondrial Dysfunction via Interactions with BAX and BCL-2.

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第一作者： Ruijie,Liu

第一单位： Department of Neurology, Henan University People's Hospital, Henan Provincial People's Hospital, Zhengzhou, Henan, China.

作者： Ruijie,Liu ^[1] ; Chenhao,Gao ^[2] ; Junkui,Shang ^[3] ; Ruihua,Sun ^[1] ; Wenjing,Wang ^[2] ; Wei,Li ^[2] ; Dandan,Gao ^[3] ; Xuejing,Huo ^[4] ; Yingying,Shi ^[2] ; Yanliang,Wang ^[2] ; Fengyu,Wang ^[2] ; Jiewen,Zhang ^[1]

作者单位： Department of Neurology, Henan University People's Hospital, Henan Provincial People's Hospital, Zhengzhou, Henan, China. ^[1] Department of Neurology, Zhengzhou University People's Hospital, Henan Provincial People's Hospital, Zhengzhou, Henan, China. ^[2] Academy of Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China. ^[3] Department of Neurology, Xinxiang Medical University, Henan Provincial People's Hospital, Zhengzhou, Henan, China. ^[4] Henan Provincial Key Laboratory of Kidney Disease and Immunology, Zhengzhou University People's Hospital, Henan Provincial People's Hospital, Zhengzhou, Henan, China. ^[5]

关键词 Apoptosis CADASIL cysteine-sparing NOTCH3 mutation flow cytometry mitochondrial dysfunction

主题词 CADASIL(CADASIL);人类(Humans);线粒体(Mitochondria);突变(Mutation);原癌基因蛋白质c-bcl-2(Proto-Oncogene Proteins c-bcl-2);受体, Notch(Receptors, Notch);bcl-2相关X蛋白质(bcl-2-Associated X Protein)

DOI 10.3233/JAD-215256

PMID 35001891

发布时间 2022-05-31

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