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TextLocation
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Abstract
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a(CHEBI:"calcium(2+)") -| (p(HGNC:IL1B) -> tscript(complex(NCH:"Nfkb Complex")))
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p(HGNC:IL1B) -> tscript(complex(NCH:"Nfkb Complex"))
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Approximately 2000 hand curated statements drawn from 57 PubMeds.
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Copyright (c) 2011-2012, Selventa. All Rights Reserved.
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BEL Framework Small Corpus Document
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Creative Commons Attribution-Non-Commercial-ShareAlike 3.0 Unported License
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1.6
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However, IL-1β-induced NF-κB activity is attenuated by increased intracellular calcium
in response to ionomycin, UTP, or thapsigargin or by overexpression of CaMKKc
and/or Akt. Ionomycin and CaMKKc overexpression increases Akt phosphorylation
on Thr308 and enzyme activity. Under these conditions or upon overexpression of
wild type Akt, IL-1β-induced IKKβ activity is diminished. Furthermore, a dominant
negative mutant of Akt abolishes IKKβ inhibition by CaMKKc and ionomycin, suggesting
that Akt acts as a mediator of CaMKK signaling to inhibit IL-1β-induced
IKK activity at an upstream target site.
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http://www.ncbi.nlm.nih.gov/pubmed/11976320
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support@belframework.org
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Selventa
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2014-07-03T14:29:32.783+02:00
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