J Biol Chem. 2001 Jul 6;276(27):25605-11. Epub 2001 Apr 27.

HIV-1 Nef promotes survival of myeloid cells by a Stat3-dependent pathway.

Briggs SD, Scholtz B, Jacque JM, Swingler S, Stevenson M, Smithgall TE.

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Department of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.

Abstract

Human immunodeficiency virus Nef is a small myristylated protein that plays a critical role in AIDS progression. Nef binds with high affinity to the SH3 domain of the myeloid-restricted tyrosine kinase Hck in vitro, identifying this Src-related kinase as a possible cellular target for Nef in macrophages. Here we show that Nef activates endogenous Hck in the granulocyte-macrophage colony-stimulating factor-dependent myeloid cell line, TF-1. Unexpectedly, Nef induced cytokine-independent TF-1 cell outgrowth and constitutive activation of the Stat3 transcription factor. Induction of survival required the Nef SH3 binding and membrane-targeting motifs and was blocked by dominant-negative Stat3 mutants. Nef also stimulated Stat3 activation in primary human macrophages, providing evidence for Stat3 as a Nef effector in a target cell for human immunodeficiency virus.

PMID:: 11328823; [PubMed - indexed for MEDLINE]

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HIV-1 Nef promotes survival of myeloid cells by a Stat3-dependent pathway.

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