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10.1038/ni.3409 http://scihub22266oqcxt.onion/10.1038/ni.3409 C4836962!4836962 !27019227     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27019227 &cmd=llinks): Failed to open stream: HTTP request failed! 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DNA polymerase-? regulates the activation of type I interferons through cytosolic RNA:DNA synthesis |pdf=|usr=}}{{27019227 }} gab.com Text DNA polymerase- regulates the activation of type I interferons through cytosolic RNA:DNA synthesis JO: Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27019227 #FOAvip Aberrant nucleic acids generated during viral replication are the main trigger for antiviral immunity, and mutations that disrupt nucleic acid metabolism can lead to autoinflammatory disorders. Here we investigated the etiology of X-linked reticulate pigmentary disorder (XLPDR), a primary immunodeficiency with autoinflammatory features. We discovered that XLPDR is caused by an intronic mutation that disrupts the expression of POLA1, which encodes the catalytic subunit of DNA polymerase-?. Unexpectedly, POLA1 deficiency resulted in increased production of type I interferons. This enzyme is necessary for the synthesis of RNA:DNA primers during DNA replication and, strikingly, we found that POLA1 is also required for the synthesis of cytosolic RNA:DNA, which directly modulates interferon activation. Together this work identifies POLA1 as a critical regulator of the type I interferon response. Twit Text FOAVip DNA polymerase- regulates the activation of type I interferons through cytosolic RNA:DNA synthesis ????Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27019227 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27019227 #FOAvip English Wikipedia <ref>{{Cite pmid|27019227 }}</ref> DNA polymerase-? regulates the activation of type I interferons through cytosolic RNA:DNA synthesis #MMPMID27019227 Starokadomskyy P ; Gemelli T ; Rios JJ ; Xing C ; Wang RC ; Li H ; Pokatayev V ; Dozmorov I ; Khan S ; Miyata N ; Fraile G ; Raj P ; Xu Z ; Xu Z ; Ma L ; Lin Z ; Wang H ; Yang Y ; Ben-Amitai D ; Orenstein N ; Mussaffi H ; Baselga E ; Tadini G ; Grunebaum E ; Sarajlija A ; Krzewski K ; Wakeland EK ; Yan N ; de la Morena MT ; Zinn AR ; Burstein E Nat Immunol 2016[May]; 17 (5 ): 495-504 PMID27019227 show ga Aberrant nucleic acids generated during viral replication are the main trigger for antiviral immunity, and mutations that disrupt nucleic acid metabolism can lead to autoinflammatory disorders. Here we investigated the etiology of X-linked reticulate pigmentary disorder (XLPDR), a primary immunodeficiency with autoinflammatory features. We discovered that XLPDR is caused by an intronic mutation that disrupts the expression of POLA1, which encodes the catalytic subunit of DNA polymerase-?. Unexpectedly, POLA1 deficiency resulted in increased production of type I interferons. This enzyme is necessary for the synthesis of RNA:DNA primers during DNA replication and, strikingly, we found that POLA1 is also required for the synthesis of cytosolic RNA:DNA, which directly modulates interferon activation. Together this work identifies POLA1 as a critical regulator of the type I interferon response. |Base Sequence [MESH] |Cells, Cultured [MESH] |Cytosol/metabolism [MESH] |DNA Polymerase I/genetics/*metabolism [MESH] |DNA/*biosynthesis/genetics [MESH] |Family Health [MESH] |Female [MESH] |Fibroblasts/cytology/metabolism [MESH] |Gene Expression Profiling [MESH] |Genetic Diseases, X-Linked/genetics/metabolism [MESH] |HEK293 Cells [MESH] |HeLa Cells [MESH] |Humans [MESH] |Immunoblotting [MESH] |Interferon Type I/*metabolism [MESH] |Male [MESH] |Microscopy, Confocal [MESH] |Mutation [MESH] |Oligonucleotide Array Sequence Analysis [MESH] |Pedigree [MESH] |Pigmentation Disorders/genetics/metabolism [MESH] |RNA/*biosynthesis/genetics [MESH]DNA polymerase-? regulates the activation of type I interferons throug(epmc).pdf DeepDyve Pubget Overpricing