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Journal of Virology, February 2001, p. 1220-1228, Vol. 75, No. 3
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.3.1220-1228.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Antiapoptotic Function of Cdk9 (TAK/P-TEFb) in U937 Promonocytic Cells

Shannon M. Foskett,1 Romi Ghose,1 Derek Ng Tang,2 Dorothy E. Lewis,2 and Andrew P. Rice1,*

Department of Molecular Virology and Microbiology1 and Department of Immunology,2 Baylor College of Medicine, Houston, Texas 77030

Received 15 May 2000/Accepted 3 November 2000

Cdk9 is the catalytic subunit of TAK (cyclinT1/P-TEFb), a cellular protein kinase that mediates human immunodeficiency virus type 1 (HIV-1) Tat transcriptional activation function. To examine Cdk9 function in cells relevant to HIV-1 infection, we used a murine leukemia virus retrovirus vector to transduce and overexpress the cDNA of a dominant negative mutant Cdk9 protein (Cdk9-dn) in Jurkat T cells and U937 promonocytic cells. In Jurkat cells, overexpression of Cdk9-dn specifically inhibited Tat transactivation and HIV-1 replication but had no inhibitory effect on induction of CD69, CD25, and interleukin-2 following T-cell activation. In U937 cells, overexpression of Cdk9-dn sensitized cells to apoptosis, especially after phorbol myristate acetate (PMA) treatment to induce differentiation to macrophage-like cells. Because Cdk9 function is induced in PMA-treated U937 cells, Cdk9 may play an antiapoptotic role during monocyte differentiation.

* Corresponding author. Mailing address: Department of Molecular Virology and Microbiology, Baylor College of Medicine, One Baylor Plaza, Mail Stop BCM-385, Houston, TX 77030. Phone: (713) 798-5774. Fax: (713) 798-3490. E-mail: arice{at}bcm.tmc.edu.

Journal of Virology, February 2001, p. 1220-1228, Vol. 75, No. 3
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.3.1220-1228.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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Copyright © 2001 by the American Society for Microbiology. All rights reserved.