Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

An internal deletion of ADAR rescued by MAVS deficiency leads to a minute phenotype.

Nucleic acids research - 6 Apr 2020

Bajad Prajakta, Ebner Florian, Amman Fabian, Szabó Brigitta, Kapoor Utkarsh, Manjali Greeshma, Hildebrandt Alwine, Janisiw Michael P, Jantsch Michael F

Abstract excerpt

The RNA-editing protein ADAR is essential for early development in the mouse. Genetic evidence suggests that A to I editing marks endogenous RNAs as 'self'. Today, different Adar knockout alleles have been generated that show a common phenotype of apoptosis, liver disintegration, elevated immune response and lethality at E12.5. All the Adar knockout alleles can be rescued by a concomitant deletion of the innate...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Adaptor Proteins, Signal Transducing
Share to Adenosine Deaminase

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Immunity, Innate

Share to Interferon-Induced Helicase, IFIH1

Share to Ribosomal Proteins

Share to RNA-Binding Proteins

Share to RNA Editing

Source

Open in PubMed Open full text

Identifiers

PMID: 31956894
DOI: 10.1093/nar/gkaa025
PMCID: PMC7102943

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

An internal deletion of ADAR rescued by MAVS deficiency leads to a minute phenotype.PMID 31956894Read ↗

Protein recoding by ADAR1-mediated RNA editing is not essential for normal development and homeostasis.Semantic proximity Read ↗

Generation of a new <i> Adar1p150 <sup>-/-</sup> </i> mouse demonstrates isoform-specific roles in embryonic development and adult homeostasisSemantic proximity Read ↗

Microgliosis and aberrant interferon response in Adar Mavs brain are rescued by PKR removal.Semantic proximity Read ↗

An Aicardi-Goutières Syndrome-Causative Point Mutation in Adar1 Gene Invokes Multiorgan Inflammation and Late-Onset Encephalopathy in Mice.Semantic proximity Read ↗

Aberrant activation of the innate immune sensor PKR by self dsRNA is prevented by direct interaction with ADAR1Semantic proximity Read ↗

ADAR1 is vital for B cell lineage development in the mouse bone marrowSemantic proximity Read ↗

The majority of A-to-I RNA editing is not required for mammalian homeostasisSemantic proximity Read ↗

RNA editing by ADAR1 prevents MDA5 sensing of endogenous dsRNA as nonself.Semantic proximity Read ↗

PKR and the Integrated Stress Response drive immunopathology caused by ADAR1 mutationSemantic proximity Read ↗

ADAR RNA editing in human disease; more to it than meets the I.Semantic proximity Read ↗

Reconfigured immunity in Adar heterozygous and Adar Mavs Eif2ak2 (PKR) triple mutant mice.Semantic proximity Read ↗

Stress-induced apoptosis associated with null mutation of ADAR1 RNA editing deaminase gene.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.