http://www.cnr.it/ontology/cnr/individuo/prodotto/ID11445
In vitro treatment of human monocyte/macrophages with myristoylated recombinant Nef of human immunodeficiency virus type 1 leads to the activation of mitogen-activated protein kinases, IkB kinases and Interferon Regulatory Factor 3 and to the release of Beta Interferon. (Articolo in rivista)
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- In vitro treatment of human monocyte/macrophages with myristoylated recombinant Nef of human immunodeficiency virus type 1 leads to the activation of mitogen-activated protein kinases, IkB kinases and Interferon Regulatory Factor 3 and to the release of Beta Interferon. (Articolo in rivista) (literal)
- Anno
- 2007-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1128/JVI.01640-06 (literal)
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1.Mangino G., 1.Percario Z.A., 2,3.Fiorucci G., 4.Vaccari G., 6.Manrique S., 7,3.Romeo G. , 5.Federico M., 6.Geyer M, 1.Affabris E. (2007)
In vitro treatment of human monocyte/macrophages with myristoylated recombinant Nef of human immunodeficiency virus type 1 leads to the activation of mitogen-activated protein kinases, IkB kinases and Interferon Regulatory Factor 3 and to the release of Beta Interferon.
in Journal of virology (Print); ASM, American society for microbiology, Washington, DC (Stati Uniti d'America)
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- 1.Mangino G., 1.Percario Z.A., 2,3.Fiorucci G., 4.Vaccari G., 6.Manrique S., 7,3.Romeo G. , 5.Federico M., 6.Geyer M, 1.Affabris E. (literal)
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- 1Department of Biology, University Roma Tre
2Institute of Molecular Biology and Pathology, CNR, Rome
3Department of Infectious, Parasitic and Immune-Mediated Diseases, ISS, Rome
4Department of Food Safety and Veterinary Public Health
5National AIDS Center, Ist. Superiore di Sanità, Rome
6Max-Planck-Institut für Molekulare Physiologie, Abteilung Physikalische Biochemie, Dortmund, Germany
7Department of Experimental Medicine and Pathology, University La Sapienza, Rome (literal)
- Titolo
- In vitro treatment of human monocyte/macrophages with myristoylated recombinant Nef of human immunodeficiency virus type 1 leads to the activation of mitogen-activated protein kinases, IkB kinases and Interferon Regulatory Factor 3 and to the release of Beta Interferon. (literal)
- Abstract
- The viral protein Nef is a virulence factor that plays multiple roles during the early and late phases of human immunodeficiency virus (HIV) replication. Nef regulates the cell surface expression of critical proteins (including down-regulation of CD4 and major histocompatibility complex class I), T-cell receptor signaling, and apoptosis, inducing proapoptotic effects in uninfected bystander cells and antiapoptotic effects in infected cells. It has been proposed that Nef intersects the CD40 ligand signaling pathway in macrophages, leading to modification in the pattern of secreted factors that appear able to recruit and activate T lymphocytes, rendering them susceptible to HIV infection. There is also increasing evidence that in vitro cell treatment with Nef induces signaling effects. Exogenous Nef treatment is able to induce apoptosis in uninfected T cells, maturation in dendritic cells, and suppression of CD40-dependent immunoglobulin class switching in B cells. Previously, we reported that Nef treatment of primary human monocyte-derived macrophages (MDMs) induces a cycloheximide-independent activation of NF-kappaB and the synthesis and secretion of a set of chemokines/cytokines that activate STAT1 and STAT3. Here, we show that Nef treatment is capable of hijacking cellular signaling pathways, inducing a very rapid regulatory response in MDMs that is characterized by the rapid and transient phosphorylation of the alpha and beta subunits of the IkappaB kinase complex and of JNK, ERK1/2, and p38 mitogen-activated protein kinase family members. In addition, we have observed the activation of interferon regulatory factor 3, leading to the synthesis of beta interferon mRNA and protein, which in turn induces STAT2 phosphorylation. All of these effects require Nef myristoylation. (literal)
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