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.

A multi-transcriptional CDKs inhibitor suppresses MYC and induces regression of ovarian tumors, indicating that targeting CDK7, 12, 13 with THZ1 may be an effective approach for treating MYC-dependent malignancies.

Application of a live-cell reporter for CDK4/6 activity reveals rapid activity changes and reversibility in the cell-cycle entry signaling program.

Detailed molecular profiling investigations alongside antitumor testing and tolerability studies in animals suggest caution when considering the clinical development of inhibitors of CDK8 and CDK19, since a clear therapeutic window could not be demonstrated with two structurally distinct, potent and selective prototype drugs.

CDKG1 is a D-cyclin dependent retinoblastoma related protein kinase whose abundance scales with cell size and controls cell division cycle number during multiple fission.

High-throughput phenotypic screening followed by unbiased target identification reveals a new molecular glue HQ461 that induces CDK12-DDB1 interaction to promote degradation of Cyclin K via the ubiquitin proteasome system.

The ZF-CxxC protein FBXL19 recruits kinase-associated Mediator to CpG islands of silent developmental genes in embryonic stem cells, which primes these genes for activation during differentiation and is required for embryonic development.

DNA concentration, cyclin levels, phosphatase activity, and CDK phosphorylation combine to directly link cell size to cell division.

Anticancer compound library screen identified many types of nucleolar stress and revealed an essential role of transcriptional cyclin-dependent kinases in nucleolar structure and function.

High-resolution mapping of RNA polymerase II transcripts shows that the directionality of mammalian promoters is determined by preferential transcriptional initiation and the opposing activities of Integrator and CDK9.