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anti-Rat (Rattus) ADAR Antibodies:
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Human Polyclonal ADAR Primary Antibody for IHC, WB - ABIN2774648
Pan, Ye, Franco, Li, Yu, Zou, Zhang, Jiao, Lin: Insulin resistance and depressive symptoms in middle-aged and elderly Chinese: findings from the Nutrition and Health of Aging Population in China Study. in Journal of affective disorders 2008
Show all 2 Pubmed References
Human Polyclonal ADAR Primary Antibody for IF, IHC (p) - ABIN513112
Liu, Chen, Yeh, Li, Wu, Chen, Chen, Yeh: ADAR2-mediated editing of miR-214 and miR-122 precursor and antisense RNA transcripts in liver cancers. in PLoS ONE 2014
Guinea Pig Polyclonal ADAR Primary Antibody for IHC, WB - ABIN2774647
Zhang, Liu, Jiang, Tian, Wang, Yu: Six novel mutations of the ADAR1 gene in Chinese patients with dyschromatosis symmetrica hereditaria. in Journal of dermatological science 2008
Show all 2 Pubmed References
The presence of ADA (show ADA Antibodies) 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 (show RNPC3 Antibodies)-4f 5'-UTR (show UTS2R Antibodies) 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.
The miRNAs that were found upregulated in DENV-infected cells did not control the production of infectious virus particles. On the other hand, miR (show MLXIP Antibodies)-3614-5p, which was upregulated in DENV-negative macrophages, reduced DENV infectivity and regulated ADAR1 expression, a protein that facilitates viral replication.
We detected high ADAR1 expression in half of the triple-negative breast cancer patients. In addition to DNA mutations, RNA editing can be related to neoantigens; hence, we need to explore non-synonymous mutations exclusively found using RNA sequencing data to identify clinically relevant neoantigens.
Editing in the STAT3 (show STAT3 Antibodies) intron is performed by ADAR1 and affects STAT3 (show STAT3 Antibodies) alternative splicing. RNA editing is one of the molecular mechanisms regulating the expression of STAT3beta.
a role for ADAR1 as a lung cancer oncogene (show RAB1A Antibodies) undergoing gene amplification-associated activation that affects downstream RNA editing patterns and patient prognosis.
In endothelial cells, ADAR1 overexpression induces CTSS (show CTSS Antibodies) RNA editing and consequently increases cathepsin S (show CTSS Antibodies) expression. ADAR1 levels and the extent of CTSS (show CTSS Antibodies) RNA editing are associated with changes in cathepsin S (show CTSS Antibodies) levels in patients with atherosclerotic vascular diseases.
the activation of the JAK (show JAK3 Antibodies)/STAT (show STAT1 Antibodies) pathway is a regulatory mechanism of ADAR1 expression and causes abnormal RNA editing profile in esophageal squamous cell carcinoma. This mechanism may serve as a new target for esophageal squamous cell carcinoma therapy
Lentiviral ADAR1 wild-type, but not an editing-defective ADAR1(E912A) mutant, induces self-renewal gene expression and impairs biogenesis of stem cell regulatory let-7 microRNAs.
ADAR1p110 isoform competitively inhibits binding of Staufen1 (show STAU1 Antibodies) to the 3'-untranslated-region dsRNAs and antagonizes Staufen1 (show STAU1 Antibodies)-mediated mRNA decay.
we have identified two novel mutations of the ADAR1 gene and explored their implications on the structure and functions of ADAR1 protein.
ADAR1 restricts LINE-1 retrotransposition.
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 (show DHX58 Antibodies)-RNA-sensing pathway mediated inflammatory reaction in response to acute liver IR.
Thus, Adarb1 (show ADARB1 Antibodies) and Adarb2 (show ADARB2 Antibodies) 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 (show ABL1 Antibodies) isoform of ADAR1 uniquely regulated the MDA5 (show IFIH1 Antibodies) pathway.
transcriptional activation of Adar1 by IFN occurs in the absence of STAT1 (show STAT1 Antibodies) by a non-canonical STAT2 (show STAT2 Antibodies)-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 (show IFNA Antibodies)-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