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10.1128/MCB.01228-14 http://scihub22266oqcxt.onion/10.1128/MCB.01228-14 C4323494!4323494 !25512613     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25512613 &cmd=llinks): Failed to open stream: HTTP request failed! 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Stabilization of ATF5 by TAK1-Nemo-like kinase critically regulates the interleukin-1?-stimulated C/EBP signaling pathway |pdf=|usr=}}{{25512613 }} gab.com Text Stabilization of ATF5 by TAK1-Nemo-like kinase critically regulates the interleukin-1 -stimulated C/EBP signaling pathway JO: Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=25512613 #FOAvip Interleukin-1? (IL-1?) is a key proinflammatory cytokine that initiates several signaling cascades, including those involving CCAAT/enhancer binding proteins (C/EBPs). The mechanism by which IL-1? propagates a signal that activates C/EBP has remained elusive. Nemo-like kinase (NLK) is a mitogen-activated protein kinase (MAPK)-like kinase associated with many pathways and phenotypes that are not yet well understood. Using a luciferase reporter screen, we found that IL-1?-induced C/EBP activation was positively regulated by NLK. Overexpression of NLK activated C/EBP and potentiated IL-1?-triggered C/EBP activation, whereas knockdown or knockout of NLK had the opposite effect. NLK interacted with activating transcription factor 5 (ATF5) and inhibited the proteasome-dependent degradation of ATF5 in a kinase-independent manner. Consistently, NLK deficiency resulted in decreased levels of ATF5. NLK cooperated with ATF5 to activate C/EBP, whereas NLK could not activate C/EBP upon knockdown of ATF5. Moreover, TAK1, a downstream effector of IL-1? that acts upstream of NLK, mimicked the ability of NLK to stabilize ATF5 and activate C/EBP. Thus, our findings reveal the TAK1-NLK pathway as a novel regulator of basal or IL-1?-triggered C/EBP activation though stabilization of ATF5. Twit Text FOAVip Stabilization of ATF5 by TAK1-Nemo-like kinase critically regulates the interleukin-1 -stimulated C/EBP signaling pathway ????Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=25512613 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25512613 #FOAvip English Wikipedia <ref>{{Cite pmid|25512613 }}</ref> Stabilization of ATF5 by TAK1-Nemo-like kinase critically regulates the interleukin-1?-stimulated C/EBP signaling pathway #MMPMID25512613 Zhang ZY ; Li SZ ; Zhang HH ; Wu QR ; Gong J ; Liang T ; Gao L ; Xing NN ; Liu WB ; Du RL ; Zhang XD Mol Cell Biol 2015[Mar]; 35 (5 ): 778-88 PMID25512613 show ga Interleukin-1? (IL-1?) is a key proinflammatory cytokine that initiates several signaling cascades, including those involving CCAAT/enhancer binding proteins (C/EBPs). The mechanism by which IL-1? propagates a signal that activates C/EBP has remained elusive. Nemo-like kinase (NLK) is a mitogen-activated protein kinase (MAPK)-like kinase associated with many pathways and phenotypes that are not yet well understood. Using a luciferase reporter screen, we found that IL-1?-induced C/EBP activation was positively regulated by NLK. Overexpression of NLK activated C/EBP and potentiated IL-1?-triggered C/EBP activation, whereas knockdown or knockout of NLK had the opposite effect. NLK interacted with activating transcription factor 5 (ATF5) and inhibited the proteasome-dependent degradation of ATF5 in a kinase-independent manner. Consistently, NLK deficiency resulted in decreased levels of ATF5. NLK cooperated with ATF5 to activate C/EBP, whereas NLK could not activate C/EBP upon knockdown of ATF5. Moreover, TAK1, a downstream effector of IL-1? that acts upstream of NLK, mimicked the ability of NLK to stabilize ATF5 and activate C/EBP. Thus, our findings reveal the TAK1-NLK pathway as a novel regulator of basal or IL-1?-triggered C/EBP activation though stabilization of ATF5. |*Gene Expression Regulation, Enzymologic [MESH] |*Signal Transduction [MESH] |Activating Transcription Factors/*metabolism [MESH] |Animals [MESH] |Base Sequence [MESH] |CCAAT-Enhancer-Binding Proteins/*metabolism [MESH] |Cell Line, Tumor [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Interleukin-1beta/*physiology [MESH] |Intracellular Signaling Peptides and Proteins/*metabolism [MESH] |Luciferases/metabolism [MESH] |MAP Kinase Kinase Kinases/*metabolism [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Microscopy, Confocal [MESH] |Molecular Sequence Data [MESH] |Phosphorylation [MESH] |Plasmids/metabolism [MESH] |Protein Serine-Threonine Kinases/*metabolism [MESH] |RNA Interference [MESH]Stabilization of ATF5 by TAK1-Nemo-like kinase critically regulates th(epmc).pdf DeepDyve Pubget Overpricing