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.

Targeting the CRL5 ubiquitin ligase complex in combination with CDK9 or MCL1 inhibition could combat innate and acquired resistance of cancer cells to MCL1-targeting therapeutics.

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

Cyclin T1 phosphorylation determines levels of P-TEFb via stabilizing interactions between cyclin T1 and CDK9.

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.

The HIV-1 Tat protein hijacks host non-degradative ubiquitination to trigger the nuclear import of the transcription elongation factor, P-TEFb.

Cancer cell antigen presentation, a requirement for immune-mediated tumor rejection, is induced by dihydroorotate dehydrogenase-inhibitor-mediated cancer cell pyrimidine nucleotide depletion via P-TEFb-dependent transcriptional upregulation of MHC-I and related genes.

TRIM28 was found to be a versatile dual-function latency contributor by bridging both suppressive epigenetic modifications and RNAP II transcriptional-pausing, and can be a novel target to develop latency-reversing agents.

Transcription elongation by the elongation factor P-TEFb promotes the epithelial–mesenchymal transition and metastasis of breast cancer cells, implicating inhibition of this factor as a potential treatment for the late stages of this cancer.