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10.1080/15476286.2016.1203501 http://scihub22266oqcxt.onion/10.1080/15476286.2016.1203501 C5449086!5449086!27362366     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       RNA+Biol 2017 ; 14 (5): 587-602 Nephropedia Template TP {{tp|p=27362366|t=2017. ADAR1 deletion induces NF?B and interferon signaling dependent liver inflammation and fibrosis |pdf=|usr=}}{{27362366}} gab.com Text ADAR1 deletion induces NF B and interferon signaling dependent liver inflammation and fibrosis JO: RNA Biol http://www.kidney.de/pget.php?&tw=1&pmid=27362366 #FOAvip Adenosine deaminase acting on RNA (ADAR) 1 binds and edits double-stranded (ds) RNA secondary structures found mainly within untranslated regions of many transcripts. In the current research, our aim was to study the role of ADAR1 in liver homeostasis. As previous studies show a conserved immunoregulatory function for ADAR1 in mammalians, we focused on its role in preventing chronic hepatic inflammation and the associated activation of hepatic stellate cells to produce extracellular matrix and promote fibrosis. We show that hepatocytes specific ADAR1 knock out (KO) mice display massive liver damage with multifocal inflammation and fibrogenesis. The bioinformatics analysis of the microarray gene-expression datasets of ADAR1 KO livers reveled a type-I interferons signature and an enrichment for immune response genes compared to control littermate livers. Furthermore, we found that in vitro silencing of ADAR1 expression in HepG2 cells leads to enhanced transcription of NF?B target genes, foremost of the pro-inflammatory cytokines IL6 and IL8. We also discovered immune cell-independent paracrine signaling among ADAR1-depleted HepG2 cells and hepatic stellate cells, leading to the activation of the latter cell type to adopt a profibrogenic phenotype. This paracrine communication dependent mainly on the production and secretion of the cytokine IL6 induced by ADAR1 silencing in hepatocytes. Thus, our findings shed a new light on the vital regulatory role of ADAR1 in hepatic immune homeostasis, chiefly its inhibitory function on the crosstalk between the NF?B and type-I interferons signaling cascades, restraining the development of liver inflammation and fibrosis. Twit Text FOAVip ADAR1 deletion induces NF B and interferon signaling dependent liver inflammation and fibrosis ????RNA Biol http://www.kidney.de/pget.php?&tw=1&pmid=27362366 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27362366 #FOAvip English Wikipedia <ref>{{Cite pmid|27362366}}</ref> ADAR1 deletion induces NF?B and interferon signaling dependent liver inflammation and fibrosis #MMPMID27362366 Ben-Shoshan SO; Kagan P; Sultan M; Barabash Z; Dor C; Jacob-Hirsch J; Harmelin A; Pappo O; Marcu-Malina V; Ben-Ari Z; Amariglio N; Rechavi G; Goldstein I; Safran M RNA Biol 2017[]; 14 (5): 587-602 PMID27362366show ga Adenosine deaminase acting on RNA (ADAR) 1 binds and edits double-stranded (ds) RNA secondary structures found mainly within untranslated regions of many transcripts. In the current research, our aim was to study the role of ADAR1 in liver homeostasis. As previous studies show a conserved immunoregulatory function for ADAR1 in mammalians, we focused on its role in preventing chronic hepatic inflammation and the associated activation of hepatic stellate cells to produce extracellular matrix and promote fibrosis. We show that hepatocytes specific ADAR1 knock out (KO) mice display massive liver damage with multifocal inflammation and fibrogenesis. The bioinformatics analysis of the microarray gene-expression datasets of ADAR1 KO livers reveled a type-I interferons signature and an enrichment for immune response genes compared to control littermate livers. Furthermore, we found that in vitro silencing of ADAR1 expression in HepG2 cells leads to enhanced transcription of NF?B target genes, foremost of the pro-inflammatory cytokines IL6 and IL8. We also discovered immune cell-independent paracrine signaling among ADAR1-depleted HepG2 cells and hepatic stellate cells, leading to the activation of the latter cell type to adopt a profibrogenic phenotype. This paracrine communication dependent mainly on the production and secretion of the cytokine IL6 induced by ADAR1 silencing in hepatocytes. Thus, our findings shed a new light on the vital regulatory role of ADAR1 in hepatic immune homeostasis, chiefly its inhibitory function on the crosstalk between the NF?B and type-I interferons signaling cascades, restraining the development of liver inflammation and fibrosis. äADAR1 deletion induces NF?B and interferon signaling dependent liver i(epmc).pdf DeepDyve Pubget Overpricing