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10.4049/jimmunol.1402830 http://scihub22266oqcxt.onion/10.4049/jimmunol.1402830 C4472943!4472943 !26019272     free     free     free 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 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 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 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\26019272 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Immunol 2015 ; 195 (1 ): 277-88 Nephropedia Template TP {{tp|p=26019272 |t=2015. Dual-Specificity Phosphatase 1 and Tristetraprolin Cooperate To Regulate Macrophage Responses to Lipopolysaccharide |pdf=|usr=}}{{26019272 }} gab.com Text Dual-Specificity Phosphatase 1 and Tristetraprolin Cooperate To Regulate Macrophage Responses to Lipopolysaccharide JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26019272 #FOAvip Dual-specificity phosphatase (DUSP) 1 dephosphorylates and inactivates members of the MAPK superfamily, in particular, JNKs, p38?, and p38? MAPKs. It functions as an essential negative regulator of innate immune responses, hence disruption of the Dusp1 gene renders mice extremely sensitive to a wide variety of experimental inflammatory challenges. The principal mechanisms behind the overexpression of inflammatory mediators by Dusp1(-/-) cells are not known. In this study, we use a genetic approach to identify an important mechanism of action of DUSP1, involving the modulation of the activity of the mRNA-destabilizing protein tristetraprolin. This mechanism is key to the control of essential early mediators of inflammation, TNF, CXCL1, and CXCL2, as well as the anti-inflammatory cytokine IL-10. The same mechanism also contributes to the regulation of a large number of transcripts induced by treatment of macrophages with LPS. These findings demonstrate that modulation of the phosphorylation status of tristetraprolin is an important physiological mechanism by which innate immune responses can be controlled. Twit Text FOAVip Dual-Specificity Phosphatase 1 and Tristetraprolin Cooperate To Regulate Macrophage Responses to Lipopolysaccharide ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26019272 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26019272 #FOAvip English Wikipedia <ref>{{Cite pmid|26019272 }}</ref> Dual-Specificity Phosphatase 1 and Tristetraprolin Cooperate To Regulate Macrophage Responses to Lipopolysaccharide #MMPMID26019272 Smallie T ; Ross EA ; Ammit AJ ; Cunliffe HE ; Tang T ; Rosner DR ; Ridley ML ; Buckley CD ; Saklatvala J ; Dean JL ; Clark AR J Immunol 2015[Jul]; 195 (1 ): 277-88 PMID26019272 show ga Dual-specificity phosphatase (DUSP) 1 dephosphorylates and inactivates members of the MAPK superfamily, in particular, JNKs, p38?, and p38? MAPKs. It functions as an essential negative regulator of innate immune responses, hence disruption of the Dusp1 gene renders mice extremely sensitive to a wide variety of experimental inflammatory challenges. The principal mechanisms behind the overexpression of inflammatory mediators by Dusp1(-/-) cells are not known. In this study, we use a genetic approach to identify an important mechanism of action of DUSP1, involving the modulation of the activity of the mRNA-destabilizing protein tristetraprolin. This mechanism is key to the control of essential early mediators of inflammation, TNF, CXCL1, and CXCL2, as well as the anti-inflammatory cytokine IL-10. The same mechanism also contributes to the regulation of a large number of transcripts induced by treatment of macrophages with LPS. These findings demonstrate that modulation of the phosphorylation status of tristetraprolin is an important physiological mechanism by which innate immune responses can be controlled. |Animals [MESH] |Chemokine CXCL1/genetics/immunology [MESH] |Chemokine CXCL2/genetics/immunology [MESH] |Dual Specificity Phosphatase 1/genetics/*immunology [MESH] |Gene Expression Regulation [MESH] |Immunity, Innate [MESH] |Interleukin-10/genetics/immunology [MESH] |Lipopolysaccharides/*pharmacology [MESH] |MAP Kinase Kinase 4/genetics/immunology [MESH] |Macrophages/drug effects/*immunology/pathology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mitogen-Activated Protein Kinase 11/genetics/immunology [MESH] |Mitogen-Activated Protein Kinase 14/genetics/immunology [MESH] |Phosphorylation [MESH] |Primary Cell Culture [MESH] |RNA Stability [MESH] |RNA, Messenger/genetics/*immunology [MESH] |Signal Transduction [MESH] |Tristetraprolin/genetics/*immunology [MESH]Dual-Specificity Phosphatase 1 and Tristetraprolin Cooperate To Regula(epmc).pdf DeepDyve Pubget Overpricing