Activated p53 induces NF-κB DNA binding but suppresses its transcriptional activation

Kawauchi, Keiko; Araki, Keigo; Tobiume, Kei; Tanaka, Nobuyuki

doi:10.1016/j.bbrc.2008.05.021

Cited by 61 publications

(52 citation statements)

References 23 publications

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“…Our data and a recent report (Kawauchi et al, 2008a) reveal physical interactions between p65 and p53, which may allow an IkB kinase a-dependent transit of CBP (Huang et al, 2007). The fact that p53 binding to a region in the N-terminal part of p65 does not disrupt IkB kinase a binding to the C-terminal transactivation domain is furthermore compatible with a transcriptionally active p53/p65 complex (Kawauchi et al, 2008a). Future studies will clarify the exact composition of this protein assembly likely comprising additional proteins.…”

Section: Control Of Activated Nf-jb By P53supporting

confidence: 69%

“…Although we could not detect a lack of ATM or CHK1 activation in HU-treated HCT-116 p53À cells, these kinases could regulate p53-dependent NF-kB actions, possibly collateral with RSK1 and MEK1 that govern the nuclear p53/p65 cross talk (Armstrong et al, 1995;Ryan et al, 2000;Bohuslav et al, 2004;Yoshida et al, 2008). Our data and a recent report (Kawauchi et al, 2008a) reveal physical interactions between p65 and p53, which may allow an IkB kinase a-dependent transit of CBP (Huang et al, 2007). The fact that p53 binding to a region in the N-terminal part of p65 does not disrupt IkB kinase a binding to the C-terminal transactivation domain is furthermore compatible with a transcriptionally active p53/p65 complex (Kawauchi et al, 2008a).…”

Section: Control Of Activated Nf-jb By P53contrasting

confidence: 52%

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Cross talk between stimulated NF-κB and the tumor suppressor p53

et al. 2010

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Nuclear factor-jB (NF-jB) and p53 critically determine cancer development and progression. Defining the cross talk between these transcription factors can expand our knowledge on molecular mechanisms of tumorigenesis. Here, we show that induction of replicational stress activates NF-jB p65 and triggers its interaction with p53 in the nucleus. Experiments with knockout cells show that p65 and p53 are both required for enhanced NF-jB activity during S-phase checkpoint activation involving ataxiatelangiectasia mutated and checkpoint kinase-1. Accordingly, the pro-inflammatory cytokine tumor necrosis factora (TNF-a) also triggers formation of a transcriptionally active complex containing nuclear p65 and p53 on jB response elements. Gene expression analyses revealed that, independent of NF-jB activation in the cytosol, TNFinduced NF-jB-directed gene expression relies on p53. Hence, p53 is unexpectedly necessary for NF-jB-mediated gene expression induced by atypical and classical stimuli. Remarkably, data from gain-and loss-of function approaches argue that anti-apoptotic NF-jB p65 activity is constitutively evoked by a p53 hot-spot mutant frequently found in tumors. Our observations suggest explanations for the outstanding question why p53 mutations rather than p53 deletions arise in tumors of various origins.

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Section: Control Of Activated Nf-jb By P53supporting

confidence: 69%

Section: Control Of Activated Nf-jb By P53contrasting

confidence: 52%

Cross talk between stimulated NF-κB and the tumor suppressor p53

et al. 2010

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“…Previous studies have demonstrated that RelA can directly bind to the Glut3 promoter (33) and repress Glut3 transcription in the presence of p53 (34). As p53 is expressed in SH-SY5Y cells (35), RelA appears to act as a transcriptional repressor of Glut3 in these cells.…”

Section: Discussionmentioning

confidence: 95%

MicroRNA-7 Promotes Glycolysis to Protect against 1-Methyl-4-phenylpyridinium-induced Cell Death

Chaudhuri

Kabaria

Choi

et al. 2015

Journal of Biological Chemistry

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“…Then, increasing OGlcNAcylation of IKK␤ that sensitizes it to activation by inflammatory cytokines such as TNF␣ may affect the positive feedback loop regulation of NF-B activation in tumors. We recently showed that activated p53 inhibits the kinase activity of IKK␤ through direct binding (27). Moreover, it has been shown that O-GlcNAcylation stabilizes p53 (28).…”

Section: Discussionmentioning

confidence: 99%

“…In conclusion, we have found a novel mechanism by which glucose metabolism enhances the IKK-NF-B signaling pathway through O-linked glycosylation of IKK␤. Because p53 suppresses IKK activity, NF-B transcriptional activity (15,27) and decreases glycolysis (14), restriction of the positive feedback loop by p53 may be an important role in the tumor surveillance system (Fig. 5C).…”

Section: Discussionmentioning

confidence: 99%