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000140512 0247_ $$2doi$$a10.1016/j.neurobiolaging.2018.11.026
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000140512 037__ $$aDZNE-2020-06834
000140512 041__ $$aEnglish
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000140512 1001_ $$0P:(DE-2719)2810282$$aPickhardt, Marcus$$b0$$eFirst author$$udzne
000140512 245__ $$aScreening of a neuronal cell model of tau pathology for therapeutic compounds.
000140512 260__ $$aAmsterdam [u.a.]$$bElsevier Science$$c2019
000140512 264_1 $$2Crossref$$3print$$bElsevier BV$$c2019-04-01
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000140512 520__ $$aWe have developed a cell-based phenotypic automated high-content screening approach for N2a cells expressing the pro-aggregant repeat domain of tau protein (tauRDΔK), which allows analysis of a chemogenomic library of 1649 compounds for their effect on the inhibition or stimulation of intracellular tau aggregation. We identified several inhibitors and stimulators of aggregation and achieved a screening reproducibility >85% for all data. We identified 18 potential inhibitors (= 1.1% of the library) and 10 stimulators (= 0.6% of the library) of tau aggregation in this cell model of tau pathology. The results provide insights into the regulation of cellular tau aggregation and the pathways involved in this process (e.g., involving signaling via p38 mitogen-activated protein kinase, histone deacetylases, vascular endothelial growth factor, rho/ROCK). For example, inhibitors of protein kinases (e.g., p38) can reduce tau aggregation, whereas inhibitors of deacetylases (histone deacetylases) can enhance aggregation. These observations are compatible with reports that phosphorylated or acetylated tau promotes pathology.
000140512 536__ $$0G:(DE-HGF)POF3-342$$a342 - Disease Mechanisms and Model Systems (POF3-342)$$cPOF3-342$$fPOF III$$x0
000140512 542__ $$2Crossref$$i2019-04-01$$uhttps://www.elsevier.com/tdm/userlicense/1.0/
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000140512 650_7 $$2NLM Chemicals$$aEnzyme Inhibitors
000140512 650_7 $$2NLM Chemicals$$aHistone Deacetylase Inhibitors
000140512 650_7 $$2NLM Chemicals$$atau Proteins
000140512 650_7 $$0EC 2.7.11.24$$2NLM Chemicals$$ap38 Mitogen-Activated Protein Kinases
000140512 650_7 $$0EC 3.5.1.98$$2NLM Chemicals$$aHistone Deacetylases
000140512 650_2 $$2MeSH$$aCell Line
000140512 650_2 $$2MeSH$$aDrug Evaluation, Preclinical: methods
000140512 650_2 $$2MeSH$$aEnzyme Inhibitors: pharmacology
000140512 650_2 $$2MeSH$$aHistone Deacetylase Inhibitors
000140512 650_2 $$2MeSH$$aHistone Deacetylases: pharmacology
000140512 650_2 $$2MeSH$$aHumans
000140512 650_2 $$2MeSH$$aModels, Biological
000140512 650_2 $$2MeSH$$aProtein Aggregation, Pathological: genetics
000140512 650_2 $$2MeSH$$aProtein Aggregation, Pathological: metabolism
000140512 650_2 $$2MeSH$$aSignal Transduction: genetics
000140512 650_2 $$2MeSH$$aSignal Transduction: physiology
000140512 650_2 $$2MeSH$$aTauopathies: drug therapy
000140512 650_2 $$2MeSH$$aTauopathies: genetics
000140512 650_2 $$2MeSH$$aTauopathies: metabolism
000140512 650_2 $$2MeSH$$ap38 Mitogen-Activated Protein Kinases: antagonists & inhibitors
000140512 650_2 $$2MeSH$$atau Proteins: metabolism
000140512 7001_ $$0P:(DE-2719)2810678$$aTassoni, Michele$$b1$$udzne
000140512 7001_ $$0P:(DE-2719)2810245$$aDenner, Philip$$b2$$udzne
000140512 7001_ $$0P:(DE-2719)2810323$$aKurkowsky, Birgit$$b3$$udzne
000140512 7001_ $$0P:(DE-2719)2810578$$aKitanovic, Ana$$b4$$udzne
000140512 7001_ $$0P:(DE-2719)2810422$$aMöhl, Christoph$$b5$$udzne
000140512 7001_ $$0P:(DE-2719)2159508$$aFava, Eugenio$$b6$$udzne
000140512 7001_ $$0P:(DE-2719)2541671$$aMandelkow, Eckhard$$b7$$eLast author$$udzne
000140512 77318 $$2Crossref$$3journal-article$$a10.1016/j.neurobiolaging.2018.11.026$$b : Elsevier BV, 2019-04-01$$p24-34$$tNeurobiology of Aging$$v76$$x0197-4580$$y2019
000140512 773__ $$0PERI:(DE-600)1498414-3$$a10.1016/j.neurobiolaging.2018.11.026$$gVol. 76, p. 24 - 34$$p24-34$$q76<24 - 34$$tNeurobiology of aging$$v76$$x0197-4580$$y2019
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