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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
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http://www.tkuhn.ch/bel2nanopub/RAW4HjC-x1vtROis7nD8NHmtBtipL1qmuit5Cd3LjdaUU#_1
http://purl.obolibrary.org/obo/RO_0002204
http://www.informatics.jax.org/marker/MGI:103556
http://www.tkuhn.ch/bel2nanopub/RAW4HjC-x1vtROis7nD8NHmtBtipL1qmuit5Cd3LjdaUU#_1
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
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http://www.tkuhn.ch/bel2nanopub/RAW4HjC-x1vtROis7nD8NHmtBtipL1qmuit5Cd3LjdaUU#_2
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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://amigo.geneontology.org/amigo/term/GO:0016301
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p(MGI:Cxcl12) -> kin(p(SFAM:"MAPK Erk1/2 Family"))
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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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SDF1alpha resulted in rapid activation of the extracellular signal-regulated kinase (ERK)1/2. This SDF1alpha-induced ERK activity was dose dependent and could be inhibited by pre-treatment of the cells with either pertussis toxin, an inactivator of G-protein-coupled receptors, or PD98059, a MEK1 inhibitor. Concomitant with ERK activation, SDF1alpha also activated the downstream transcription factor Ets, a substrate for ERK phosphorylation. Further, downstream activation of genes associated with cell survival, differentiation and migration was assessed using a G-protein-coupled receptor pathway-focused microarray. We found that 23 genes, including PDK1, Egr-1, Grm5, and E-selectin, were up-regulated by SDF1alpha.
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Selventa
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2014-07-03T14:32:42.539+02:00
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