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Matches in Nanopublications for { ?s ?p ?o <http://www.tkuhn.ch/bel2nanopub/RAElaX19tWulTS8RKgmfUNaz5nFWN7tXkUmw0A6WY8kn8#provenance>. }

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_6 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 _6 provenance.
assertion wasDerivedFrom large_corpus.bel provenance.
assertion wasDerivedFrom _5 provenance.
assertion hadPrimarySource 16236716 provenance.
_5 wasQuotedFrom 16236716 provenance.
_5 value "Repression of these SMC1{beta} promoter constructs by E2F6 was confirmed by inhibition of reporter gene expression by overexpressed E2F6 (Fig. 2C). A point mutant of E2F6 defective in DNA binding (E68) (6) had no effect on reporter gene expression, demonstrating that repression of SMC1{beta} by E2F6 depends on sequence-specific DNA-binding. The -26 promoter had equal activity in wild-type and E2f6-/- cells and was not repressed by the coexpression of E2F6. This finding suggests that an E2F6-responsive site is located between nucleotides -26 and -129 of the SMC1{beta} promoter. Examination of this part of the promoter sequence showed that it contains a potential E2F binding site (see Fig. 2D). To test whether this E2F site is required for repression of the SMC1{beta} promoter by E2F6, we mutated the E2F element and analyzed the activity of the mutated reporter construct in E2f6+/+ and E2f6-/- cells (Fig. 2E). The mutated reporter gene had equal activity in E2f6+/+ and E2f6-/- cells, demonstrating that the E2F site is required for repression by E2F6. " provenance.