Abstract
In a recent study, Farrelly, Zheng, and colleagues used a histone proteomics approach and patient-derived neurons to show increase in histone variant H2A.Z acetylation associated with schizophrenia (SCZ). They identified the bromo- and extraterminal (BET) protein BRD4 as an H2A.Z acetylation 'reader', and showed that a BRD4 inhibitor ameliorated the SCZ-associated transcriptional signature, revealing a new candidate target for treatment.
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