2023
DOI: 10.1016/j.molmet.2023.101771
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Metabolic protein kinase signalling in neuroblastoma

William J. Smiles,
Luca Catalano,
Victoria E. Stefan
et al.
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Cited by 4 publications
(4 citation statements)
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“…Overall, this results in the self-renewal of tumour cells [ 45 ]. In fact, targeted therapy for MYCN is usually not possible since there are two extended α-helices in the DNA binding domain that do not allow for interaction with small molecules [ 46 ].…”
Section: Neuroblastoma and Oxidative Stressmentioning
confidence: 99%
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“…Overall, this results in the self-renewal of tumour cells [ 45 ]. In fact, targeted therapy for MYCN is usually not possible since there are two extended α-helices in the DNA binding domain that do not allow for interaction with small molecules [ 46 ].…”
Section: Neuroblastoma and Oxidative Stressmentioning
confidence: 99%
“…These cells can shift from glycolysis for oxidative phosphorylation when glucose availability is limited. Overall, MYCN amplification can promote both glycolysis and oxidative phosphorylation in NB [ 46 ].…”
Section: Neuroblastoma and Oxidative Stressmentioning
confidence: 99%
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“…In the therapeutic studies of esophageal squamous cell carcinoma, MAP2K3 inhibitors have been reported to be effective in inhibiting cell growth. MAP2K3 can mediate cellular responses to external stimuli by phosphorylating and activating the p38-MAPK signaling pathway ( 8 ). When cells are subjected to external stimuli, activated MAP3K activates MAP2K3 to phosphorylate and activate the p38-MAPK signaling pathway.…”
Section: Introductionmentioning
confidence: 99%