Human Platelet Derived Mitochondrial OPA-1 Isoforms and Interaction With TDP-43 in Neurodegenerative Diseases.

Missouri medicine Pub Date : 2024-01-01
Su Han Lee, Duyen Pham, Edina Kosa, Abdulbaki Agbas
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引用次数: 0

Abstract

Optic atrophy 1(OPA1) is a GTPase protein that controls mitochondrial fusion, cristae integrity, and mtDNA maintenance. In neurodegenerative diseases such as Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), the mitochondrial network morphology is compromised. Studies on TAR-DNA binding protein 43 (TDP-43) has been the focus in our lab. OPA1 and TDP-43 interaction may shed a light on how aberrant TDP-43 interacts with OPA1, which will lead to mitochondrial dysfunction. The preliminary study tested the idea of whether OPA1 and TDP-43 are physically interacting in human platelet derived mitochondria obtained from healthy human subjects.

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人血小板衍生线粒体 OPA-1 异构体及与神经退行性疾病中 TDP-43 的相互作用
视神经萎缩1(OPA1)是一种控制线粒体融合、嵴完整性和mtDNA维持的GTPase蛋白。在阿尔茨海默病(AD)、肌萎缩性脊髓侧索硬化症(ALS)和帕金森病(PD)等神经退行性疾病中,线粒体网络形态受到损害。对 TAR-DNA 结合蛋白 43(TDP-43)的研究一直是我们实验室的重点。OPA1和TDP-43的相互作用可能会揭示异常的TDP-43如何与OPA1相互作用,从而导致线粒体功能障碍。初步研究测试了 OPA1 和 TDP-43 是否在健康人血小板线粒体中发生物理相互作用。
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