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Department of Cell and Molecular Biology, Umeà University, S-901 87 Umeå, Sweden [S. W. E. L.], and Institute of Cancer Studies, University of Birmingham Medical School, Birmingham B15 2TJ, United Kingdom [M. R.]
The EBV-encoded latent membrane protein 1 (LMP1) suppresses appoptosis in B lymphocytes through up-regulation of Bcl-2. However, the maximum induction of Bcl-2 by LMP1 takes about 48–72 h. We show in this report that up-regulation of the Bcl-2 homologue Mcl-1 by LMP1 preceded the induction of Bcl-2 and that the up-regulation was transient; therefore, Mcl-1 levels decreased when Bcl-2 levels started to increase. This finding supports the hypothesis that Mcl-1 functions as a rapidly inducible, short-term effector of cell viability. LMP1 also blocked the decline in the Mcl-1 levels in response to apoptotic stimulation triggered by elevated cyclic AMP. This effect of LMP1 was associated with a delayed cell death in the EBV-negative Burkitt lymphoma cell line BL41. The maintenance of Mcl-1 expression by LMP1 is likely to be a crucial immediate-early response that enables cells to survive until Bcl-2 can be up-regulated.
1 This study was supported by the Swedish Cancer Society and Lion's Cancer Research Foundation, Umeå University.
2 To whom requests for reprints should be addressed.
Received 6/ 7/96. Accepted 8/28/96.
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