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J Neurosci. 2007 Dec 12;27(50):13579-80. doi: 10.1523/JNEUROSCI.4821-07.2007.
2
Moderate reduction of gamma-secretase attenuates amyloid burden and limits mechanism-based liabilities.适度降低γ-分泌酶可减轻淀粉样蛋白负担并限制基于机制的不良反应。
J Neurosci. 2007 Oct 3;27(40):10849-59. doi: 10.1523/JNEUROSCI.2152-07.2007.
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Alzheimer research forum discussion: gain or loss of function - time to shake up assumptions on gamma-secretase in Alzheimer disease?阿尔茨海默病研究论坛讨论:功能获得还是功能丧失——是时候撼动关于阿尔茨海默病中γ-分泌酶的假设了?
J Alzheimers Dis. 2007 Jun;11(3):399-417. doi: 10.3233/jad-2007-11315.
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Genetic Deletion of Tumor Necrosis Factor-α Attenuates Amyloid-β Production and Decreases Amyloid Plaque Formation and Glial Response in the 5XFAD Model of Alzheimer's Disease.肿瘤坏死因子-α基因缺失可减少淀粉样β生成并降低阿尔茨海默病 5XFAD 模型中的淀粉样斑块形成和神经胶质反应。
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Monoamine oxidase B is elevated in Alzheimer disease neurons, is associated with γ-secretase and regulates neuronal amyloid β-peptide levels.单胺氧化酶 B 在阿尔茨海默病神经元中升高,与 γ-分泌酶相关,并调节神经元淀粉样 β-肽水平。
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Aβ reduction in BACE1 heterozygous null 5XFAD mice is associated with transgenic APP level.β-分泌酶1(BACE1)杂合缺失的5XFAD小鼠中淀粉样前体蛋白(Aβ)的减少与转基因淀粉样前体蛋白(APP)水平相关。
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Activation of peroxisome proliferator-activated receptor α stimulates ADAM10-mediated proteolysis of APP.过氧化物酶体增殖物激活受体α的激活刺激了ADAM10介导的淀粉样前体蛋白的蛋白水解。
Proc Natl Acad Sci U S A. 2015 Jul 7;112(27):8445-50. doi: 10.1073/pnas.1504890112. Epub 2015 Jun 15.
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Regulation of gamma-secretase activating protein by the 5Lipoxygenase: in vitro and in vivo evidence.5-脂氧合酶对γ-分泌酶激活蛋白的调控:体内外证据
Sci Rep. 2015 Jun 16;5:11086. doi: 10.1038/srep11086.

引用本文的文献

1
Discovery of a Tetrahydrobenzisoxazole Series of γ-Secretase Modulators.γ-分泌酶调节剂的四氢苯并异恶唑系列的发现。
ACS Med Chem Lett. 2017 Sep 19;8(10):1002-1006. doi: 10.1021/acsmedchemlett.7b00178. eCollection 2017 Oct 12.
2
gamma-Secretase heterogeneity in the Aph1 subunit: relevance for Alzheimer's disease.Aph1亚基中的γ-分泌酶异质性:与阿尔茨海默病的相关性
Science. 2009 May 1;324(5927):639-42. doi: 10.1126/science.1171176. Epub 2009 Mar 19.

本文引用的文献

1
Moderate reduction of gamma-secretase attenuates amyloid burden and limits mechanism-based liabilities.适度降低γ-分泌酶可减轻淀粉样蛋白负担并限制基于机制的不良反应。
J Neurosci. 2007 Oct 3;27(40):10849-59. doi: 10.1523/JNEUROSCI.2152-07.2007.
2
A specific amyloid-beta protein assembly in the brain impairs memory.大脑中一种特定的β-淀粉样蛋白聚集体会损害记忆。
Nature. 2006 Mar 16;440(7082):352-7. doi: 10.1038/nature04533.
3
Persistent amyloidosis following suppression of Abeta production in a transgenic model of Alzheimer disease.在阿尔茨海默病转基因模型中,抑制β淀粉样蛋白生成后持续存在的淀粉样变性。
PLoS Med. 2005 Dec;2(12):e355. doi: 10.1371/journal.pmed.0020355. Epub 2005 Nov 15.
4
Characterization of the reconstituted gamma-secretase complex from Sf9 cells co-expressing presenilin 1, nicastrin [correction of nacastrin], aph-1a, and pen-2.对共表达早老素1、尼卡斯特林[纠正为nicastrin]、APH-1A和PEN-2的Sf9细胞中重组γ-分泌酶复合物的表征。
Biochemistry. 2005 Mar 22;44(11):4450-7. doi: 10.1021/bi0481500.
5
Modulation of notch processing by gamma-secretase inhibitors causes intestinal goblet cell metaplasia and induction of genes known to specify gut secretory lineage differentiation.γ-分泌酶抑制剂对Notch加工的调节会导致肠道杯状细胞化生,并诱导已知可指定肠道分泌谱系分化的基因。
Toxicol Sci. 2004 Nov;82(1):341-58. doi: 10.1093/toxsci/kfh254. Epub 2004 Aug 19.
6
Notch1 functions as a tumor suppressor in mouse skin.Notch1在小鼠皮肤中作为一种肿瘤抑制因子发挥作用。
Nat Genet. 2003 Mar;33(3):416-21. doi: 10.1038/ng1099. Epub 2003 Feb 18.
7
Notch signaling in lymphocyte development.Notch信号通路在淋巴细胞发育中的作用
Semin Immunol. 2002 Dec;14(6):395-404. doi: 10.1016/s104453230200074x.
8
gamma-Secretase, Notch, Abeta and Alzheimer's disease: where do the presenilins fit in?γ-分泌酶、Notch、β淀粉样蛋白与阿尔茨海默病:早老素在其中扮演什么角色?
Nat Rev Neurosci. 2002 Apr;3(4):281-90. doi: 10.1038/nrn785.
9
Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse.用β-淀粉样蛋白免疫可减轻PDAPP小鼠的阿尔茨海默病样病理变化。
Nature. 1999 Jul 8;400(6740):173-7. doi: 10.1038/22124.

Moderate reduction of gamma-secretase: is there a therapeutic sweet spot?

作者信息

Choi Se Hoon, Norstrom Eric

机构信息

Committee on Neurobiology, University of Chicago, Chicago, Illinois 60637, USA.

出版信息

J Neurosci. 2007 Dec 12;27(50):13579-80. doi: 10.1523/JNEUROSCI.4821-07.2007.

DOI:10.1523/JNEUROSCI.4821-07.2007
PMID:18077669
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6673637/
Abstract
摘要