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In the context of HBV infection, PRMT1 is recruited to cccDNA and catalyzes H4R3me2a modification, which, in turn, alters the acetylation status of cccDNA, ultimately resulting in the suppression of HBV transcription (Figure 7F) [195]

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The peptide influences both endothelial nitric oxide synthase (eNOS), which produces the beneficial, vasodilating form of nitric oxide, and inducible nitric oxide synthase (iNOS), which can produce excessive amounts that contribute to inflammation and tissue damage