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.

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.

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.

Cyclin-dependentkinase 2 (Cdk2), the master regulator of S phase events during the cell cycle, controls the earliest step in the motile ciliogenesis pathway in quiescent multiciliatedairway epithelial cells.

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.

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.

CDK9 inhibition in human cells uncovers that Pol II pause duration regulates the frequency of productive transcription initiation.

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.

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