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The presence of ADA activity in zebrafish brain may be important to regulate the adenosine/inosine levels in the CNS of this species
These findings suggest a role of NS4A in the interaction of BVDV with ADAR that favors virus replication.
our data shows that ADAR is essential for proper temperature adaptation, a key behavior trait that is essential for survival of flies in the wild. Moreover, our results suggest a more general role of ADAR in regulating RNA secondary structures in vivo
Deficiencies in the RNA-editing gene Adar increase sleep due to synaptic dysfunction in glutamatergic neurons.
The study demonstrates that neuronal excitability is linked to dADAR expression levels in individual neurons.
loss of Adar increases quantal size, reduces the number of quanta of neurotransmitter released and perturbs the calcium dependence of synaptic release
results demonstrate a novel role for dADAR protein in rnp-4f 5'-UTR alternative intron splicing regulation which is consistent with a previously proposed model.
Data suggeset that RNA editing enzyme ADAR-mediated editing is more widespread than previously indicated and largely occurs cotranscriptionally.
the solution structure of the N-terminal dsRNA binding domain (dsRBD) of dADAR
Abolishing dADAR auto-regulation dramatically remodels the landscape of re-coding events in a site-specific manner.
network-wide temporal and spatial regulation of ADAR activity can tune the complex system of RNA-editing sites and modulate multiple ethologically relevant behavioral modalities.
Our study is the first to systematically characterize the temporal and spatial expression of full-length and truncated dADAR mRNA and protein isoforms during Drosophila embryogenesis.
genetic analysis of dADAR substrates in Drosophila
importance of ADAR in maintenance of neuronal function and regulatory role in the expression of genes encoding reactive oxygen species scavengers.
Two predominant isoforms of dAdar are expressed in gonads and dAdar is transcribed from both the embryonic and the adult promoters.
This is the first reported DSH case with chilblains, harbouring a novel heterozygous in-frame deletion mutation of the third dsRBD in ADAR1.
Stably introduced into cancer cell lines, the system reports on elevated endogenous ADAR1 editing activity induced by interferon as well as knockdown of ADAR1 and ADAR2. In a single-well setup we used the reporter in HeLa cells to screen a small molecule library of 33 000 compounds
Here, the authors describe ADAR1 role as a regulator of innate and antiviral immune function in hepatitis C virus infection, both in vitro and in patients. Polymorphisms within ADAR1 gene were found significantly associated to poor clinical outcome to hepatitis C therapy and advanced liver fibrosis in a cohort of hepatitis C virus and HIV-1 coinfected patients.
The multiple myeloma transcriptome is aberrantly hyperedited because of the overexpression of ADAR1. These events were associated with patients' survival independent of 1q21 amplifications and could affect patients' responsiveness to different treatment regimes.
the interplay of the Zalpha domain from ADAR1 and MBD3 may regulate the transition of the DNA conformation between B- and Z-DNA and thereby modulate chromatin accessibility, resulting in alterations in gene expression
ADAR1 polymorphisms protected against severe liver disease in HIV/HCV-coinfected patients.
AZIN1 RNA editing levels and ADAR1 expression were significantly elevated in gastric cancer tissues compared with matched normal mucosa.
tRNA deamination by ADAT requires substrate-specific recognition mechanisms and can be inhibited by terminal restriction fragments.
ADAR1 regulated endothelial cell survival which was mediated by FGFR2/PI3K/Akt pathway.
Changes in expression levels of ADAR1 and ADAR2 may represent an important regulatory mechanism in idiopathic pulmonary fibrosis, by regulating the processing of key miRNAs such as miRNA-21.
Higher expression of ADAR1 into the cytoplasm resulted to be an independent prognostic factor
tumor-derived IFN resulting in chronic signaling creates a cellular state primed to respond to dsRNA accumulation, rendering Interferon stimulated gene-positive tumors susceptible to ADAR loss.
Four novel ADAR1 mutations were identified in Chinese pedigrees with dyschromatosis symmetrica hereditaria.
DAR1 p110 could strongly enhance the adhesion of HCC tumor cells to ECM, which was usually regarded as the initiation of tumor invasion. Such phenotype was caused due to up-regulation of ITGA2 both in mRNA and protein level.
ADAR1 promotes viral replication by acting as an RNA sensing inhibitor, by editing viral RNA and by inhibiting PKR.
essential gene for the survival of a subset of lung cancer cell lineswhich possess a high interferon gene expression signature
We confirmed the role of ADAR1 in this regulation using a shRNA in a breast cancer cell line (ZR-75-1). Altogether, these results revealed a significant association between the mRNA editing in genes related to cancer-relevant pathways and clinical outcomes, suggesting an important role of ADAR1 expression and function in breast cancer.
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.
This study investigates the genome-wide binding preferences of the nuclear constitutive isoforms ADAR1-p110 and ADAR2 on human miRNA species by RNA immunoprecipitation of ADAR-bound small RNAs .
The adenosine deaminase RNA-specific binding protein (ADAR1)-dependent and RNA-editing-independent regulation of invasion, mediated by Integrin beta3 (ITGB3) suggests a central involvement of ADAR1 in cancer progression and metastasis.
These findings suggest that prevention of MDA5 sensing of endogenous dsRNA by ADAR1-mediated RNA editing is required for preventing both innate immune responses and T cell-mediated autoimmunity.
ADAR1 functions as a checkpoint that limits anti-tumour immunity by preventing the sensing of endogenous dsRNA. Loss of function of ADAR1 improves responses to PD-1 blockade and overcomes common mechanisms of resistance to immunotherapy.
a novel ADAR1 protective effect for maintaining intestinal homeostasis, is reported.
ADAR1p150 plays a key role in complexing with Dicer and promoting the expression of miRNA-222, the latter of which suppresses the expression of the target gene PTEN during VMC. Our work reveals a previously unknown role of ADAR1p150 in gene expression in VMC.
ADAR1 modulates macrophage M2 polarization via the ADAR1-miR-21-Foxo1-IL-10 axis.
ADAR1 (Gene ID: ADAR) belongs to the ADAR family, which catalyzes the conversion of adenosine into inosine (A-to-I) in pre-mRNA.
ADAR1 silencing reduces engraftment of myeloma in vivo.
ADAR1 functions other than RNA editing are reviewed.
protein recoding arising from ADAR1-mediated editing is not essential for organismal homeostasis
These findings shed a new light on the vital regulatory role of ADAR1(Adenosine deaminase) in hepatic immune homeostasis, chiefly its inhibitory function on the crosstalk between the NFkappaB and type-I interferons signaling cascades, restraining the development of liver inflammation and fibrosis.
ADAR1-mediated RNA editing is essential for normal erythropoiesis.
Knockout of ADAR1 dramatically inhibited injury-induced neointima formation and restored vascular smooth muscle cell remodeling.
we identified a novel ADAR1-dependent protective contribution through which hepatocytes guard against aberrant cytosolic RLR-RNA-sensing pathway mediated inflammatory reaction in response to acute liver IR.
Thus, Adarb1 and Adarb2 have nearly exclusive expression within brain tissue, while Adar has more appreciable expression across multiple tissues.
After fear conditioning protocol, mRNA expression of ADAR1 increased in amygdala and hippocampus.
ADAR1 is an essential molecule for maintaining adult liver homeostasis and, in turn, morphological and functional integrity.
The p150 isoform of ADAR1 uniquely regulated the MDA5 pathway.
transcriptional activation of Adar1 by IFN occurs in the absence of STAT1 by a non-canonical STAT2-dependent pathway in mouse but not human cells.
A-to-I editing of endogenous dsRNA is the essential function of ADAR1, preventing the activation of the cytosolic dsRNA response by endogenous transcripts.
ADAR1 mutations causing Aicardi-Goutieres syndrome affect the activity of the interferon-inducible cytoplasmic isoform more severely than the nuclear isoform.
This gene encodes the enzyme responsible for RNA editing by site-specific deamination of adenosines. This enzyme destabilizes double-stranded RNA through conversion of adenosine to inosine. Mutations in this gene have been associated with dyschromatosis symmetrica hereditaria. Alternative splicing results in multiple transcript variants.
double-stranded RNA-specific adenosine deaminase
, dsRNA adenosine deaminase
, adenosine deaminase, RNA-specific
, RNA-specific adenosine deaminase
, adenosine deaminase acting on RNA
, adenosine deaminases acting on RNA
, hypoxia, anoxia, sensitive 2
, 136 kDa double-stranded RNA-binding protein
, adenosine deaminase acting on RNA 1-A
, interferon-induced protein 4
, interferon-inducible protein 4
, RNA adenosine deaminase 1
, RNA-specific adenosine deaminase p110 form
, RNA-specific adenosine deaminase p150 form