Abstract
The family of Cyclin-Dependent Kinases (CDKs) can be subdivided into two major functional groups based on their roles in cell cycle and/or transcriptional control. This review is centered on CDK9, which is activated by T-type cyclins and cyclin K generating distinct Positive-Transcription Elongation Factors termed P-TEFb. P-TEFb positively regulates transcriptional elongation by phosphorylating the C-terminal domain (CTD) of RNA polymerase II (RNA pol II), as well as negative elongation factors, which block elongation by RNA pol II shortly after the initiation of transcription. Work over the past few years has led to a dramatic increase in our understanding of how productive transcriptional elongation occurs. This review will briefly describe the mechanisms regulating the activity of T-type cyclin/CDK9 complexes and discuss how these complexes regulate gene expression. For further information, the reader is directed to excellent existing reviews on transcriptional elongation and HIV transcription.
