Stimulation of insulin signaling and inhibition of JNK-AP1 activation protect cells from amyloid-β-induced signaling dysregulation and inflammatory response

From National Research Council Canada

DOIResolve DOI: https://doi.org/10.3233/JAD-131949
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Affiliation
  1. National Research Council of Canada. Human Health Therapeutics
FormatText, Article
Subjectactin; amyloid beta protein; amyloid beta protein[1-42]; anthra[1,9 cd]pyrazol 6(2h) one; early growth response factor 2; granulocyte macrophage colony stimulating factor; insulin; interleukin 2; interleukin 23; interleukin 23p19; interleukin 32; interleukin 6; interleukin 8; macrophage inflammatory protein 1beta; monocyte chemotactic protein 1; protein c jun; stress activated protein kinase; transcription factor AP 1; transcription factor E2F1; tumor necrosis factor alpha; tumor suppressor protein; cell growth; cell viability; cytokine release; cytotoxicity; densitometry; gene expression; human cell; immunoblotting; in vitro study; inflammation; insulin treatment; lipid oxidation; negative feedback; oxidative stress; protein expression; protein phosphorylation; signal transduction; transcription initiation; Western blotting
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LanguageEnglish
Peer reviewedYes
NPARC number21272247
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Record created2014-07-23
Record modified2020-04-22
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