Nanopublications

Matches in Nanopublications for { ?s ?p ?o <http://www.tkuhn.ch/bel2nanopub/RA7pcf8b78X0k3XoClf75k2Qqh004jkndkz3X703AaDP8#provenance>. }

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_5 label "Selventa" provenance.
large_corpus.bel title "BEL Framework Large Corpus Document" provenance.
large_corpus.bel description "Approximately 61,000 statements." provenance.
large_corpus.bel version "20131211" provenance.
large_corpus.bel authoredBy _5 provenance.
assertion wasDerivedFrom large_corpus.bel provenance.
assertion wasDerivedFrom _4 provenance.
assertion hadPrimarySource 17568773 provenance.
_4 wasQuotedFrom 17568773 provenance.
_4 value "Foxh1 and Smads bind the Mixl1 promoter and mediate the TGFbeta-dependent induction of Mixl1. (A, C, F, G, I) HepG2 cells were transiently transfected with the Mixl1-luc reporter, Foxh1 and Smads (S2, S3, S4), Cripto, ActRIB or ActRII, as indicated. Error bars represent standard deviation of the mean. (B, D, E, H) EMSA. A 248-bp Mixl1 promoter fragment containing a wild-type or mutated Foxh1-binding site was incubated with bacterially expressed proteins (B, E) or crude extracts from COS-1 cells transiently transfected with the indicated DNA (D, H). Protein?DNA complexes were visualized by autoradiography. For supershift assays (D, H), anti-myc (M), anti-Flag (F), and anti-Smad4 (S4) antibodies were added to the reactions.Co-expression of Foxh1 with the Mixl1-luc reporter yielded strong TGFbeta-dependent activation of the Mixl1-luc reporter (Figure 1A). Direct binding of Foxh1 to the Mixl1 promoter fragment was confirmed by electrophoretic mobility shift assays (EMSA) using bacterially expressed Foxh1 (Figure 1B). Moreover, Smad2 and Smad4 enhanced both the basal and TGFbeta-induced Foxh1-dependent activation of the Mixl1-luc reporter (Figure 1C)." provenance.