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Literature summary for 3.5.4.37 extracted from
- Editing of cellular self-RNAs by adenosine deaminase ADAR1 suppresses innate immune stress responses (2016), J. Biol. Chem., 291, 6158-6168 .
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Mus musculus | Q99MU3 | - |
- |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| embryonic fibroblast | - |
Mus musculus | - |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| ADAR1 | - |
Mus musculus |
General Information
| General Information | Comment | Organism |
|---|---|---|
| malfunction | interferon treatment of Adar1-/-x02cells lacking both the p110 constitutive and p150 interferon-inducible ADAR1 proteins induces formation of stress granules, whereas neither wild-type nor Adar2x02-/-x02 cells display a comparable stress granule response following interferon treatment. Phosphorylation of protein synthesis initiation factor eIF2alpha at Ser51 is increased in interferon-treated Adar1x02-/-x02cells but not in either wild-type or Adar2x02-/- cells following interferon treatment | Mus musculus |
| physiological function | the majority of editing in mouse embryo fibroblasts is carried out by ADAR1. ADAR1 p150 as the major A-to-I editor in mouse embryo fibroblasts, acts as a feedback suppressor of innate immune responses otherwise triggered by self-RNAs possessing regions of double-stranded character | Mus musculus |
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Release 2023.1 (January 2023)
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