IκB Kinase Promotes Tumorigenesis through Inhibition of Forkhead FOXO3a (PII:S0092-8674(04)00302-2)

By M. Hu, Dung‐Fang Lee, W. Xia, L. Golfman, Ou-Yang Fu, Jer-Yen Yang, Y. Zou, Shilai Bao, N. Hanada, H. Saso and 2 more. 2007

753 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/60e9f126eb1a1497e7d4cdc4dfcab7554b71bc0e

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In Molecular Biology

1. J. Villén
2. M. Hayden
3. Steven P. Gygi
4. S. Ghosh
5. A. Brunet
6. Robert F. Schwabe
7. Dervis A M Salih
8. R. Jove

Citations in the corpus

• A conserved MST-FOXO signaling pathway mediates oxidative-stress responses and extends life span. (2006, positive): “In a similar vein, the role of FOXOs in pathological states including cancer and diabetes mellitus (Hu et al., 2004; Nakae et al., 2002) points to the possibility that misregulation of MST-FOXO signaling might contribute to the pathogenesis of these disorders.”
• FoxO transcription factors; Regulation by AKT and 14-3-3 proteins. (2011, positive): “S644 is targeted by IKKb and this phosphorylation inhibits FoxO3 function by increasing its nuclear exclusion and degradation [113,114].”
• Integrating cell-signalling pathways with NF-κB and IKK function (2007, positive): “Consistent with its anti-apoptotic role, IKKβ has been shown to phosphorylate and inhibit FOXO3a, a transcription factor and tumour suppressor that can induce either apoptosis or cell-cycle arres”
• Redox regulation of FoxO transcription factors (2015, neutral): “Other IKKβ S644 [325] FoxO3a: inactivation, nuclear exclusion, degradation↑ [325]”
• ERK promotes tumorigenesis by inhibiting FOXO3a via MDM2-mediated degradation (2008, neutral): “FOXO3a was shown to be associated with tumour suppression activit”
• Deubiquitination and Stabilization of PD-L1 by CSN5 (2016, positive): “…cytokine TNF-a, which is mainly secreted by macrophages, promotes tumor growth by inducing cell survival (Wang et al., 2012), proliferation (Hu et al., 2004), angiogenesis (Lee et al., 2007), and epithelial-tomesenchymal transition (Li et al., 2012) via NF-kB activation. e aggressiveness.”
• FOXO transcription factors at the interface between longevity and tumor suppression (2005, neutral): “The degradation of FOXO transcription factors is mediated by the ubiquitin–proteasome pathway (Matsuzaki et al., 2003; Plas and Thompson, 2003; Aoki et al., 2004; Hu et al., 2004; Huang et al., 2005).”
• FoxO transcription factors in the maintenance of cellular homeostasis during aging. (2008, positive): “In line with these studies, the loss of FoxO transcriptional activity renders progenitor cells or tumor cells resistant to the cytostatic effects of extracellular effectors such as TGFb, which may contribute to tumor development (Figure 2) [30,33 ,34 ,84,85].”
• Off the beaten pathway: the complex cross talk between Notch and NF-κB (2008, positive): “44 IKK β also phosphorylates and inactivates proapoptotic transcription factor FOXO3a”