CDK9 has the intrinsic property to shuttle between nucleus and cytoplasm, and enhanced expression of cyclin T1 promotes its nuclear localization.

CDK9 in association with cyclin T constitutes the P-TEFb complex that stimulates transcription elongation of RNAPII transcripts by phosphorylation of the CTD of RNAPII. Here we report subcellular distribution of P-TEFb in terms of localization of CDK9 and cyclin T1. We found that cyclin T1 is exclusively nuclear and it ...
is present in nuclear-speckled structures. CDK9, albeit mainly nuclear, was also visualized in the cytoplasm. We determined that CDK9 is actively exported from the nucleus, and that leptomycin B (LMB), a specific inhibitor of nuclear export, inhibits this process. Interestingly, enforced expression of cyclin T1 enhances nuclear localization of CDK9. These findings reveal a novel control mechanism for the function of the P-TEFb complex.
Mesh Terms:
3T3 Cells, Active Transport, Cell Nucleus, Animals, COS Cells, Cell Nucleus, Cercopithecus aethiops, Cyclin T, Cyclin-Dependent Kinase 9, Cyclin-Dependent Kinases, Cyclins, Cytoplasm, HeLa Cells, Humans, Mice, Protein Transport, Subcellular Fractions
J. Cell. Physiol.
Date: Aug. 01, 2002
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