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Given that the phenotype is highly variable, it is likely that residual TPK1 activity and/or other cellular kinases (albeit at a lower extent and favored by the mass action of high thiamine doses) may also phosphorylate thiamine, thereby partly circumventing the metabolic block

reported that elevated TNF- and IL-6 levels promote osteoclast differentiation and activation while inhibiting osteoblast function [5556], which aligns with our experimental observations

GSH degradation has been believed to occur primarily in the extracellular space

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