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Literature summary for 2.3.2.2 extracted from

  • Reuter, S.; Schnekenburger, M.; Cristofanon, S.; Buck, I.; Teiten, M.H.; Daubeuf, S.; Eifes, S.; Dicato, M.; Aggarwal, B.B.; Visvikis, A.; Diederich, M.
    Tumor necrosis factor alpha induces gamma-glutamyltransferase expression via nuclear factor-kappaB in cooperation with Sp1 (2009), Biochem. Pharmacol., 77, 397-411.
    View publication on PubMed
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Organism

Organism UniProt Comment Textmining
Homo sapiens
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Source Tissue

Source Tissue Comment Organism Textmining
K-562 cell
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 Homo sapiens
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MEG-01 cell
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 Homo sapiens
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Expression

Organism Comment Expression
Homo sapiens tumor necrosis factor TNFalpha induces GGT promoter transactivation, mRNA and protein synthesis, as well as enzymatic activity. Remicade, a clinically used anti-TNFalpha antibody, small interfering RNA against p50 and p65 nuclear factor NF-kB isoforms, curcumin, a well characterized natural NF-kB inhibitor, as well as a dominant negative inhibitor IkBa, prevent GGT activation at various levels. Over-expression of receptor of TNFalpha-1, TNFR-associated factor-2 TRAF2, TNFR-1 associated death domain TRADD, dominant negative IkBa or NF-kB p65 further confirm GGT promoter activation via NF-kB.Mutation of the NF-kB site located at 110 additionally inhibits TNFalpha-induced promoter induction up