Regulatory subunit of the cyclin-dependent kinase pair (CDK9/cyclin-T1) complex, also called positive transcription elongation factor B (P-TEFb), which is proposed to facilitate the transition from abortive to productive elongation by phosphorylating the CTD (carboxy-terminal domain) of the large subunit of RNA polymerase II (RNA Pol II). In case of HIV or SIV infections, binds to the transactivation domain of the viral nuclear transcriptional activator, Tat, thereby increasing Tat's affinity for the transactivating response RNA element (TAR RNA). Serves as an essential cofactor for Tat, by promoting RNA Pol II activation, allowing transcription of viral genes. Cyclin-T1 is the predominant cyclin that associates with CDK9 to form a heterodimer called P-TEFb. P-TEFb forms a complex with AFF4/AF5Q31. Interacts with the transactivation region of HIV-1, HIV-2 and SIV Tat. Component of a complex which is at least composed of HTATSF1/Tat-SF1, P-TEFb complex, RNA pol II, SUPT5H, and NCL/nucleolin. Component of the 7SK snRNP complex at least composed of P-TEFb (composed of CDK9 and CCNT1/cyclin-T1), HEXIM1, HEXIM2, BCDIN3, SART3 proteins and 7SK and U6 snRNAs. Interacts with MDFIC. Ubiquitously expressed. Belongs to the cyclin family. Cyclin C subfamily. Note: This description may include information from UniProtKB.
Molecular Function: protein binding; snRNA binding; DNA binding; chromatin binding; protein kinase binding
Biological Process: transcription from RNA polymerase II promoter; transcription initiation from RNA polymerase II promoter; transcription, DNA-dependent; viral reproduction; positive regulation of viral transcription; cell cycle; protein amino acid phosphorylation; cell division; virus-host interaction; transforming growth factor beta receptor signaling pathway; RNA elongation from RNA polymerase II promoter; positive regulation of transcription from RNA polymerase II promoter; gene expression; regulation of cyclin-dependent protein kinase activity
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.