
@ARTICLE{Gabay2022-gw,
  title    = "Landscape of adenosine-to-inosine {RNA} recoding across human
              tissues",
  author   = "Gabay, Orshay and Shoshan, Yoav and Kopel, Eli and Ben-Zvi, Udi
              and Mann, Tomer D and Bressler, Noam and Cohen-Fultheim, Roni and
              Schaffer, Amos A and Roth, Shalom Hillel and Tzur, Ziv and
              Levanon, Erez Y and Eisenberg, Eli",
  abstract = "RNA editing by adenosine deaminases changes the information
              encoded in the mRNA from its genomic blueprint. Editing of
              protein-coding sequences can introduce novel, functionally
              distinct, protein isoforms and diversify the proteome. The
              functional importance of a few recoding sites has been
              appreciated for decades. However, systematic methods to uncover
              these sites perform poorly, and the full repertoire of recoding
              in human and other mammals is unknown. Here we present a new
              detection approach, and analyze 9125 GTEx RNA-seq samples, to
              produce a highly-accurate atlas of 1517 editing sites within the
              coding region and their editing levels across human tissues.
              Single-cell RNA-seq data shows protein recoding contributes to
              the variability across cell subpopulations. Most highly edited
              sites are evolutionary conserved in non-primate mammals,
              attesting for adaptation. This comprehensive set can facilitate
              understanding of the role of recoding in human physiology and
              diseases.",
  journal  = "Nat. Commun.",
  volume   =  13,
  number   =  1,
  pages    = "1184",
  month    =  mar,
  year     =  2022,
  url      = "http://dx.doi.org/10.1038/s41467-022-28841-4",
  language = "en",
  issn     = "2041-1723",
  pmid     = "35246538",
  doi      = "10.1038/s41467-022-28841-4",
  pmc      = "PMC8897444"
}



@ARTICLE{Picardi2017-gn,
  title    = "{REDIportal}: a comprehensive database of {A-to-I} {RNA} editing
              events in humans",
  author   = "Picardi, Ernesto and D'Erchia, Anna Maria and Lo Giudice, Claudio
              and Pesole, Graziano",
  abstract = "RNA editing by A-to-I deamination is the prominent
              co-/post-transcriptional modification in humans. It is carried
              out by ADAR enzymes and contributes to both transcriptomic and
              proteomic expansion. RNA editing has pivotal cellular effects and
              its deregulation has been linked to a variety of human disorders
              including neurological and neurodegenerative diseases and cancer.
              Despite its biological relevance, many physiological and
              functional aspects of RNA editing are yet elusive. Here, we
              present REDIportal, available online at
              http://srv00.recas.ba.infn.it/atlas/, the largest and
              comprehensive collection of RNA editing in humans including more
              than 4.5 millions of A-to-I events detected in 55 body sites from
              thousands of RNAseq experiments. REDIportal embeds RADAR database
              and represents the first editing resource designed to answer
              functional questions, enabling the inspection and browsing of
              editing levels in a variety of human samples, tissues and body
              sites. In contrast with previous RNA editing databases,
              REDIportal comprises its own browser (JBrowse) that allows users
              to explore A-to-I changes in their genomic context, empathizing
              repetitive elements in which RNA editing is prominent.",
  journal  = "Nucleic Acids Res.",
  volume   =  45,
  number   = "D1",
  pages    = "D750--D757",
  month    =  jan,
  year     =  2017,
  url      = "http://dx.doi.org/10.1093/nar/gkw767",
  language = "en",
  issn     = "0305-1048, 1362-4962",
  pmid     = "27587585",
  doi      = "10.1093/nar/gkw767",
  pmc      = "PMC5210607"
}


@ARTICLE{Chung2018-gh,
  title    = "Human {ADAR1} Prevents Endogenous {RNA} from Triggering
              Translational Shutdown",
  author   = "Chung, Hachung and Calis, Jorg J A and Wu, Xianfang and Sun, Tony
              and Yu, Yingpu and Sarbanes, Stephanie L and Dao Thi, Viet Loan
              and Shilvock, Abigail R and Hoffmann, H-Heinrich and Rosenberg,
              Brad R and Rice, Charles M",
  abstract = "Type I interferon (IFN) is produced when host sensors detect
              foreign nucleic acids, but how sensors differentiate self from
              nonself nucleic acids, such as double-stranded RNA (dsRNA), is
              incompletely understood. Mutations in ADAR1, an
              adenosine-to-inosine editing enzyme of dsRNA, cause
              Aicardi-Gouti{\`e}res syndrome, an autoinflammatory disorder
              associated with spontaneous interferon production and neurologic
              sequelae. We generated ADAR1 knockout human cells to explore
              ADAR1 substrates and function. ADAR1 primarily edited Alu
              elements in RNA polymerase II (pol II)-transcribed mRNAs, but not
              putative pol III-transcribed Alus. During the IFN response, ADAR1
              blocked translational shutdown by inhibiting hyperactivation of
              PKR, a dsRNA sensor. ADAR1 dsRNA binding and catalytic activities
              were required to fully prevent endogenous RNA from activating
              PKR. Remarkably, ADAR1 knockout neuronal progenitor cells
              exhibited MDA5 (dsRNA sensor)-dependent spontaneous interferon
              production, PKR activation, and cell death. Thus, human ADAR1
              regulates sensing of self versus nonself RNA, allowing pathogen
              detection while avoiding autoinflammation.",
  journal  = "Cell",
  volume   =  172,
  number   =  4,
  pages    = "811--824.e14",
  month    =  feb,
  year     =  2018,
  url      = "http://dx.doi.org/10.1016/j.cell.2017.12.038",
  keywords = "ADAR1; AGS; Aicardi-Goutieres syndrome; Alu elements; MDA5; PKR;
              RNA editing; innate immunity; neuronal progenitor cells;
              translation; type I interferon",
  language = "en",
  issn     = "0092-8674, 1097-4172",
  pmid     = "29395325",
  doi      = "10.1016/j.cell.2017.12.038",
  pmc      = "PMC5831367"
}

