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.

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.

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.

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

CBP/p300 acetylation of histone H3 at promoters and enhancers stimulates transcriptional elongation through recruitment of the super-elongation complex and BRD4.

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.

In fusion-positive rhabdomyosarcoma, CHD4 positively regulates super-enhancer-mediated gene expression by allowing a chromatin architecture at these cis-regulatory regions, which is permissive to the binding of the transcription factor PAX3-FOXO1.

RNAi screening in planarians finds that inhibition of the TEC-family protein tyrosine kinase tec-1 increases the regeneration of neurons through enhancement of cell survival.

Mitotic labeling defines a change in cell division kinetics from growth to homeostasis and identifies slowly cycling cells in the adult tendon.