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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
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http://www.tkuhn.ch/bel2nanopub/RABJxfvSUljX1H8y-HHreYq5NRYfrDiTqaskXpuGhxb6o#_1
http://semanticscience.org/resource/SIO_000139
http://www.tkuhn.ch/bel2nanopub/RABJxfvSUljX1H8y-HHreYq5NRYfrDiTqaskXpuGhxb6o#_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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http://purl.obolibrary.org/obo/RO_0002204
http://www.informatics.jax.org/marker/MGI:1861437
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http://resource.belframework.org/belframework/20131211/namespace/selventa-legacy-diseases/cardiomyocyte%20hypertrophy
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kin(p(MGI:Gsk3b)) -| path(SDIS:"cardiomyocyte hypertrophy")
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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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This observation, together with the very rapid kinetics of GSK3-beta phosphorylation in response to aortic coarctaction, supports the hypothesis that melusin selectively senses the biomechanical stimuli. In contrast to other kinases, GSK3-beta is highly active in unstimulated cells and becomes inactivated by phosphorylation of serine 9 in response to several stimuli28. Recent studies have shown that this inactivation is required for cardiac hypertrophy. In cardiomyocytes, active GSK3-beta phosphorylates the transcription factors NF-AT and GATA4, inducing their translocation from the nucleus to the cytoplasm and thus inhibiting their transcriptional activity25-27. In addition, active GSK3-beta also induces inhibition of elF2B, a principal initiation factor regulating protein synthesis.
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Selventa
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2014-07-03T14:31:57.570+02:00
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