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10.1016/j.immuni.2017.03.014 http://scihub22266oqcxt.onion/10.1016/j.immuni.2017.03.014 C5501252!5501252 !28410990     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28410990 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Immunity 2017 ; 46 (4 ): 635-648 Nephropedia Template TP {{tp|p=28410990 |t=2017. Tyrosine Kinase SYK Licenses MyD88 Adaptor Protein to Instigate IL-1?-Mediated Inflammatory Disease |pdf=|usr=}}{{28410990 }} gab.com Text Tyrosine Kinase SYK Licenses MyD88 Adaptor Protein to Instigate IL-1 -Mediated Inflammatory Disease JO: Immunity http://www.kidney.de/pget.php?&tw=1&pmid=28410990 #FOAvip Mice carrying a hypomorphic point mutation in the Ptpn6 gene (Ptpn6(spin) mice) develop an inflammatory skin disease that resembles neutrophilic dermatosis in humans. Here, we demonstrated that interleukin-1? (IL-1?) signaling through IL-1R and MyD88 in both stromal and immune cells drive inflammation in Ptpn6(spin) mice. We further identified SYK as a critical kinase that phosphorylates MyD88, promoted MyD88-dependent signaling and mediates dermatosis in Ptpn6(spin) mice. Our studies further demonstrated that SHP1 encoded by Ptpn6 binds and suppresses SYK activation to inhibit MyD88 phosphorylation. Downstream of SHP1 and SYK-dependent counterregulation of MyD88 tyrosine phosphorylation, we have demonstrated that the scaffolding function of receptor interacting protein kinase 1 (RIPK1) and tumor growth factor-? activated kinase 1 (TAK1)-mediating signaling were required to spur inflammatory disease. Overall, these studies identify SHP1 and SYK crosstalk as a critical regulator of MyD88 post-translational modifications and IL-1-driven inflammation. Twit Text FOAVip Tyrosine Kinase SYK Licenses MyD88 Adaptor Protein to Instigate IL-1 -Mediated Inflammatory Disease ????Immunity http://www.kidney.de/pget.php?&tw=1&pmid=28410990 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28410990 #FOAvip English Wikipedia <ref>{{Cite pmid|28410990 }}</ref> Tyrosine Kinase SYK Licenses MyD88 Adaptor Protein to Instigate IL-1?-Mediated Inflammatory Disease #MMPMID28410990 Gurung P ; Fan G ; Lukens JR ; Vogel P ; Tonks NK ; Kanneganti TD Immunity 2017[Apr]; 46 (4 ): 635-648 PMID28410990 show ga Mice carrying a hypomorphic point mutation in the Ptpn6 gene (Ptpn6(spin) mice) develop an inflammatory skin disease that resembles neutrophilic dermatosis in humans. Here, we demonstrated that interleukin-1? (IL-1?) signaling through IL-1R and MyD88 in both stromal and immune cells drive inflammation in Ptpn6(spin) mice. We further identified SYK as a critical kinase that phosphorylates MyD88, promoted MyD88-dependent signaling and mediates dermatosis in Ptpn6(spin) mice. Our studies further demonstrated that SHP1 encoded by Ptpn6 binds and suppresses SYK activation to inhibit MyD88 phosphorylation. Downstream of SHP1 and SYK-dependent counterregulation of MyD88 tyrosine phosphorylation, we have demonstrated that the scaffolding function of receptor interacting protein kinase 1 (RIPK1) and tumor growth factor-? activated kinase 1 (TAK1)-mediating signaling were required to spur inflammatory disease. Overall, these studies identify SHP1 and SYK crosstalk as a critical regulator of MyD88 post-translational modifications and IL-1-driven inflammation. |Animals [MESH] |Flow Cytometry [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Immunoblotting [MESH] |Inflammation/genetics/*immunology/metabolism [MESH] |Interleukin-1alpha/genetics/*immunology/metabolism [MESH] |MAP Kinase Kinase Kinases/genetics/immunology/metabolism [MESH] |Mice, Knockout [MESH] |Models, Immunological [MESH] |Mutation [MESH] |Myeloid Differentiation Factor 88/genetics/*immunology/metabolism [MESH] |Phosphorylation [MESH] |Protein Tyrosine Phosphatase, Non-Receptor Type 6/genetics/immunology/metabolism [MESH] |Receptor-Interacting Protein Serine-Threonine Kinases/genetics/immunology/metabolism [MESH] |Receptors, Interleukin-1/immunology/metabolism [MESH] |Signal Transduction/genetics/immunology [MESH] |Skin Diseases/genetics/*immunology/metabolism [MESH]Tyrosine Kinase SYK Licenses MyD88 Adaptor Protein to Instigate IL-1?-(epmc).pdf DeepDyve Pubget Overpricing