P-TEFb

TL;DR: It is proposed that Tat directs cyclin T-CDK9 to RNAPII through cooperative binding to TAR RNA, and confers a requirement for sequences in the loop of TAR that are not recognized by Tat alone.

TL;DR: Proteomic analysis revealed that Brd4 interacts with cyclinT1 and Cdk9 that constitutes core positive transcription elongation factor b (P-TEFb) and is a positive regulatory component of P- TEFb, which alternately interacts with Brd 4 and the inhibitory subunit to maintain functional equilibrium in the cell.

TL;DR: Phylogenetic analyses of the components of the human elongation control machinery indicate that the number of mechanisms utilized to regulate P-TEFb function increased as organisms developed more complex developmental patterns.

TL;DR: It is shown that in stress-induced cells, the 7SK/HEXIM1-bound P-TEFb is quantitatively converted into the Brd4-associated form, which is necessary to form the transcriptionally active P-teFb, recruits P- TEFb to a promoter, and enables P-TFb to contact the Mediator complex, a potential target for the Br d4-mediated recruitment.

TL;DR: The identification and purification from HeLa nuclear extract of a third protein factor required for DRB-sensitive transcription, termed negative elongation factor (NELF), cooperates with DSIF and strongly represses pol II elongation.