Title : Loss of p53 enhances catalytic activity of IKKbeta through O-linked beta-N-acetyl glucosamine modification.

Pub. Date : 2009 Mar 3

PMID : 19202066






3 Functional Relationships(s)
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1 Recently, we have shown that p53 regulates glucose metabolism through the IKK-NF-kappaB pathway and that, in the absence of p53, the positive feedback loop between IKK-NF-kappaB and glycolysis has an integral role in oncogene-induced cell transformation. Glucose tumor protein p53 Homo sapiens
2 In p53-deficient cells, the O-GlcNAcylated IKKbeta and the activating phosphorylation of IKK were decreased by p65/NF-kappaB knockdown or glucose depletion. Glucose tumor protein p53 Homo sapiens
3 Taken together, we propose a novel mechanism for the enhancement of NF-kappaB activity by loss of p53, which evokes positive feedback regulation from enhanced glucose metabolism to IKK in oncogenesis. Glucose tumor protein p53 Homo sapiens