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Validated All-in-One™ qPCR Primer for ADAR(NM_001111.3) Search again
Product ID:
HQP000472
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ADAR1, AGS6, DRADA, DSH, DSRAD, G1P1, IFI-4, IFI4, K88DSRBP, P136
Gene Description:
adenosine deaminase RNA specific
Target Gene Accession:
NM_001111.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
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. Alternate transcriptional splice variants, encoding different isoforms, have been characterized. [provided by RefSeq].
Gene References into function
- crystallization and diffraction results when complexed with a chimeric oligonucleotide
- overexpression inhibits HDV RNA replication and compromises virus viabiltiy
- Up-regulation of type I interferon inducible 150kDa ADAR1 is associated with induction of A to G transcript mutations in systemic lupus erythematosus (SLE) T lymphocytes.
- The IFN-inducible RNA-specific adenosine deaminase ADAR1 promoter possesses a KCS-like (KCS-l) element.
- ADAR1 is primarily responsible for editing HDV RNA at the amber/W site during HDV infection.
- Results identify regions in human adenosine deaminase that acts on RNA (ADAR1) that interfere with nuclear localization and mediate cytoplasmic accumulation.
- ADAR1 has a role in protein translation independent of RNA editing
- mutations involved in causing dyschromatosis symmetrica hereditaria have been identified in the gene that encodes double-stranded RNA-specific adenosine deaminase (DSRAD) as the disease gene
- ADAR1 variants are differentially regulated during acute inflammation: the localization of these variants and of A-to-I RNA editing in the cytoplasm, nucleus, and nucleolus is intracellularly reorganized in response to inflammatory stimulation
- the intracellular distribution of the various ADAR1 isoforms is determined by NLS-c, NES, NoLS, and a regulatory motif
- This is the first report on DSRAD as the causative gene of dyschromatosis symmetrica hereditaria in the Chinese population.
- data add new variants to the repertoire of ADAR mutations in Dyschromatosis symmetrica hereditaria
- Atomic force microscopy imaging of the Zalpha domain of ADAR1 complexed with supercoiled plasmid Z-DNA.
- R1155W missense mutation is a new mutation in exon 15 of DSRAD, the pathogenic gene of dyschromatosis symmetrica hereditaria
- Frame-shift mutations in the DSRAD gene could cause dyschromatosis symmetrica hereditaria in the chinese population.
- We report 16 novel mutations containing six missense substitutions, two splice site mutations, six frameshift mutations, and two nonsense mutations found in Japanese patients with dyschromatosis symmetrica hereditaria.
- ADAR1 has the potential both to change information content through editing of mRNA and to regulate gene expression through interacting with NF90
- Identification of a deletion mutation in the ADAR gene of a Chinese family with Dyschromatosis symmetrica hereditaria is reported.
- induction of ADAR1-L may at least partially cause the antiviral effect of IFN-alpha in natural immune response to HDV as well as in case of therapeutic administration of IFN
- 10 novel mutations responsible for dyschromatosis symmetrica hereditaria: p.Q102fsX123, p.T369fsX374, p.S664fsX677, p.R892L, p.I913R, p.R916Q, p.P990fsX1016, p.C1081S, p.C1169F, and p.K1187X.
- ADAR1-L induces mutations in the viral RNA which leads to a loss of viral protein function and reduced viral infectivity, and contributes to the innate antiviral immune response.
- reports two novel mutations c.2116 G > A (E706K) and c.2848 C > T (Q950X) in the DSRAD gene identified in two Chinese pedigrees with DSH
- Missense mutation of the double-stranded RNA-specific adenosine deaminase gene is associated with dyschromatosis symmetrica hereditaria
- ADAR1 interacts with dsRNA-activated protein kinase PKR, inhibits its kinase activity, and suppresses the alpha subunit of eukaryotic initiation factor 2 (eIF-2alpha) phosphorylation, and thus increases host susceptibility to viral infection.
- 5 families and 3 sporadic patients with dyschromatosis symmetrica hereditaria in a Chinese Han population were studied. By direct sequencing, 5 novel ADAR gene mutations and 3 mutations described previously were identified, all were heterozygous.
- Novel deletion mutation of gene in a Chinese family with Dyschromatosis Symmetrica Hereditaria
- G to A mutation at the position 3,125 in exon 12 of the DSRAD gene induces a R1042H change in the putative deaminase domain of DSRAD. This, among other DSRAD mutations, is characteristic to dyschromatosis symmetrica hereditaria
- A deletion mutation (c.2447G > A) in the ADAR gene has been detected in this in a pedigree with dyschromatosis symmetrical hereditar, which is probably one of the molecular bases of the pathogenesis of the disease.
- elevated levels of ADAR1, as found in astrocytomas, do indeed interfere with ADAR2 specific editing activity, and the endogenous ADAR1 can form heterodimers with ADAR2 in astrocytes
- Six novel mutations of the ADAR1 gene are reported in Chinese patients with dyschromatosis symmetrica hereditaria.
- suggests a regulatory pathway by a combination of ADAR1 A-to-I editing enzyme and RNA degradation presumably with the aid of hUpf1
- The mutation is a novel heterozygous nucleotide T-->C transition at position 3617 in exon 15 of the DSRAD gene, which induces a M1206T change in the putative deaminase domain of DSRAD.
- histological findings in dyschromatosis symmetrica hereditaria mainly induced by the ADAR1 gene mutations.
- These data suggested the role of ADAR in modulation of HIV-1 replication.
- Four novel mutations of the ADAR1 gene have been reported in patients with dyschromatosis symmetrica hereditaria.
- Overexpressed ADAR1 specifically edits a yet unknown cellular substrate, which in turn affects plasmid-based gene expression.