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10.1111/cei.12764 http://scihub22266oqcxt.onion/10.1111/cei.12764 C4837237!4837237 !26724675     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 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\26724675 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Clin+Exp+Immunol 2016 ; 184 (2 ): 183-96 Nephropedia Template TP {{tp|p=26724675 |t=2016. Downstream activation of NF-?B in the EDA-A1/EDAR signalling in Sjögren s syndrome and its regulation by the ubiquitin-editing enzyme A20 |pdf=|usr=}}{{26724675 }} gab.com Text Downstream activation of NF- B in the EDA-A1/EDAR signalling in Sjögren s syndrome and its regulation by the ubiquitin-editing enzyme A20 JO: Clin Exp Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26724675 #FOAvip Sjögren's syndrome (SS) is an autoimmune disease and the second most common chronic systemic rheumatic disorder. Prevalence of primary SS in the general population has been estimated to be approximately 1-3%, whereas secondary SS has been observed in 10-20% of patients with rheumatoid arthritis, systemic lupus erythematosus (SLE) and scleroderma. Despite this, its exact aetiology and pathogenesis are largely unexplored. Nuclear factor-kappa B (NF-?B) signalling mechanisms provide central controls in SS, but how these pathways intersect the pathological features of this disease is unclear. The ubiquitin-editing enzyme A20 (tumour necrosis factor-?-induced protein 3, TNFAIP3) serves as a critical inhibitor on NF-?B signalling. In humans, polymorphisms in the A20 gene or a deregulated expression of A20 are often associated with several inflammatory disorders, including SS. Because A20 controls the ectodysplasin-A1 (EDA-A1)/ectodysplasin receptor (EDAR) signalling negatively, and the deletion of A20 results in excessive EDA1-induced NF-?B signalling, this work investigates the expression levels of EDA-A1 and EDAR in SS human salivary glands epithelial cells (SGEC) and evaluates the hypothesis that SS SGEC-specific deregulation of A20 results in excessive EDA1-induced NF-?B signalling in SS. Our approach, which combines the use of siRNA-mediated gene silencing and quantitative pathway analysis, was used to elucidate the role of the A20 target gene in intracellular EDA-A1/EDAR/NF-?B pathway in SS SGEC, holding significant promise for compound selection in drug discovery. Twit Text FOAVip Downstream activation of NF- B in the EDA-A1/EDAR signalling in Sjögren s syndrome and its regulation by the ubiquitin-editing enzyme A20 ????Clin Exp Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26724675 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26724675 #FOAvip English Wikipedia <ref>{{Cite pmid|26724675 }}</ref> Downstream activation of NF-?B in the EDA-A1/EDAR signalling in Sjögren s syndrome and its regulation by the ubiquitin-editing enzyme A20 #MMPMID26724675 Sisto M ; Barca A ; Lofrumento DD ; Lisi S Clin Exp Immunol 2016[May]; 184 (2 ): 183-96 PMID26724675 show ga Sjögren's syndrome (SS) is an autoimmune disease and the second most common chronic systemic rheumatic disorder. Prevalence of primary SS in the general population has been estimated to be approximately 1-3%, whereas secondary SS has been observed in 10-20% of patients with rheumatoid arthritis, systemic lupus erythematosus (SLE) and scleroderma. Despite this, its exact aetiology and pathogenesis are largely unexplored. Nuclear factor-kappa B (NF-?B) signalling mechanisms provide central controls in SS, but how these pathways intersect the pathological features of this disease is unclear. The ubiquitin-editing enzyme A20 (tumour necrosis factor-?-induced protein 3, TNFAIP3) serves as a critical inhibitor on NF-?B signalling. In humans, polymorphisms in the A20 gene or a deregulated expression of A20 are often associated with several inflammatory disorders, including SS. Because A20 controls the ectodysplasin-A1 (EDA-A1)/ectodysplasin receptor (EDAR) signalling negatively, and the deletion of A20 results in excessive EDA1-induced NF-?B signalling, this work investigates the expression levels of EDA-A1 and EDAR in SS human salivary glands epithelial cells (SGEC) and evaluates the hypothesis that SS SGEC-specific deregulation of A20 results in excessive EDA1-induced NF-?B signalling in SS. Our approach, which combines the use of siRNA-mediated gene silencing and quantitative pathway analysis, was used to elucidate the role of the A20 target gene in intracellular EDA-A1/EDAR/NF-?B pathway in SS SGEC, holding significant promise for compound selection in drug discovery. |DNA-Binding Proteins/genetics/*metabolism [MESH] |Ectodysplasins/*metabolism [MESH] |Edar Receptor/*metabolism [MESH] |Epithelial Cells/metabolism [MESH] |Humans [MESH] |I-kappa B Proteins/genetics [MESH] |Intracellular Signaling Peptides and Proteins/genetics/*metabolism [MESH] |NF-KappaB Inhibitor alpha [MESH] |NF-kappa B/*metabolism [MESH] |Nuclear Proteins/genetics/*metabolism [MESH] |RNA Interference [MESH] |RNA, Small Interfering/genetics [MESH] |Salivary Glands/cytology/metabolism [MESH] |Signal Transduction [MESH] |Sjogren's Syndrome/*pathology [MESH]Downstream activation of NF-?B in the EDA-A1/EDAR signalling in Sjögre(epmc).pdf DeepDyve Pubget Overpricing