BRD9 provides the first actionable therapeutic target in synovial sarcoma tumours that is both biochemically and functionally linked to the SS18-SSX fusion protein which drives disease development.

A new potent and selective CDK9 inhibitor induces the expression of the proto-oncogene MYC via a mechanism that depends on the bromodomain protein BRD4.

Acetylation of the circadian transcription factor BMAL1 by the acetyltransferase TIP60 is crucial for recruitment of the pause release factors to clock gene promoters and productive elongation of these genes.

The structure of receptor-ligand complex reveals the ligand binding selectivity among different dopamine receptor subtypes and also shows how this ligand class inhibits receptor activity.

The maintenance of memory CD4 T cells in mice relies on a continual and strikingly high level of replenishment from naive precursors, and older memory T cells may resist the influx of newer ones.

JMJD6 helps BRD4 to recruit CDK9 to RNA Polymerase II by disrupting 7SK snRNP complex.

Mathematical modeling reveals that long-term immunological memory is maintained in a manner that is even more dynamic than previously thought.

Targeting the transcription factor c-Myc via one of its coactivator proteins is a promising strategy for cancer therapy.