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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://www.nanopub.org/nschema#Nanopublication
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http://www.tkuhn.ch/bel2nanopub/RAwjjOXJC8FZjTH4dq7GZBYDCT5-n33Gr3StSWqOcHV08#_1
http://purl.obolibrary.org/obo/RO_0002204
http://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=11920
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http://www.w3.org/1999/02/22-rdf-syntax-ns#object
http://resource.belframework.org/belframework/20131211/namespace/selventa-legacy-diseases/T-cell%20apoptosis
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http://www.w3.org/2000/01/rdf-schema#label
p(HGNC:FAS) -> path(SDIS:"T-cell apoptosis")
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http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel
http://purl.org/dc/elements/1.1/description
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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activation of protein kinase C (PKC) by phorbol 12-myristate 13-acetate (PMA) mimicked the effects of IFN-alpha2 [in inhibiting t-cell apoptosis]. Furthermore, the bis-indolylmaleimide GF 109203X, a specific inhibitor of PKC, inhibited the effect of PMA as well as that of IFN-alpha2 on Apo-1/Fas-induced apoptosis. These results point to a PKC-dependent mechanism of transient interaction between the intracellular signaling along the IFN-alpha2 and the Apo-1/Fas pathway (downstream of MAPK signaling
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http://www.w3.org/ns/prov#wasQuotedFrom
http://www.ncbi.nlm.nih.gov/pubmed/8977313
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http://www.w3.org/2000/01/rdf-schema#label
Selventa
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http://www.w3.org/ns/prov#hadPrimarySource
http://www.ncbi.nlm.nih.gov/pubmed/8977313
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http://www.w3.org/ns/prov#wasDerivedFrom
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http://www.tkuhn.ch/bel2nanopub/RAwjjOXJC8FZjTH4dq7GZBYDCT5-n33Gr3StSWqOcHV08#pubinfo
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2014-07-03T14:33:55.488+02:00
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