Do proteomics analyses provide insights into reduced oxidative stress in the brain of an Alzheimer disease transgenic mouse model with an M631L amyloid precursor protein substitution and thereby the importance of amyloid-beta-resident methionine 35 in Alzheimer disease pathogenesis?

SultanaR.; RobinsonR.A.S.; BaderLangeM.; FioriniA.; GalvanV.; FombonneJ.; BakerA.; GorostizaO.; ZhangJ.; CaiJ.; PierceW.M.; BredesenD.E.; AllanButterfieldD.

首页> 外文期刊>Antioxidants and redox signalling >Do proteomics analyses provide insights into reduced oxidative stress in the brain of an Alzheimer disease transgenic mouse model with an M631L amyloid precursor protein substitution and thereby the importance of amyloid-beta-resident methionine 35 in Alzheimer disease pathogenesis?

【24h】

Do proteomics analyses provide insights into reduced oxidative stress in the brain of an Alzheimer disease transgenic mouse model with an M631L amyloid precursor protein substitution and thereby the importance of amyloid-beta-resident methionine 35 in Alzheimer disease pathogenesis?

机译：蛋白质组学分析是否可提供有关M631L淀粉样蛋白前体蛋白替代的阿尔茨海默氏病转基因小鼠模型脑部氧化应激降低的见解，以及淀粉样蛋白-β-蛋氨酸35在阿尔茨海默氏病发病机理中的重要性？

获取原文

获取原文并翻译 | 示例

掌桥外文数据库（机构版） >>

开具论文收录证明 >>

文献代查 >>

页面导航

摘要
著录项
相似文献
相关主题

摘要

The single methionine (Met/M) residue of amyloid-beta (Aβ) peptide, at position 35 of the 42-mer, has important relevance for Aβ-induced oxidative stress and neurotoxicity. Recent in vivo brain studies in a transgenic (Tg) Alzheimer disease (AD) mouse model with Swedish and Indiana familial AD mutations in human amyloid precursor protein (APP) (referred to as the J20 Tg mouse) demonstrated increased levels of oxidative stress. However, the substitution of the Met631 residue of APP to leucine (Leu/L) (M631L in human APP numbering, referred to as M631L Tg and corresponding to residue 35 of Aβ1-42) resulted in no significant in vivo oxidative stress levels, thereby supporting the hypothesis that Met-35 of Aβ contributes to oxidative insult in the AD brain. It is conceivable that oxidative stress mediated by Met-35 of Aβ is important in regulating numerous downstream effects, leading to differential levels of relevant biochemical pathways in AD. Therefore, in the current study using proteomics, we tested the hypothesis that several brain proteins involved in pathways such as energy and metabolism, antioxidant activity, proteasome degradation, and pH regulation are altered in J20Tg versus M631L Tg AD mice.

机译：淀粉样β（Aβ）肽的单个蛋氨酸（Met / M）残基位于42-mer的35位，与Aβ诱导的氧化应激和神经毒性具有重要的关系。最近在人类淀粉样蛋白前体蛋白（APP）（称为J20 Tg小鼠）中具有瑞典和印第安纳家族AD突变的转基因（Tg）阿尔茨海默病（AD）小鼠模型中的体内大脑研究表明，氧化应激水平升高。然而，将APP的Met631残基替换为亮氨酸（Leu / L）（人APP编号中的M631L，称为M631L Tg，对应于Aβ1-42的残基35）导致体内氧化应激水平不显着，因此支持Aβ的Met-35有助于AD脑氧化损伤的假说。可以想象，由Aβ的Met-35介导的氧化应激在调节众多下游效应中很重要，从而导致AD中相关生化途径的水平不同。因此，在当前使用蛋白质组学的研究中，我们测试了以下假设：J20Tg与M631L Tg AD小鼠相比，参与能量和代谢，抗氧化活性，蛋白酶体降解和pH调节等途径的几种脑蛋白发生了改变。

著录项

来源
《Antioxidants and redox signalling》 |2012年第11期|共8页
作者
SultanaR.; RobinsonR.A.S.; BaderLangeM.; FioriniA.; GalvanV.; FombonneJ.; BakerA.; GorostizaO.; ZhangJ.; CaiJ.; PierceW.M.; BredesenD.E.; AllanButterfieldD.;
展开▼
作者单位

展开▼
收录信息
原文格式 PDF
正文语种 eng
中图分类基础医学;
关键词

相似文献

外文文献
专利

1. Do proteomics analyses provide insights into reduced oxidative stress in the brain of an Alzheimer disease transgenic mouse model with an M631L amyloid precursor protein substitution and thereby the importance of amyloid-beta-resident methionine 35 in Alzheimer disease pathogenesis? [J] . SultanaR., RobinsonR.A.S., BaderLangeM., Antioxidants and redox signalling . 2012,第11期

机译：蛋白质组学分析是否可提供有关M631L淀粉样蛋白前体蛋白替代的阿尔茨海默氏病转基因小鼠模型脑部氧化应激降低的见解，以及淀粉样蛋白-β-蛋氨酸35在阿尔茨海默氏病发病机理中的重要性？
2. Do proteomics analyses provide insights into reduced oxidative stress in the brain of an Alzheimer disease transgenic mouse model with an M631L amyloid precursor protein substitution and thereby the importance of amyloid-beta-resident methionine 35 in Alzheimer disease pathogenesis? [J] . SultanaR., RobinsonR.A.S., BaderLangeM., Antioxidants and redox signalling . 2012,第11期

机译：蛋白质组学分析是否为具有M631L淀粉样蛋白前体蛋白质取代的阿尔茨海默病转基因小鼠模型的脑中的脑大脑中的洞察力提供了深入的氧化应激，从而在阿尔茨海默病发病机制中的淀粉样蛋白β-血液蛋氨酸35的重要性？
3. DIFFERENTIAL EXPRESSION AND REDOX PROTEOMICS ANALYSES OF AN ALZHEIMER DISEASE TRANSGENIC MOUSE MODEL: EFFECTS OF THE AMYLOID-beta PEPTIDE OF AMYLOID PRECURSOR PROTEIN [J] . R. A. S. ROBINSON, M. B. LANGE, R. SULTANA, Neuroscience: An International Journal under the Editorial Direction of IBRO . 2011,第Null期

机译：老年痴呆症转基因小鼠模型的差异表达和氧化还原蛋白质组学分析：淀粉样前体蛋白的淀粉样β肽的影响
4. Proteomic Imaging of amyloids in Brains from Amyloid Precursor Protein (APP) Transgenic Mice in comparison with Human Alzheimer Amyloid [C] . Masaya Ikegawa, Tomohiro Miyasaka, Noriyuki Iwasaki, ASMS Conference on Mass Spectrometry and Allied Topics . 2015

机译：淀粉样蛋白前体蛋白（APP）转基团的淀粉样蛋白淀粉样蛋白蛋白质组学成像与人阿尔茨海默蛋白相比
5. Amyloid beta-peptide (1-42)-mediated oxidative stress and neurotoxicity: I. The role of methionine 35. II. Proteomic identification of specifically oxidized proteins in models of Alzheimer's disease. [D] . Boyd-Kimball, Debra Lynn. 2004

机译：淀粉样β-肽（1-42）介导的氧化应激和神经毒性：I.蛋氨酸的作用35. II。蛋白质组学鉴定阿尔茨海默病模型中特定氧化的蛋白质。
6. Do Proteomics Analyses Provide Insights into Reduced Oxidative Stress in the Brain of an Alzheimer Disease Transgenic Mouse Model with an M631L Amyloid Precursor Protein Substitution and Thereby the Importance of Amyloid-Beta-Resident Methionine 35 in Alzheimer Disease Pathogenesis? [O] . Rukhsana Sultana, Renã A. S. Robinson, Miranda Bader Lange, -1

机译：蛋白质组学分析是否能为减少M631L淀粉样前体蛋白替代的阿尔茨海默氏病转基因小鼠模型的大脑中的氧化应激提供见解从而使淀粉样β-常驻蛋氨酸35在阿尔茨海默氏病发病机理中的重要性？
7. Do Proteomics Analyses Provide Insights into Reduced Oxidative Stress in the Brain of an Alzheimer Disease Transgenic Mouse Model with an M631L Amyloid Precursor Protein Substitution and Thereby the Importance of Amyloid-Beta-Resident Methionine 35 in Alzheimer Disease Pathogenesis? [O] . Rukhsana Sultana, Renã A. S. Robinson, Miranda Bader Lange, 2012

机译：蛋白质组学分析是否为具有M631L淀粉样蛋白前体蛋白质取代的阿尔茨海默病转基因小鼠模型的脑中的脑部中的氧化胁迫降低，从而在阿尔茨海默病发病机制中的淀粉样蛋白 - β-植物蛋氨酸35的重要性？

Do proteomics analyses provide insights into reduced oxidative stress in the brain of an Alzheimer disease transgenic mouse model with an M631L amyloid precursor protein substitution and thereby the importance of amyloid-beta-resident methionine 35 in Alzheimer disease pathogenesis?

摘要

著录项

相似文献

相关主题

期刊订阅