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Molecular and Cellular Biology, September 1998, p. 4986-4993, Vol. 18, No. 9
Division of Pediatric Oncology, Dana-Farber
Cancer Institute, and Department of Pediatrics, Harvard Medical
School, Boston, Massachusetts 02115
Received 1 December 1997/Returned for modification 30 December
1997/Accepted 29 May 1998
The Rho family of small GTP-binding proteins is involved in the
regulation of cytoskeletal structure, gene transcription, specific cell
fate development, and transformation. We demonstrate in this report
that overexpression of an activated form of Rho enhances AP-1 activity
in Jurkat T cells in the presence of phorbol myristate acetate (PMA),
but activated Rho (V14Rho) has little or no effect on NFAT, Oct-1, and
NF-
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Copyright © 1998, American Society for Microbiology. All rights reserved.
The Small GTP-Binding Protein Rho Potentiates
AP-1 Transcription in T Cells
B enhancer element activities under similar conditions.
Overexpression of a V14Rho construct incapable of membrane
localization (CAAX deleted) abolishes PMA-induced AP-1 transcriptional
activation. The effect of Rho on AP-1 is independent of the
mitogen-activated protein kinase pathway, as a dominant-negative MEK
and a MEK inhibitor (PD98059) did not affect Rho-induced AP-1 activity.
V14Rho binds strongly to protein kinase C
(PKC
) in vivo; however,
deletion of the CAAX site on V14Rho severely diminished this
association. Evidence for a role for PKC
as an effector of
Rho was obtained by the observation that coexpression of the
N-terminal domain of PKC
blocked the effects of activated Rho
plus PMA on AP-1 transcriptional activity. These data suggest that Rho
potentiates AP-1 transcription during T-cell activation.
*
Corresponding author. Mailing address: Division of
Pediatric Oncology, Dana-Farber Cancer Institute, 44 Binney St.,
Harvard Medical School, Boston, MA 02115. Phone: (617) 632-3564. Fax: (617) 632-4367. E-mail:
steven_burakoff{at}dfci.harvard.edu.
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