Previous Article | Next Article ![]()
Molecular and Cellular Biology, September 2001, p. 5797-5805, Vol. 21, No. 17
CRC Centre for Cell and Molecular Biology,
Institute of Cancer Research, London SW3 6JB, United Kingdom
Received 11 September 2000/Returned for modification 3 November
2000/Accepted 7 June 2001
During T-cell activation, c-Myb is induced upon interleukin 2 (IL-2) stimulation and is required for correct proliferation of cells.
In this paper, we provide evidence that IL-2-mediated induction of the
c-myb gene occurs via the phosphoinositide 3-kinase (PI3K)
signaling pathway, that protein kinase B (PKB) is the principal transducer of this signal, and that activation of the c-myb
promoter can be abolished by deletion of conserved E2F and NF-
0270-7306/01/$04.00+0 DOI: 10.1128/MCB.21.17.5797-5805.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
c-myb Transcription Is Activated by
Protein Kinase B (PKB) following Interleukin 2 Stimulation of T Cells
and Is Required for PKB-Mediated Protection from Apoptosis

B
binding sites. We show that Myb is required to protect activated
peripheral T cells from bcl-2-independent apoptosis and that
overexpression of oncogenic v-Myb is antiapoptotic. Overexpression of a
Myb dominant-negative transgene abrogates PKB-mediated protection from
apoptosis. Taken together, these results suggest that induction of
c-myb transcription is an important downstream event for
PKB-mediated protection of T cells from programmed cell death.
*
Corresponding author. Mailing address: CRC Centre for
Cell and Molecular Biology, Institute of Cancer Research, 237 Fulham Rd., London SW3 6JB, United Kingdom. Phone: 44 20 7878 3846. Fax: 44 20 7352 3299. E-mail: kathy{at}icr.ac.uk.
Present address: MRC Laboratory of Molecular Biology, Cambridge CB2
2QH, United Kingdom.
This article has been cited by other articles:
| J. Bacteriol. | J. Virol. | Eukaryot. Cell |
|---|
| Microbiol. Mol. Biol. Rev. | Clin. Vaccine Immunol. | All ASM Journals |
|---|