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

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

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.

The sigma subunit of bacterial RNA polymerase, classically known as an initiation factor, can also operate as an elongation factor with effects that vary with growth phase.

Natural genetic variation reveals how DNA sequence impacts core transcriptional processes of initiation, pause, and termination.

Quantification of all the major on- and off-pathway kinetic parameters in the transcription elongation cycle reveals that RNA polymerase II translocates slowly in a linear, non-branched Brownian ratchet mechanism.

Seven distinct cryo-electron microscopy structures delineate the elaborate mechanism for how E. coli Mfd, a transcription repair coupling factor, disassembles the RNA polymerase transcription elongation complex to initiate transcription-coupled repair.

High-throughput and ultra-stable magnetic tweezers reveal that Remdesivir induces a long-lived backtrack pause upon incorporation by the coronavirus polymerase, and SARS-CoV-2 is able to evade interferon-induced antiviral ddhCTP.

Tat uses unexpected regulatory mechanisms to reprogram target immune cells to promote viral replication and rewire pathways beneficial for HIV.

MYCN and TFIIIC exert a censoring function during early transcription, limiting the accumulation of inactive RNAPII at the promoter and facilitating promoter-proximal degradation of nascent RNA.