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http://purl.bioontology.org/ontology/MSH/D017209
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http://purl.obolibrary.org/obo/BFO_0000066
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kin(p(HGNC:MAPK8)) -> bp(MESHPP:Apoptosis)
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p(HGNC:KRT8,pmod(P,S,73)) -| (kin(p(HGNC:MAPK8)) -> bp(MESHPP:Apoptosis))
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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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We generated transgenic mice that overexpress the human disease-associated K8 Gly61-to-Cys (G61C) variant and showed that G61C predisposes to liver injury and apoptosis and dramatically inhibits K8 phosphorylation at serine 73 (S73) via stress-activated kinases. This led us to generate mice that overexpress K8 S73-to-Ala (S73A), which mimicked the susceptibility of K8 G61C mice to injury, thereby providing a molecular link between K8 phosphorylation and disease-associated mutation. Upon apoptotic stimulation, G61C and S73A hepatocytes have persistent and increased nonkeratin proapoptotic substrate phosphorylation by stress-activated kinases, compared with wild-type hepatocytes, in association with an inability to phosphorylate K8 S73. Our findings provide the first direct link between patient-related human keratin variants and liver disease predisposition. The highly abundant cytoskeletal protein K8, and possibly other keratins with the conserved S73-containing phosphoepitope, can protect tissue from injury by serving as a phosphate \"sponge\" for stress-activated kinases and thereby provide a novel nonmechanical function for intermediate filament proteins.
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Selventa
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2014-07-03T14:30:43.899+02:00
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