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Mechanistic studies reveal that SFN significantly downregulates programmed death-ligand 1 (PD-L1) expression on tumor cells through multiple mechanisms, including direct covalent modification of cysteine residues on STAT1, which inhibits its transcriptional activity and blocks IFN--induced PD-L1 expression (75)

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Retinoic acid-mediated increase in TrkA expression is sufficient to elicit NGF-dependent survival of sympathetic neurons

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