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BET proteins bind the lytic origins of replication [MutuI ChIP-seq]

ABSTRACT: Lytic infection by the Epstein-Barr virus (EBV) poses numerous health risks, such as infectious mononucleosis and lymphoproliferative disorder. We demonstrate that JQ1 and other BET inhibitors block two different steps in the sequential cascade of the EBV life cycle: expression of the immediate-early gene BZLF1 and lytic genome replication. This represents a novel mode of action for antiviral drugs that may increase efficacy and decrease emergence of resistance. The ChIP-seq data below show that the BET proteins bind to both EBV lytic origins of replication.

ORGANISM(S): Homo sapiens human gammaherpesvirus 4

PROVIDER: GSE84213 | GEO | 2017/06/30

SECONDARY ACCESSION(S): PRJNA328409

REPOSITORIES: GEO

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BET proteins bind the lytic origins of replication [MutuI ChIP-seq]

Project description:BET proteins bind the lytic origins of replication [MutuI ChIP-seq]

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