Yifei Liao

This study shows that NAD metabolism supports CTCF-cohesin chromatin regulation in EBV-transformed B-cells and identifies NAMPT inhibition as a potential therapeutic strategy.

This study uses a genome-wide CRISPR-Cas9 screen to identify host factors essential for EBV B cell infection, revealing new pathways and potential therapeutic targets.

This study shows that methionine restriction induces ferroptosis in EBV-transformed B cells by promoting transsulfuration and glutathione synthesis, and that targeting methionine metabolism can impair tumor growth.

This study identifies JunB as a key dependency factor in EBV-infected B cells that represses p18INK4c, revealing a potential therapeutic target for EBV-associated cancers.

This paper identifies STEEP1 as a host factor critical for LMP1 trafficking and signaling using a CRISPR-Cas9 screen, showing its role in NF-kB and MAP kinase pathway activation.

This study identifies viral lncRNAs that regulate EBV reactivation by interacting with CTCF and modulating enhancer-promoter looping.

This paper identifies that EBV's BALF0/1 protein degrades B-cell receptor complexes by subverting caveolin and ERAD pathways, enhancing viral secretion.

This study investigates how GC cytokines regulate EBV latency gene expression and epigenetic remodeling, revealing distinct roles for STAT3 and STAT5 in silencing EBNA and activating LMP1 promoters.