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Showing 1–7 of 7 results
Advanced filters: Author: Ram M. Adar Clear advanced filters

  • The autoinflammatory pathology associated with alteration of the ZBD domain of the RNA-editing enzyme ADAR1 is driven by signalling that is dependent on the nucleotide sensor ZBP1.

    • Nicholas W. Hubbard
    • Joshua M. Ames
    • Andrew Oberst
    Research
    Nature
    Volume: 607, P: 769-775

  • Yanick Crow and colleagues show that mutations in ADAR1 cause the autoimmune disorder Aicardi-Goutières syndrome, accompanied by upregulation of interferon-stimulated genes. ADAR1 encodes an enzyme that catalyzes the deamination of adeonosine to inosine in double-stranded RNA, and the findings suggest a possible role for RNA editing in limiting the accumulation of repeat-derived RNA species.

    • Gillian I Rice
    • Paul R Kasher
    • Yanick J Crow
    Research
    Nature Genetics
    Volume: 44, P: 1243-1248

  • A survey of known human DNA editing sites with an RNA editing site prediction algorithm suggests APOBEC-mediated RNA editing may produce some of the same protein variants, with the possibility of affecting multiple areas of health.

    • Melissa Van Norden
    • Zackary Falls
    • Peter L. Elkin
    ResearchOpen Access
    Communications Biology
    Volume: 7, P: 1-10

  • Mutations in LSM11 and RNU7-1, which encode components of the replication-dependent histone pre-mRNA–processing complex, cause an autoinflammatory syndrome due to enhanced interferon signaling mediated by the cGAS–STING pathway, showing an essential role for nuclear histones in suppressing the immunogenicity of self-DNA.

    • Carolina Uggenti
    • Alice Lepelley
    • Yanick J. Crow
    Research
    Nature Genetics
    Volume: 52, P: 1364-1372

  • This overview of the ENCODE project outlines the data accumulated so far, revealing that 80% of the human genome now has at least one biochemical function assigned to it; the newly identified functional elements should aid the interpretation of results of genome-wide association studies, as many correspond to sites of association with human disease.

    • Ian Dunham
    • Anshul Kundaje
    • Ewan Birney
    ResearchOpen Access
    Nature
    Volume: 489, P: 57-74