1. ¹Departments of Medicine, Microbiology and Immunology, Rosalind Russell Medical Research Center, University of California, San Francisco, CA, USA
2. ²Cancer Research Institute, University of California, San Francisco, CA, USA
3. ³Department of Molecular Genetics, Nagoya City University Medical School, Nagoya, Japan

Correspondence: BM Peterlin, Box 0703 UCSF, 3rd and Parnassus Avenues, San Francisco, CA 94143-0703, USA. E-mail: matija@itsa.ucsf.edu

Received 26 January 2003; Revised 24 April 2003; Accepted 19 May 2003.

Abstract

c-Myc promotes cellular proliferation, sensitizes cells to apoptosis and prevents differentiation. It binds cyclin T1 structurally and functionally from the positive transcription elongation factor b (P-TEFb). The cyclin-dependent kinase 9 (Cdk9) in P-TEFb then phosporylates the C-terminal domain of RNA polymerase II, which is required for the transition from initiation to elongation of eukaryotic transcription. Inhibiting P-TEFb blocks the transcription of its target genes as well as cellular proliferation and apoptosis induced by c-Myc.