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Journal of Virology, December 1998, p. 9881-9888, Vol. 72, No. 12
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Tat-Associated Kinase, TAK, Activity Is Regulated by Distinct
Mechanisms in Peripheral Blood Lymphocytes and Promonocytic
Cell Lines
Christine H.
Herrmann,1,*
Richard G.
Carroll,2
Ping
Wei,3,
Katherine A.
Jones,3 and
Andrew P.
Rice1
Division of Molecular Virology, Baylor
College of Medicine, Houston, Texas 770301;
H. M. Jackson Foundation, Military HIV Research Program,
Bethesda, Maryland 208892; and
Regulatory Biology Laboratory, The Salk Institute for
Biological Studies, La Jolla, California 920373
Received 4 August 1998/Accepted 10 September 1998
TAK, a multisubunit cellular protein kinase that specifically
associates with the human immunodeficiency virus Tat proteins and
hyperphosphorylates the carboxyl-terminal domain of RNA polymerase II,
is a cofactor for Tat and mediates its transactivation function. The
catalytic subunit of TAK has been identified as cyclin-dependent kinase Cdk9, and its regulatory partner has been identified as cyclin
T1; these proteins are also components of positive transcription elongation factor P-TEFb. TAK activity is up-regulated upon activation of peripheral blood lymphocytes and following macrophage
differentiation of promonocytic cell lines. We have found that
activation of peripheral blood lymphocytes results in increased mRNA
and protein levels of both Cdk9 and cyclin T1. Cdk9 and cyclin T1
induction occurred in purified CD4+ primary T cells
activated by a variety of stimuli. In contrast, phorbol ester-induced
differentiation of promonocytic cell lines into macrophage-like
cells produced a large induction of cyclin T1 protein expression from
nearly undetectable levels, while Cdk9 protein levels remained at a
constant high level. Measurements of cyclin T1 mRNA levels in a
promonocytic cell line suggested that regulation of cyclin T1 occurs at
a posttranscriptional level. These results suggest that cyclin T1 and
TAK function may be required in differentiated monocytes and further
show that TAK activity can be regulated by distinct mechanisms in
different cell types.
*
Corresponding author. Mailing address: Baylor College
of Medicine, Division of Molecular Virology, One Baylor Plaza, Houston, TX 77030. Phone: (713) 798-6428. Fax: (713) 798-3490. E-mail: herrmann{at}bcm.tmc.edu.

Present address: 15711 Mahogany Circle, Gaithersburg, MD
20878.
Journal of Virology, December 1998, p. 9881-9888, Vol. 72, No. 12
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
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