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http://purl.uniprot.org/citations/25692705http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25692705http://www.w3.org/2000/01/rdf-schema#comment"Dysfunction in Ataxia-telangiectasia mutated (ATM), a central component of the DNA repair machinery, results in Ataxia Telangiectasia (AT), a cancer-prone disease with a variety of inflammatory manifestations. By analyzing AT patient samples and Atm(-/-) mice, we found that unrepaired DNA lesions induce type I interferons (IFNs), resulting in enhanced anti-viral and anti-bacterial responses in Atm(-/-) mice. Priming of the type I interferon system by DNA damage involved release of DNA into the cytoplasm where it activated the cytosolic DNA sensing STING-mediated pathway, which in turn enhanced responses to innate stimuli by activating the expression of Toll-like receptors, RIG-I-like receptors, cytoplasmic DNA sensors, and their downstream signaling partners. This study provides a potential explanation for the inflammatory phenotype of AT patients and establishes damaged DNA as a cell intrinsic danger signal that primes the innate immune system for a rapid and amplified response to microbial and environmental threats."xsd:string
http://purl.uniprot.org/citations/25692705http://purl.org/dc/terms/identifier"doi:10.1016/j.immuni.2015.01.012"xsd:string
http://purl.uniprot.org/citations/25692705http://purl.uniprot.org/core/author"Weiss S."xsd:string
http://purl.uniprot.org/citations/25692705http://purl.uniprot.org/core/author"Nilsson J.A."xsd:string
http://purl.uniprot.org/citations/25692705http://purl.uniprot.org/core/author"Lienenklaus S."xsd:string
http://purl.uniprot.org/citations/25692705http://purl.uniprot.org/core/author"Gekara N.O."xsd:string
http://purl.uniprot.org/citations/25692705http://purl.uniprot.org/core/author"Nilsson L.M."xsd:string
http://purl.uniprot.org/citations/25692705http://purl.uniprot.org/core/author"Kroger A."xsd:string
http://purl.uniprot.org/citations/25692705http://purl.uniprot.org/core/author"Resch U."xsd:string
http://purl.uniprot.org/citations/25692705http://purl.uniprot.org/core/author"Anugula S."xsd:string
http://purl.uniprot.org/citations/25692705http://purl.uniprot.org/core/author"Erttmann S.F."xsd:string
http://purl.uniprot.org/citations/25692705http://purl.uniprot.org/core/author"Ek T."xsd:string
http://purl.uniprot.org/citations/25692705http://purl.uniprot.org/core/author"Hartlova A."xsd:string
http://purl.uniprot.org/citations/25692705http://purl.uniprot.org/core/author"Raffi F.A."xsd:string
http://purl.uniprot.org/citations/25692705http://purl.uniprot.org/core/author"Schmalz A.M."xsd:string
http://purl.uniprot.org/citations/25692705http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/25692705http://purl.uniprot.org/core/name"Immunity"xsd:string
http://purl.uniprot.org/citations/25692705http://purl.uniprot.org/core/pages"332-343"xsd:string
http://purl.uniprot.org/citations/25692705http://purl.uniprot.org/core/title"DNA damage primes the type I interferon system via the cytosolic DNA sensor STING to promote anti-microbial innate immunity."xsd:string
http://purl.uniprot.org/citations/25692705http://purl.uniprot.org/core/volume"42"xsd:string
http://purl.uniprot.org/citations/25692705http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25692705
http://purl.uniprot.org/citations/25692705http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/25692705
http://purl.uniprot.org/uniprot/#_A0A125R9I3-mappedCitation-25692705http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25692705
http://purl.uniprot.org/uniprot/#_D3Z0Q2-mappedCitation-25692705http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25692705