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      HIV-1 Nef promotes survival of TF-1 macrophages by inducing Bcl-XL expression in an extracellular signal-regulated kinase-dependent manner.

      The Journal of Biological Chemistry
      Apoptosis, Blotting, Western, Cell Death, Cell Line, Tumor, Cell Survival, Chromones, pharmacology, DNA-Binding Proteins, metabolism, Dimerization, Enzyme Activation, Enzyme Inhibitors, Flavonoids, Gene Products, nef, physiology, Genes, Dominant, Granulocyte-Macrophage Colony-Stimulating Factor, Green Fluorescent Proteins, Humans, MAP Kinase Signaling System, Macrophages, virology, Mitogen-Activated Protein Kinase 3, Morpholines, Proto-Oncogene Proteins c-bcl-2, biosynthesis, RNA, Ribonucleases, STAT3 Transcription Factor, Signal Transduction, T-Lymphocytes, Time Factors, Trans-Activators, Up-Regulation, Virus Replication, bcl-X Protein

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          Abstract

          The Nef protein of human immunodeficiency virus-1 (HIV-1) is essential for the progression from human and simian immunodeficiency virus infection to full-blown AIDS. Recent studies indicate that Nef generates anti-apoptotic signals in HIV-infected T cells, suppressing cell death early in infection to allow productive viral replication. Previous work from our laboratory has shown that Nef also promotes proliferation of myeloid cells through a signal transducer and activator of transcription 3-dependent pathway. Here we demonstrate that Nef suppresses cell death induced by cytokine deprivation in the human macrophage precursor cell line, TF-1. Nef selectively induced up-regulation of Bcl-XL, an anti-apoptotic gene that is also regulated by granulocyte/macrophage-colony stimulating factor in this cell line. Activation of the extracellular signal-regulated kinase (Erk) mitogen-activated protein kinase pathway also correlated with the survival of TF-1/Nef cells. Using the selective mitogen-activated protein kinase kinase inhibitor PD98059, we found that Nef-induced Erk signaling is essential for Bcl-XL up-regulation and cell survival. In contrast, expression of Bcl-XL and TF-1 survival was not affected by dominant-negative signal transducer and activator of transcription 3. These data suggest that Nef produces survival signals in myeloid cells through Erk-mediated Bcl-XL induction, a pathway distinct from Nef survival pathways recently reported in T lymphocytes.

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