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10.1016/j.immuni.2015.11.001 http://scihub22266oqcxt.onion/10.1016/j.immuni.2015.11.001 C4654992!4654992 !26588779     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26588779 &cmd=llinks): Failed to open stream: HTTP request failed! 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Isoforms of RNA-Editing Enzyme ADAR1 Independently Control Nucleic Acid Sensor MDA5-Driven Autoimmunity and Multi-organ Development |pdf=|usr=}}{{26588779 }} gab.com Text Isoforms of RNA-Editing Enzyme ADAR1 Independently Control Nucleic Acid Sensor MDA5-Driven Autoimmunity and Multi-organ Development JO: Immunity http://www.kidney.de/pget.php?&tw=1&pmid=26588779 #FOAvip Mutations in ADAR, which encodes the ADAR1 RNA-editing enzyme, cause Aicardi-Goutières syndrome (AGS), a severe autoimmune disease associated with an aberrant type I interferon response. How ADAR1 prevents autoimmunity remains incompletely defined. Here, we demonstrate that ADAR1 is a specific and essential negative regulator of the MDA5-MAVS RNA sensing pathway. Moreover, we uncovered a MDA5-MAVS-independent function for ADAR1 in the development of multiple organs. We showed that the p150 isoform of ADAR1 uniquely regulated the MDA5 pathway, whereas both the p150 and p110 isoforms contributed to development. Abrupt deletion of ADAR1 in adult mice revealed that both of these functions were required throughout life. Our findings delineate genetically separable roles for both ADAR1 isoforms in vivo, with implications for the human diseases caused by ADAR mutations. Twit Text FOAVip Isoforms of RNA-Editing Enzyme ADAR1 Independently Control Nucleic Acid Sensor MDA5-Driven Autoimmunity and Multi-organ Development ????Immunity http://www.kidney.de/pget.php?&tw=1&pmid=26588779 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26588779 #FOAvip English Wikipedia <ref>{{Cite pmid|26588779 }}</ref> Isoforms of RNA-Editing Enzyme ADAR1 Independently Control Nucleic Acid Sensor MDA5-Driven Autoimmunity and Multi-organ Development #MMPMID26588779 Pestal K ; Funk CC ; Snyder JM ; Price ND ; Treuting PM ; Stetson DB Immunity 2015[Nov]; 43 (5 ): 933-44 PMID26588779 show ga Mutations in ADAR, which encodes the ADAR1 RNA-editing enzyme, cause Aicardi-Goutières syndrome (AGS), a severe autoimmune disease associated with an aberrant type I interferon response. How ADAR1 prevents autoimmunity remains incompletely defined. Here, we demonstrate that ADAR1 is a specific and essential negative regulator of the MDA5-MAVS RNA sensing pathway. Moreover, we uncovered a MDA5-MAVS-independent function for ADAR1 in the development of multiple organs. We showed that the p150 isoform of ADAR1 uniquely regulated the MDA5 pathway, whereas both the p150 and p110 isoforms contributed to development. Abrupt deletion of ADAR1 in adult mice revealed that both of these functions were required throughout life. Our findings delineate genetically separable roles for both ADAR1 isoforms in vivo, with implications for the human diseases caused by ADAR mutations. |Adaptor Proteins, Signal Transducing/metabolism [MESH] |Adenosine Deaminase/*metabolism [MESH] |Animals [MESH] |Autoimmune Diseases of the Nervous System/metabolism [MESH] |Autoimmunity/*physiology [MESH] |DEAD-box RNA Helicases/*metabolism [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Interferon Type I/metabolism [MESH] |Interferon-Induced Helicase, IFIH1 [MESH] |Mice [MESH] |Nervous System Malformations/metabolism [MESH] |Protein Isoforms/*metabolism [MESH] |RNA Editing/*physiology [MESH] |RNA-Binding Proteins/metabolism [MESH] |RNA/*metabolism [MESH]Isoforms of RNA-Editing Enzyme ADAR1 Independently Control Nucleic Aci(epmc).pdf DeepDyve Pubget Overpricing