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http://purl.obolibrary.org/obo/RO_0002204
http://www.informatics.jax.org/marker/MGI:96570
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http://amigo.geneontology.org/amigo/term/GO:0016301
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p(MGI:Inhba) -> kin(p(MGI:Acvr1c))
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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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As shown in Fig. 3A, activins AB and B augmented (SBE)4-lux reporter activity in MIN6 cells. To verify that activin isoforms signal is mediated via ALK7 in MIN6 cells, we measured the activity of the dominant negative ALK7 construct (D/N ALK7 cDNA). D/N ALK7 cDNA lacks the intracellular kinase domain but retains the extracellular and transmembrane domains. The specificity of D/N ALK7 was confirmed in HEK293 cells (Fig. 3B). The activity of ALK4-dependent activin signaling was barely affected in the D/N ALK7 construct, but the ALK7-augmented response to activins B and AB was significantly inhibited. Thus, D/N ALK7 is a dominant negative inhibitor of ALK7 signaling but not of the ALK4 pathway ( Fig. 3B). As shown in Fig. 3C, D/N ALK7 completely blocked the responses of MIN6 cells to activins AB and B, confirming that activin isoforms signal via ALK7 in MIN6 cells
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Selventa
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2014-07-03T14:32:22.482+02:00
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