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.

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

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.

Yeast bromodomain-containing factors Bdf1/2 offer insights into the biological role of the BET family of transcriptional regulators, which is a promising target in cancer therapy.

Genetics and biochemical analyses reveal an evolutionarily conserved mechanism to regulate gene isoform expression by mTORC1 and implicate possible gene isoform imbalance in cancer and neurological disorders with mTORC1 pathway dysregulation.

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.

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.