We are analyzing https://link.springer.com/article/10.1007/s00439-017-1837-0.

Title:
ADAR RNA editing in human disease; more to it than meets the I | Human Genetics
Description:
We review the structures and functions of ADARs and their involvements in human diseases. ADAR1 is widely expressed, particularly in the myeloid component of the blood system, and plays a prominent role in promiscuous editing of long dsRNA. Missense mutations that change ADAR1 residues and reduce RNA editing activity cause Aicardi–Goutières Syndrome, a childhood encephalitis and interferonopathy that mimics viral infection and resembles an extreme form of Systemic Lupus Erythmatosus (SLE). In Adar1 mouse mutant models aberrant interferon expression is prevented by eliminating interferon activation signaling from cytoplasmic dsRNA sensors, indicating that unedited cytoplasmic dsRNA drives the immune induction. On the other hand, upregulation of ADAR1 with widespread promiscuous RNA editing is a prominent feature of many cancers and particular site-specific RNA editing events are also affected. ADAR2 is most highly expressed in brain and is primarily required for site-specific editing of CNS transcripts; recent findings indicate that ADAR2 editing is regulated by neuronal excitation for synaptic scaling of glutamate receptors. ADAR2 is also linked to the circadian clock and to sleep. Mutations in ADAR2 could contribute to excitability syndromes such as epilepsy, to seizures, to diseases involving neuronal plasticity defects, such as autism and Fragile-X Syndrome, to neurodegenerations such as ALS, or to astrocytomas or glioblastomas in which reduced ADAR2 activity is required for oncogenic cell behavior. The range of human disease associated with ADAR1 mutations may extend further to include other inflammatory conditions while ADAR2 mutations may affect psychiatric conditions.
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Keywords {🔍}

pubmed, article, google, scholar, cas, rna, editing, central, adar, cell, human, biol, enzyme, receptor, zhang, deaminase, adenosine, sci, atoi, domain, activity, rnaediting, nat, doublestranded, oconnell, mol, dsrna, gene, usa, chem, keegan, mutations, interferon, res, structure, binding, proc, natl, acad, wang, liu, yang, higuchi, gallo, glutamate, leukemia, rich, bass, genet, emeson,

Topics {✒️}

double-stranded-rna-specific adenosine deaminase cdc14b/skp2/p21/p27 axis double-stranded rna-protein interactions double-stranded rna-binding domains month download article/chapter als/ftd c9orf72 expansion left-handed z-dna double-strand rna substrate rna-editing enzyme adar1 high-throughput multiplex sequencing microrna-376a promotes invasiveness human rna-editing deaminase rna-editing enzyme adar2 z-dna binding domain dsrna-binding domain complexed serotonin 2c receptor double-stranded rna ligand-gated ion channels full article pdf amino acid code pre-mrna encoding rna editing enzyme rna editing signature adar adenosine deaminases site-specific editing livingston jh adenosine deaminase acting adar rna editing leucine-rich export signal greger ih ampa-type glutamate receptors ampa receptor channels chronic myeloid leukemia privacy choices/manage cookies dsrna binding domain hyperphagia-mediated obesity brown ba 2nd acute myeloid leukemia nuclear rna editing rna editing gene ackert-bicknell cl sequence-specific readout rna editing occurs rna-editing enzymes recoding rna editing messenger rna editing profiling rna editing glutamate receptor subunit regulates rna rhythm ampa receptor regulation

Questions {❓}

Buckingham SD, Kwak S, Jones AK, Blackshaw SE, Sattelle DB (2008) Edited GluR2, a gatekeeper for motor neurone survival?
King AE, Woodhouse A, Kirkcaldie MT, Vickers JC (2016) Excitotoxicity in ALS: overstimulation, or overreaction?

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         description:We review the structures and functions of ADARs and their involvements in human diseases. ADAR1 is widely expressed, particularly in the myeloid component of the blood system, and plays a prominent role in promiscuous editing of long dsRNA. Missense mutations that change ADAR1 residues and reduce RNA editing activity cause Aicardi–Goutières Syndrome, a childhood encephalitis and interferonopathy that mimics viral infection and resembles an extreme form of Systemic Lupus Erythmatosus (SLE). In Adar1 mouse mutant models aberrant interferon expression is prevented by eliminating interferon activation signaling from cytoplasmic dsRNA sensors, indicating that unedited cytoplasmic dsRNA drives the immune induction. On the other hand, upregulation of ADAR1 with widespread promiscuous RNA editing is a prominent feature of many cancers and particular site-specific RNA editing events are also affected. ADAR2 is most highly expressed in brain and is primarily required for site-specific editing of CNS transcripts; recent findings indicate that ADAR2 editing is regulated by neuronal excitation for synaptic scaling of glutamate receptors. ADAR2 is also linked to the circadian clock and to sleep. Mutations in ADAR2 could contribute to excitability syndromes such as epilepsy, to seizures, to diseases involving neuronal plasticity defects, such as autism and Fragile-X Syndrome, to neurodegenerations such as ALS, or to astrocytomas or glioblastomas in which reduced ADAR2 activity is required for oncogenic cell behavior. The range of human disease associated with ADAR1 mutations may extend further to include other inflammatory conditions while ADAR2 mutations may affect psychiatric conditions.
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