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  1. Article: Influenza virus-induced AP-1-dependent gene expression requires activation of the JNK signaling pathway.

    Ludwig, S / Ehrhardt, C / Neumeier, E R / Kracht, M / Rapp, U R / Pleschka, S

    The Journal of biological chemistry

    2001  Volume 276, Issue 14, Page(s) 10990–10998

    Abstract: ... we show that influenza virus infection induces AP-1-dependent gene expression in productively infected ... of virus-induced JNK activation, reduced AP-1 activity, and impaired transactivation of the IFN-beta promoter ... compared with the levels from control cells. Therefore, we conclude that virus-induced activation of JNK ...

    Abstract Influenza A virus infection of cells results in the induction of a variety of antiviral cytokines, including those that are regulated by transcription factors of the activating protein-1 (AP-1) family. Here we show that influenza virus infection induces AP-1-dependent gene expression in productively infected cells but not in cells that do not support viral replication. Among the AP-1 factors identified to bind to their cognate DNA element during viral infections of Madin-Darby canine kidney and U937 cells are those that are regulated via phosphorylation by JNKs. Accordingly, we observed that induction of AP-1-dependent gene expression correlates with a strong activation of JNK in permissive cells, which appears to be caused by viral RNA accumulation during replication. Blockade of JNK signaling at several levels of the cascade by transient expression of dominant negative kinase mutants and inhibitory proteins resulted in inhibition of virus-induced JNK activation, reduced AP-1 activity, and impaired transactivation of the IFN-beta promoter. Virus yields from transfected and infected cells in which JNK signaling was inhibited were higher compared with the levels from control cells. Therefore, we conclude that virus-induced activation of JNK and AP-1 is part of the innate antiviral response of the cell.
    MeSH term(s) Animals ; Cell Line ; Gene Expression Regulation, Viral ; Humans ; Influenza, Human/genetics ; Influenza, Human/metabolism ; Influenza, Human/virology ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Kinase 4 ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Orthomyxoviridae/physiology ; Signal Transduction ; Transcription Factor AP-1/metabolism ; Virus Replication
    Chemical Substances Transcription Factor AP-1 ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; MAP Kinase Kinase 4 (EC 2.7.12.2) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2)
    Language English
    Publishing date 2001-01-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M009902200
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Influenza virus-induced AP-1-dependent gene expression requires activation of the JNK signaling pathway.

    Ludwig, S / Ehrhardt, C / Neumeier, E R / Kracht, M / Rapp, U R / Pleschka, S

    The Journal of biological chemistry

    2001  Volume 276, Issue 24, Page(s) 10990–10998

    Abstract: ... we show that influenza virus infection induces AP-1-dependent gene expression in productively infected ... of virus-induced JNK activation, reduced AP-1 activity, and impaired transactivation of the IFN-beta promoter ... compared with the levels from control cells. Therefore, we conclude that virus-induced activation of JNK ...

    Abstract Influenza A virus infection of cells results in the induction of a variety of antiviral cytokines, including those that are regulated by transcription factors of the activating protein-1 (AP-1) family. Here we show that influenza virus infection induces AP-1-dependent gene expression in productively infected cells but not in cells that do not support viral replication. Among the AP-1 factors identified to bind to their cognate DNA element during viral infections of Madin-Darby canine kidney and U937 cells are those that are regulated via phosphorylation by JNKs. Accordingly, we observed that induction of AP-1-dependent gene expression correlates with a strong activation of JNK in permissive cells, which appears to be caused by viral RNA accumulation during replication. Blockade of JNK signaling at several levels of the cascade by transient expression of dominant negative kinase mutants and inhibitory proteins resulted in inhibition of virus-induced JNK activation, reduced AP-1 activity, and impaired transactivation of the IFN-beta promoter. Virus yields from transfected and infected cells in which JNK signaling was inhibited were higher compared with the levels from control cells. Therefore, we conclude that virus-induced activation of JNK and AP-1 is part of the innate antiviral response of the cell.
    MeSH term(s) Activating Transcription Factor 2 ; Cell Line ; Cyclic AMP Response Element-Binding Protein/metabolism ; DNA/metabolism ; DNA-Directed DNA Polymerase/metabolism ; Enzyme Activation ; Gene Expression Regulation, Viral ; HeLa Cells ; Humans ; Influenza A virus/physiology ; Interferon-beta/genetics ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Kinase 4 ; MAP Kinase Kinase 7 ; MAP Kinase Signaling System ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Phosphorylation ; Promoter Regions, Genetic ; Protein Binding ; RNA, Viral/metabolism ; Species Specificity ; Transcription Factor AP-1/physiology ; Transcription Factors/metabolism ; U937 Cells ; Virus Replication
    Chemical Substances Activating Transcription Factor 2 ; Cyclic AMP Response Element-Binding Protein ; RNA, Viral ; Transcription Factor AP-1 ; Transcription Factors ; Interferon-beta (77238-31-4) ; DNA (9007-49-2) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; MAP Kinase Kinase 4 (EC 2.7.12.2) ; MAP Kinase Kinase 7 (EC 2.7.12.2) ; MAP2K4 protein, human (EC 2.7.12.2) ; MAP2K7 protein, human (EC 2.7.12.2) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2) ; DNA-Directed DNA Polymerase (EC 2.7.7.7)
    Language English
    Publishing date 2001-06-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Corrected and Republished Article
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The clinically approved proteasome inhibitor PS-341 efficiently blocks influenza A virus and vesicular stomatitis virus propagation by establishing an antiviral state.

    Dudek, Sabine Eva / Luig, Christina / Pauli, Eva-Katharina / Schubert, Ulrich / Ludwig, Stephan

    Journal of virology

    2010  Volume 84, Issue 18, Page(s) 9439–9451

    Abstract: ... activation of NF-kappaB as well as the JNK/AP-1 pathway. This coincides with enhanced expression of antiviral ... approach for antiviral intervention. The classical virus-induced activation of the NF-kappaB pathway ... an antiviral state mediated by the NF-kappaB-dependent expression of antivirus-acting gene products. ...

    Abstract Recently it has been shown that the proinflammatory NF-kappaB pathway promotes efficient influenza virus propagation. Based on these findings, it was suggested that NF-kappaB blockade may be a promising approach for antiviral intervention. The classical virus-induced activation of the NF-kappaB pathway requires proteasomal degradation of the inhibitor of NF-kappaB, IkappaB. Therefore, we hypothesized that inhibition of proteasomal IkappaB degradation should impair influenza A virus (IAV) replication. We chose the specific proteasome inhibitor PS-341, which is a clinically approved anticancer drug also known as Bortezomib or Velcade. As expected, PS-341 treatment of infected A549 cells in a concentration range that was not toxic resulted in a significant reduction of progeny virus titers. However, we could not observe the proposed suppression of NF-kappaB-signaling in vitro. Rather, PS-341 treatment resulted in an induction of IkappaB degradation and activation of NF-kappaB as well as the JNK/AP-1 pathway. This coincides with enhanced expression of antiviral genes, such as interleukin-6 and, most importantly, MxA, which is a strong interferon (IFN)-induced suppressor of influenza virus replication. This suggests that PS-341 may act as an antiviral agent via induction of the type I IFN response. Accordingly, PS-341 did not affect virus titers in Vero cells, which lack type I IFN genes, but strongly inhibited replication of vesicular stomatitis virus (VSV), a highly IFN-sensitive pathogen. Thus, we conclude that PS-341 blocks IAV and VSV replication by inducing an antiviral state mediated by the NF-kappaB-dependent expression of antivirus-acting gene products.
    MeSH term(s) Antiviral Agents/pharmacology ; Boronic Acids/pharmacology ; Bortezomib ; Cell Line ; Epithelial Cells/virology ; GTP-Binding Proteins/biosynthesis ; Humans ; Influenza A virus/drug effects ; Interferon Type I/biosynthesis ; Interferon Type I/immunology ; Interleukin-6/biosynthesis ; Myxovirus Resistance Proteins ; Pyrazines/pharmacology ; Vesiculovirus/drug effects
    Chemical Substances Antiviral Agents ; Boronic Acids ; Interferon Type I ; Interleukin-6 ; MX1 protein, human ; Myxovirus Resistance Proteins ; Pyrazines ; Bortezomib (69G8BD63PP) ; GTP-Binding Proteins (EC 3.6.1.-)
    Language English
    Publishing date 2010-06-30
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/JVI.00533-10
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: JNK2 and IKKbeta are required for activating the innate response to viral infection.

    Chu, W M / Ostertag, D / Li, Z W / Chang, L / Chen, Y / Hu, Y / Williams, B / Perrault, J / Karin, M

    Immunity

    1999  Volume 11, Issue 6, Page(s) 721–731

    Abstract: ... dsRNA-responsive pathway is PKR independent and involves Jun kinase (JNK) activation leading ... to stimulation of AP-1. Both IKKbeta and JNK2 are essential for efficient induction of type I IFN and ... We now describe two such pathways. The first pathway leading to NF-kappaB depends on the dsRNA-responsive ...

    Abstract Viral infection or double-stranded (ds) RNA induce interferons (IFN) and other cytokines. Transcription factors mediating IFN induction are known, but the signaling pathways that regulate them are less clear. We now describe two such pathways. The first pathway leading to NF-kappaB depends on the dsRNA-responsive protein kinase (PKR), which in turn activates IKB kinase (IKK) through the IKKbeta subunit. The second viral-and dsRNA-responsive pathway is PKR independent and involves Jun kinase (JNK) activation leading to stimulation of AP-1. Both IKKbeta and JNK2 are essential for efficient induction of type I IFN and other cytokines in response to viral infection or dsRNA. This study establishes a general role for these kinases in activation of innate immune responses.
    MeSH term(s) 3T3 Cells ; Animals ; Cell Line, Transformed ; Enzyme Activation ; Gene Expression Regulation ; Humans ; I-kappa B Kinase ; Interferon-alpha/genetics ; Interferon-beta/genetics ; JNK Mitogen-Activated Protein Kinases ; Mice ; Mice, Knockout ; Mitogen-Activated Protein Kinase 9 ; Mitogen-Activated Protein Kinases/metabolism ; Promoter Regions, Genetic ; Protein Kinases/genetics ; Protein Kinases/immunology ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/immunology ; Protein-Serine-Threonine Kinases/metabolism ; Recombinant Fusion Proteins/genetics ; Recombinant Fusion Proteins/metabolism ; Vesicular stomatitis Indiana virus/immunology ; eIF-2 Kinase/genetics ; eIF-2 Kinase/metabolism
    Chemical Substances Interferon-alpha ; Recombinant Fusion Proteins ; Interferon-beta (77238-31-4) ; Protein Kinases (EC 2.7.-) ; Mitogen-Activated Protein Kinase 9 (EC 2.7.1.24) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; eIF-2 Kinase (EC 2.7.11.1) ; CHUK protein, human (EC 2.7.11.10) ; Chuk protein, mouse (EC 2.7.11.10) ; I-kappa B Kinase (EC 2.7.11.10) ; IKBKB protein, human (EC 2.7.11.10) ; IKBKE protein, human (EC 2.7.11.10) ; Ikbkb protein, mouse (EC 2.7.11.10) ; Ikbke protein, mouse (EC 2.7.11.10) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 1999-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/s1074-7613(00)80146-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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