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http://www.tkuhn.ch/bel2nanopub/RAiHPhj4YdVr_ZxNDUVnOAOyPyQZjGdaIBsx7uvj7QfAQ
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http://www.tkuhn.ch/bel2nanopub/RAiHPhj4YdVr_ZxNDUVnOAOyPyQZjGdaIBsx7uvj7QfAQ#_1
http://semanticscience.org/resource/SIO_000139
http://www.tkuhn.ch/bel2nanopub/RAiHPhj4YdVr_ZxNDUVnOAOyPyQZjGdaIBsx7uvj7QfAQ#_2
http://www.tkuhn.ch/bel2nanopub/RAiHPhj4YdVr_ZxNDUVnOAOyPyQZjGdaIBsx7uvj7QfAQ#_1
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http://amigo.geneontology.org/amigo/term/GO:0042789
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http://purl.obolibrary.org/obo/BFO_0000066
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http://amigo.geneontology.org/amigo/term/GO:0034976
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bp(GO:"response to endoplasmic reticulum stress") -> tscript(p(HGNC:ATF6))
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel
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BEL Framework Large Corpus Document
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1.4
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A dominant negative form of ATF6 blocked ER stress induction of both ATF6 site and GRP78 reporter genes. We further found that GAL4-ATF6 could be activated by ER stress. These results demonstrate that ATF6 is a direct target of the ER stress response. A proximal sensor of the ER stress response, human IRE1 (hIRE1), was sufficient to activate the ATF6 reporter gene, while a dominant negative form of hIRE1 blocked ER stress activation, suggesting that hIRE1 is upstream of ATF6 in the ER stress signaling pathway.
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http://www.w3.org/ns/prov#wasQuotedFrom
http://www.ncbi.nlm.nih.gov/pubmed/10856300
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Selventa
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http://www.tkuhn.ch/bel2nanopub/RAiHPhj4YdVr_ZxNDUVnOAOyPyQZjGdaIBsx7uvj7QfAQ
http://purl.org/dc/terms/created
2014-07-03T14:29:51.318+02:00
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