Ribonuclease H2 mutations induce a cGAS/STING‐dependent innate immune response

@inproceedings{Mackenzie2016RibonucleaseHM,
  title={Ribonuclease H2 mutations induce a cGAS/STING‐dependent innate immune response},
  author={Karen J. Mackenzie and Paula Carroll and Laura A. Lettice and Žygimantė Tarnauskaitė and K Vasumathi Reddy and Flora L Dix and Ailsa Revuelta and Erika Abbondati and Rachel E Rigby and Bj{\"o}rn Rabe and Fiona M. Kilanowski and Graeme Grimes and Adeline Fluteau and Paul S. Devenney and Robert E Hill and Martin A M Reijns and Andrew P. Jackson},
  booktitle={The EMBO journal},
  year={2016}
}
Aicardi-Goutières syndrome (AGS) provides a monogenic model of nucleic acid-mediated inflammation relevant to the pathogenesis of systemic autoimmunity. Mutations that impair ribonuclease (RNase) H2 enzyme function are the most frequent cause of this autoinflammatory disorder of childhood and are also associated with systemic lupus erythematosus. Reduced processing of eitherRNA:DNAhybrid or genome-embedded ribonucleotide substrates is thought to lead to activation of a yet undefined nucleic… CONTINUE READING
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