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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/RA8RTmnOwEtxyfAy-5iUivnhiD7ypLavwgr9h0sYcmZ-A#_1
http://semanticscience.org/resource/SIO_000139
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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://amigo.geneontology.org/amigo/term/GO:0042789
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http://purl.obolibrary.org/obo/RO_0002204
http://www.informatics.jax.org/marker/MGI:99252
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tscript(p(MGI:Egr4)) -> r(MGI:Slc12a5)
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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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Electrophoretic mobility shift assay confirmed specific Egr4 binding to Egr4(KCC2). Interference RNA-mediated knock-down of Egr4 and a dominant-negative isoform of Egr4 significantly inhibited KCC2 reporter induction and endogenous KCC2 expression in cultured neurons. Together, the results indicate an important role for Egr4 in the developmental upregulation of KCC2 gene expression.
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Selventa
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2014-07-03T14:33:07.732+02:00
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