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Given the central role of ER stress and MYCN in driving NEPC progression, we hypothesized that exogenous supplementation of NO could restore the S-nitrosylation of MYCN, thereby reducing ER stress and mitigating the aggressive behavior of NEPC cells
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Adenosine activates ADORA2B receptors, which stimulate SphK1 activity, promote glycolysis, and boost 2,3-BPG production, a molecule that lowers hemoglobin’s affinity for oxygen
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