Regulation of P-TEFb activity during transcription. A) P-TEFb is inactivated in the large complex. After given stimuli (UV radition, cytokines, hypertrophic signals), active P-TEFb is released from the large complex by activity of signaling pathways downstream of these stimuli. Then, P-TEFb is recruited to the responsive promoter/s either by a specific activator (pink oval) such as MyoD or a co-activator, such as Brd4 (violet oval). P-TEFb is engaged at the promoters with poised RNAPII phosphorylated on Ser5 (light blue oval with letter S5) in CTD mediated by TFIIH. P-TEFb initiates transcription elongation by phosphorylating Ser2 of CTD in RNAPII (red oval with letter S2), DSIF or NELF (red ovals with letter P). Still, activity of P-TEFb can be controlled by two additional mechanisms. B) If there is a co-factor (acetyltransferase, mediator, corepressor) associating with P-TEFb at the promoter, then the activity of P-TEFb will depend on particular posttranslational modifications mediated by these co-factors, for example acetylation of Lys44 and 48 in CDK9 (white oval with letters Ac). C) Also, signaling pathways activated by given stimuli can modify components of the small complex, for example phosphorylation of CDK9 on Thr28 and Thr186 (white oval with letter P), and additionally modulate final activity of P-TEFb. Khaki barrels represent nucleosomes, and +1 depicts transcription start site.