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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

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Date
2001-09
ICR Author
Weston, Kathleen
Author
Lauder, A
Castellanos, A
Weston, K
Type
Journal Article
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Abstract
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-kappaB 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.
URI
https://repository.icr.ac.uk/handle/internal/2830
DOI
https://doi.org/10.1128/MCB.21.17.5797-5805.2001
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  • Other ICR Research
Language
eng
License start date
2001-09
Citation
MOLECULAR AND CELLULAR BIOLOGY, 2001, 21 pp. 5797 - 5805
Publisher
AMER SOC MICROBIOLOGY

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