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http://scihub22266oqcxt.onion/ 11441823!ä!11441823 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Biol+Chem 2001 ; 276 (24): 10990-8 Nephropedia Template TP {{tp|p=11441823|t=2001. Influenza virus-induced AP-1-dependent gene expression requires activation of the JNK signaling pathway |pdf=|usr=}}{{11441823}} gab.com Text Influenza virus-induced AP-1-dependent gene expression requires activation of the JNK signaling pathway JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=11441823 #FOAvip 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. Twit Text FOAVip Influenza virus-induced AP-1-dependent gene expression requires activation of the JNK signaling pathway ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=11441823 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=11441823 #FOAvip English Wikipedia <ref>{{Cite pmid|11441823}}</ref> Influenza virus-induced AP-1-dependent gene expression requires activation of the JNK signaling pathway #MMPMID11441823 Ludwig S; Ehrhardt C; Neumeier ER; Kracht M; Rapp UR; Pleschka S J Biol Chem 2001[Jun]; 276 (24): 10990-8 PMID11441823show ga 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. |*Gene Expression Regulation, Viral[MESH] |*JNK Mitogen-Activated Protein Kinases[MESH] |*MAP Kinase Kinase 4[MESH] |*MAP Kinase Signaling System[MESH] |Activating Transcription Factor 2[MESH] |Cell Line[MESH] |Cyclic AMP Response Element-Binding Protein/metabolism[MESH] |DNA-Directed DNA Polymerase/metabolism[MESH] |DNA/metabolism[MESH] |Enzyme Activation[MESH] |HeLa Cells[MESH] |Humans[MESH] |Influenza A virus/*physiology[MESH] |Interferon-beta/genetics[MESH] |MAP Kinase Kinase 7[MESH] |Mitogen-Activated Protein Kinase Kinases/*metabolism[MESH] |Phosphorylation[MESH] |Promoter Regions, Genetic[MESH] |Protein Binding[MESH] |RNA, Viral/metabolism[MESH] |Species Specificity[MESH] |Transcription Factor AP-1/*physiology[MESH] |Transcription Factors/metabolism[MESH] |U937 Cells[MESH]Influenza virus-induced AP-1-dependent gene expression requires activa(epmc).pdf DeepDyve Pubget Overpricing