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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]

The results of IP showed that SLC7A11 could interact with Sec24C rather than other isoforms (Fig

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