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10.4049/jimmunol.1301601 http://scihub22266oqcxt.onion/10.4049/jimmunol.1301601 24929003!ä!24929003 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2014 ; 193 (2): 840-8 Nephropedia Template TP {{tp|p=24929003|t=2014. DOK3 is required for IFN-beta production by enabling TRAF3/TBK1 complex formation and IRF3 activation |pdf=|usr=}}{{24929003}} gab.com Text DOK3 is required for IFN-beta production by enabling TRAF3/TBK1 complex formation and IRF3 activation JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24929003 #FOAvip The downstream of kinase (DOK) family of adaptors is generally involved in the negative regulation of signaling pathways. DOK1, 2, and 3 were shown to attenuate TLR4 signaling by inhibiting Ras-ERK activation. In this study, we elucidated a novel role for DOK3 in IFN-beta production. Macrophages lacking DOK3 were impaired in IFN-beta synthesis upon influenza virus infection or polyinosinic-polyribocytidylic acid stimulation. In the absence of DOK3, the transcription factor IFN regulatory factor 3 was not phosphorylated and could not translocate to the nucleus to activate ifn-beta gene expression. Interestingly, polyinosinic-polyribocytidylic acid-induced formation of the upstream TNFR-associated factor (TRAF) 3/TANK-binding kinase (TBK) 1 complex was compromised in dok3(-/-) macrophages. DOK3 was shown to bind TBK1 and was required for its activation. Furthermore, we demonstrated that overexpression of DOK3 and TBK1 could significantly enhance ifn-beta promoter activity. DOK3 was also shown to bind TRAF3, and the binding of TRAF3 and TBK1 to DOK3 required the tyrosine-rich C-terminal domain of DOK3. We further revealed that DOK3 was phosphorylated by Bruton's tyrosine kinase. Hence, DOK3 plays a critical and positive role in TLR3 signaling by enabling TRAF3/TBK1 complex formation and facilitating TBK1 and IFN regulatory factor 3 activation and the induction of IFN-beta production. Twit Text FOAVip DOK3 is required for IFN-beta production by enabling TRAF3/TBK1 complex formation and IRF3 activation ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24929003 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24929003 #FOAvip English Wikipedia <ref>{{Cite pmid|24929003}}</ref> DOK3 is required for IFN-beta production by enabling TRAF3/TBK1 complex formation and IRF3 activation #MMPMID24929003 Kim SS; Lee KG; Chin CS; Ng SK; Pereira NA; Xu S; Lam KP J Immunol 2014[Jul]; 193 (2): 840-8 PMID24929003show ga The downstream of kinase (DOK) family of adaptors is generally involved in the negative regulation of signaling pathways. DOK1, 2, and 3 were shown to attenuate TLR4 signaling by inhibiting Ras-ERK activation. In this study, we elucidated a novel role for DOK3 in IFN-beta production. Macrophages lacking DOK3 were impaired in IFN-beta synthesis upon influenza virus infection or polyinosinic-polyribocytidylic acid stimulation. In the absence of DOK3, the transcription factor IFN regulatory factor 3 was not phosphorylated and could not translocate to the nucleus to activate ifn-beta gene expression. Interestingly, polyinosinic-polyribocytidylic acid-induced formation of the upstream TNFR-associated factor (TRAF) 3/TANK-binding kinase (TBK) 1 complex was compromised in dok3(-/-) macrophages. DOK3 was shown to bind TBK1 and was required for its activation. Furthermore, we demonstrated that overexpression of DOK3 and TBK1 could significantly enhance ifn-beta promoter activity. DOK3 was also shown to bind TRAF3, and the binding of TRAF3 and TBK1 to DOK3 required the tyrosine-rich C-terminal domain of DOK3. We further revealed that DOK3 was phosphorylated by Bruton's tyrosine kinase. Hence, DOK3 plays a critical and positive role in TLR3 signaling by enabling TRAF3/TBK1 complex formation and facilitating TBK1 and IFN regulatory factor 3 activation and the induction of IFN-beta production. |Adaptor Proteins, Signal Transducing/genetics/*metabolism[MESH] |Animals[MESH] |Blotting, Western[MESH] |Cells, Cultured[MESH] |Gene Expression[MESH] |HEK293 Cells[MESH] |Host-Pathogen Interactions[MESH] |Humans[MESH] |Interferon Regulatory Factor-3/genetics/*metabolism[MESH] |Interferon-beta/genetics/*metabolism[MESH] |Macrophages/cytology/metabolism/virology[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |Microscopy, Confocal[MESH] |Orthomyxoviridae/physiology[MESH] |Phosphorylation/drug effects[MESH] |Poly I-C/pharmacology[MESH] |Promoter Regions, Genetic/genetics[MESH] |Protein Binding[MESH] |Protein Serine-Threonine Kinases/genetics/*metabolism[MESH] |Reverse Transcriptase Polymerase Chain Reaction[MESH] |Signal Transduction/drug effects/genetics[MESH] |TNF Receptor-Associated Factor 3/genetics/*metabolism[MESH]DOK3 is required for IFN-beta production by enabling TRAF3/TBK1 comple(epmc).pdf DeepDyve Pubget Overpricing