3.5.4.37: double-stranded RNA adenine deaminase
This is an abbreviated version!
For detailed information about double-stranded RNA adenine deaminase, go to the full flat file.
Word Map on EC 3.5.4.37
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3.5.4.37
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inosine
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a-to-i
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deaminases
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deamination
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adenosine-to-inosine
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hereditaria
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rna-editing
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pre-mrnas
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dyschromatosis
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symmetrica
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z-dna
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duplex
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ampa
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left-handed
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unedited
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glur-b
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recoding
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site-selective
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macules
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interferon-inducible
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mda5
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hypopigmented
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ifn-inducible
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dsrbds
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interferon-stimulated
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ca2+-permeable
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5-ht2cr
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dicer
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samhd1
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genodermatosis
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rig-i
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hypermutation
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ifn-stimulated
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pigmentary
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interferonopathy
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autoinflammatory
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medicine
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inosine-containing
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dsrna-binding
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drug development
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protein-rna
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antigenome
- 3.5.4.37
- inosine
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a-to-i
- deaminases
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deamination
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adenosine-to-inosine
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hereditaria
-
rna-editing
- pre-mrnas
-
dyschromatosis
-
symmetrica
- z-dna
- duplex
- ampa
-
left-handed
-
unedited
-
glur-b
-
recoding
-
site-selective
-
macules
-
interferon-inducible
- mda5
-
hypopigmented
-
ifn-inducible
-
dsrbds
-
interferon-stimulated
-
ca2+-permeable
-
5-ht2cr
- dicer
- samhd1
-
genodermatosis
- rig-i
-
hypermutation
-
ifn-stimulated
-
pigmentary
-
interferonopathy
-
autoinflammatory
- medicine
-
inosine-containing
-
dsrna-binding
- drug development
-
protein-rna
-
antigenome
Reaction
Synonyms
ADAR, ADAR1, ADAR1L, ADAR1S, ADAR2, ADAR2 deaminase, adenosine deaminase acting on RNA 1, adenosine deaminase acting on RNA-1, APOBEC1, bADAR1a, CiADAR1, dADAR, double-stranded RNA adenosine deaminase, double-stranded RNA-specific adenosine deaminase, double-stranded RNA-specific adenosine deaminase 1, double-stranded-RNA-specific adenosine deaminase 1, DRADA1, dsRAD, dsRNA adenosine deaminase, hADAR1, hADAR1a, hADAR2, hADAR2-D
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General Information
General Information on EC 3.5.4.37 - double-stranded RNA adenine deaminase
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malfunction
metabolism
physiological function
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ADAR1 knockout embryos die at day 11.5 to 12. ADAR1 is not completely necessary for cell survival because some cells survive without ADAR1. ADAR1 is dispensable in pluripotent cells for their survival and proliferation
malfunction
ADAR1-/- homozygous embryos die at E11.0 to E12.5. Widespread apoptosis is detected in many tissues of ADAR1-/- embryos collected live at E10.5 to E11.5, despite their normal gross appearance
malfunction
homozygosity for two different null alleles of ADAR1 causes a consistent embryonic phenotype appearing early at embryonic day 11 and leading to death between embryonic days 11.5 and 12.5. This phenotype manifests a rapidly disintegrating liver structure, along with severe defects in definitive hematopoiesis, encompassing both erythroid and myeloid/granuloid progenitors as well as spleen colonyforming activity from the aorta-gonad-mesonephros region and fetal liver
malfunction
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knockdown of ADAR2 expression markedly impairs glucose-stimulated insulin secretion in the rat insulinoma INS-1 cells and primary pancreatic islets and significantly diminishes KCl-stimulated secretion of exogenous human growth hormone or endogenous chromogranin B protein in the rat adrenal pheochromocytoma PC12 cells
malfunction
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the ADAR2 knockout phenotype can be attributed to the lack of editing of the GluR-B receptor. ADAR1 deficiency results in an embryonic lethal phenotype
malfunction
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knock-down of ADAR1 increases HIV-1 replication in primary macrophages
malfunction
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loss of ADAR1 induces endoplasmic reticulum stress and activation of interferon signaling, and alters expression in WNT targets, followed by intestinal inflammation and crypt apoptosis
malfunction
A-to-I underediting at the glutamine (Q)/arginine (R) site of the glutamate receptor subunit B (GluR-B) is associated with the pathogenesis and invasiveness of glioma and is confirmed in the glioma cell lines U87, U251 and A172 compared with that in normal human astrocytes. The expression of ADAR2 mRNA was not significantly altered in the glioma cell lines. Aberrant alternative splicing pattern of ADAR2 downregulates A-to-I editing in glioma
malfunction
dysregulation of A-to-I editing by ADAR1 can have profound consequences, ranging from effects on cell growth and development to autoimmune disorders
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
malfunction
knockdown of ADAR by RNA interference induces formation of pseudo-diapause embryos, which lack resistance to the stresses and exhibit high levels of apoptosis
malfunction
knockdown of ADARa in lung adenocarcinoma cells with amplified ADAR leads to decreased migration and invasion
ADAR1 is an essential enzyme for normal development. The interferon-inducible ADAR1p150 is involved in immune responses to both exogenous and endogenous triggers, whereas the functions of the constitutively expressed ADAR1p110 are variable. ADAR1 is involved in the recognition of self versus non-self dsRNA. This provides potential explanations for its links to hematopoiesis, type I interferonopathies, and viral infections. Editing in both coding and noncoding sequences results in diseases ranging from cancers to neurological abnormalities. Furthermore, editing of noncoding sequences, like microRNAs, can regulate protein expression, while editing of Alu sequences can affect translational efficiency and editing of proximal sequences. Identifications of long noncoding RNA and retrotransposons as editing targets expand the effects of A-to-I editing. Besides editing, ADAR1 also interacts with other dsRNA-binding proteins in editing-independent manners
metabolism
ADAR2 is the main enzyme responsible for A-to-I editing in humans
metabolism
role of ADAR1 as a suppressor of dsRNA-triggered innate immune responses
metabolism
the enzyme (ADAR1) regulates the phosphorylation of activation of protein kinase (PKR) and eukaryotic translation initiation factor 2 alpha (eIF2) in both an IFN-dependent and IFN-independent manner, and its inhibitory effect on the IFN production partially contributes to its proviral effect. The enzyme promotes the Zika virus replication by inhibiting the activation of protein kinase PKR
metabolism
the enzyme contributes to resistance to stress in Artemia diapause embryos
metabolism
the enzyme is an essential gene for the survival of a subset of cancer cell lines. ADAR1-dependent cell lines display increased expression of interferon-stimulated genes. Activation of type I interferon signaling in the context of ADAR1 deficiency can induce cell lethality in non-ADAR1-dependent cell lines
ADAR1 has the potential both to change information content through editing of mRNA and to regulate gene expression through interacting with the NF90 family proteins
physiological function
ADAR1 is required for cell survival and embryo development by protecting against stress-induced apoptosis
physiological function
ADAR1 plays an essential role in adult hematopoiesis through its RNA editing activity in hematopoietic progenitor cells
physiological function
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ADAR2-editing activity inhibits glioblastoma growth through the modulation of the CDC14B/Skp2/p21/p27 axis
physiological function
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editing of RNA changes the read-out of information from DNA by altering the nucleotide sequence of a transcript. One type of RNA editing found in all metazoans uses double-stranded RNA (dsRNA) as a substrate and results in the deamination of adenosine to give inosine, which is translated as guanosine
physiological function
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the enzyme is implicated in the antiviral immune response
physiological function
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the enzyme is involved in RNA editing in order to generate many different mRNAs from the same gene, increasing the transcriptome and then the proteome. The most frequent RNA editing mechanism in mammals involves the conversion of specific adenosines into inosines by the ADAR family of enzymes. This editing event can change both the sequence and the secondary structure of RNA molecules, with important consequences on both the final proteins and regulatory RNAs. Alteration in RNA editing has been connected to numerous human pathologies and is important in tumor progression. RNA editing on non-coding RNA can affect the secondary (and consequently the tertiary) structure of the RNAs and then modulate and/or prevent RNA-protein and RNA-RNA interactions. RNA editing on non-coding portions of the transcripts could influence splicing, localization, stability and translation efficiency of the transcripts
physiological function
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ADAR1 is essential for intestinal homeostasis and stem cell maintenance by suppressing endoplasmic reticulum stress and interferon signaling
physiological function
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ADAR1 restricts HIV-1 replication post-transcriptionally in macrophages harboring HIV-1 provirus
physiological function
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ADAR1 significantly promotes equine infectious anemia virus replication and infectivity
physiological function
A-to-I editing of endogenous dsRNA is the essential function of ADAR1, preventing the activation of the cytosolic dsRNA response by endogenous transcripts
physiological function
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equine ADAR1 (eADAR1) is a positive regulator of equine infectious anemia virus (EIAV). eADAR1 significantly promotes EIAV replication, and the enhancement of viral protein expression is associated with the long terminal repeat (LTR) and Rev response element regions. The RNA binding domain 1 of eADAR1 is essential only for enhancing LTR-mediated gene expression. eADAR1 increases the EIAV infectivity
physiological function
the enzyme (ADAR2) is a radar enzyme that maintains a degree of editing in the miRNA population and balances miRNA expression, maintaining them at physiological, that is, safe, levels. Whenever ADAR2 is impaired (that is, in glioblastoma), miRNA homeostasis is altered and this may contribute to cancer progression. The major effect of ADAR2 is to reduce the expression of a large number of miRNAs, most of which act as onco-miRNAs. ADAR2 can edit miR-222/221 and miR-21 precursors and decrease the expression of the corresponding mature onco-miRNAs in vivo and in vitro, with important effects on cell proliferation and migration
physiological function
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the enzyme is proposed to contribute to the adaptation of equine infectious anemia virus from horses to donkeys
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