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MOBP and HIP1 in multiple system atrophy: New α-synuclein partners in glial cytoplasmic inclusions implicated in the disease pathogenesis
Neuropathology and Applied Neurobiology ( IF 4.0 ) Pub Date : 2020-12-23 , DOI: 10.1111/nan.12688
Conceição Bettencourt 1, 2 , Yasuo Miki 1, 3 , Ignazio S Piras 4 , Rohan de Silva 2, 5 , Sandrine C Foti 1, 6 , Joshua S Talboom 4 , Tamas Revesz 1, 5, 6 , Tammaryn Lashley 1, 6 , Robert Balazs 1, 6 , Emmanuelle Viré 7 , Thomas T Warner 1, 2, 5 , Matt J Huentelman 4 , Janice L Holton 1, 2
Affiliation  

Multiple system atrophy (MSA) is a fatal neurodegenerative disease. Similar to Parkinson's disease (PD), MSA is an α-synucleinopathy, and its pathological hallmark consists of glial cytoplasmic inclusions (GCIs) containing α-synuclein (SNCA) in oligodendrocytes. We previously identified consistent changes in myelin-associated oligodendrocyte basic protein (MOBP) and huntingtin interacting protein 1 (HIP1) DNA methylation status in MSA. We hypothesized that if differential DNA methylation at these loci is mechanistically relevant for MSA, it should have downstream consequences on gene regulation.

中文翻译:

多系统萎缩中的 MOBP 和 HIP1:神经胶质细胞质内含物中的新 α-突触核蛋白伙伴与疾病发病机制有关

多系统萎缩(MSA)是一种致命的神经退行性疾病。与帕金森病(PD)类似,MSA是一种α-突触核蛋白病,其病理特征是少突胶质细胞中含有α-突触核蛋白(SNCA)的胶质细胞质包涵体(GCI)。我们之前发现 MSA 中髓磷脂相关少突胶质细胞碱性蛋白 ( MOBP ) 和亨廷顿蛋白相互作用蛋白 1 ( HIP1 ) DNA 甲基化状态的一致变化。我们假设,如果这些位点的差异 DNA 甲基化在机制上与 MSA 相关,那么它应该对基因调控产生下游影响。
更新日期:2020-12-23
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