p53 regulates glucose metabolism through an IKK-NF-κB pathway and inhibits cell transformation

By K. Kawauchi, Keigo Araki, K. Tobiume, N. Tanaka. Nature Cell Biology, 2008

658 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/afec2a4bdf125c5e0ec6fce2b30487bf779ed830

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Citations in the corpus

Analysis of cancer metabolism by imaging hyperpolarized nuclei: prospects for translation to clinical research. (2011, background): “[21] Kawauchi K, Araki K, Tobiume K, and Tanaka N (2008).”
Role of interleukin-6 in cancer progression and therapeutic resistance (2016, background): “induced p53 regulates glycolytic metabolism through NF-kBmediated mechanism, which also increases GLUT-2 and GLUT-4 receptors on the cells to enhance glycolysis [125].”
NF-κB, an Active Player in Human Cancers (2014, positive): “Tanaka and colleagues showed that NF-κ B activation in p53 −/− mouse embryonic fibroblasts (MEF) can increase glucose uptake by upregulating the expression of glucose transporter 3 (GLUT3) and maintaining a high glycolytic flux (37).”
Tumor suppression in the absence of p53-mediated cell cycle arrest, apoptosis, and senescence (2012, positive): “For example p53 suppresses the expression of glucose transporters such as GLUT3 (Kawauchi et al., 2008; Schwartzenberg-Bar-Yoseph et al., 2004), although the precise mechanism of this repression needs further elucidation.”
Reprogramming of glucose, fatty acid and amino acid metabolism for cancer progression (2015, positive): “suppressed by p53 [37].”
c-Myc and Cancer Metabolism (2012, positive): “Other work also suggests that p53-mediated regulation of glucose metabolism may be dependent on the transcription factor NFkB (65).”
Blinded by the Light: The Growing Complexity of p53. (2009, background): “These recently uncovered functions include modulating glucose uptake (Kawauchi et al., 2008), dampening glycolysis (Bensaad et al., 2006; Kondoh et al., 2005), and enhancing mitochondrial respiration (Ma et al., 2007).”
AMP-activated protein kinase inhibits NF-κB signaling and inflammation: impact on healthspan and lifespan (2011, background): “[70] observed that the lack of p53 protein expression clearly increased the rate of glycolysis and significantly stimulated the activity of NF-κB signaling.”
Cancer cell metabolism: Warburg and beyond. (2008, background): “Other work also suggests that p53-mediated regulation of glucose metabolism may be dependent on the transcription factor NF-κB (Kawauchi et al., 2008).”