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http://www.tkuhn.ch/bel2nanopub/RAAeR4YvnzQpFdtgxtG1CVUZN-Cv-PKQSX_FruS43bxdU#_1
http://purl.obolibrary.org/obo/BFO_0000066
http://purl.bioontology.org/ontology/MSH/D008099
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bp(GO:"response to endoplasmic reticulum stress") -> bp(MESHPP:"Insulin Resistance")
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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BEL Framework Large Corpus Document
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1.4
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http://www.w3.org/ns/prov#value
Targeting of JNK using a synthetic inhibitor and/or an inhibitory peptide has been demonstrated to improve insulin action in obese mice and reduce atherosclerosis in the apoE-deficient rodent model (52, 53). These results directly demonstrate the therapeutic potential of JNK inhibitors in diabetes. TZDs, high-affinity ligands of PPARg, which are given clinically as insulin-sensitizing agents, likely improve insulin action through multiple mechanisms, including both activating lipid metabolism and reducing production of inflammatory mediators such as TNFalpha It has recently been demonstrated that mice in which the chaperone ORP150 is transgenically or adenovirally overexpressed exhibited reduced ER stress and improved insulin tolerance compared with controls, whereas reduction of the expression of this molecule in liver results in increased ER stress and insulin resistance
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Selventa
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2014-07-03T14:30:35.092+02:00
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