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Validated All-in-One™ qPCR Primer for ADARB1(NM_001112.4) Search again
Product ID:
HQP149282
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ADAR2, DRABA2, DRADA2, NEDHYMS, RED1
Gene Description:
adenosine deaminase RNA specific B1
Target Gene Accession:
NM_001112.4(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 pre-mRNA editing of the glutamate receptor subunit B by site-specific deamination of adenosines. Studies in rat found that this enzyme acted on its own pre-mRNA molecules to convert an AA dinucleotide to an AI dinucleotide which resulted in a new splice site.
Gene References into function
- overexpression inhibits HDV RNA replication and compromises virus viability
- Adenosine to inosine RNA editing requires formation of a ternary complex on the GluR-B R/G site
- short inhibitory RNA-mediated knockdown of host ADAR1 expression but not that of ADAR2 led to decreased HDV amber/W editing and virus production
- the Q/R site of GluRs editing is regulated in a regional manner and the GluR2 Q/R site editing is critically regulated by ADAR2 in human brain
- assayed enzymatic activity of N-terminal deletion constructs of hADAR2 to determine the role of the double-stranded RNA binding motifs and the intervening linker peptide
- Inositol hexakisphosphate is buried within the catalytic domain of ADAR2 and is required for editing of transfer RNA.
- results show that bipolar affective disorder may not be caused by mutations in ADARB1.
- Serum adenosine deaminase (ADA) activity of active Behcet's disease (BD) was higher than that of inactive BD (P < 0.01), but erythrocyte ADA activity was found to be lower in active BD than inactive BD (P < 0.01).
- CD26 and cell surface adenosine deaminase are selectively expressed on ALK-positive, but not on ALK-negative, anaplastic large cell lymphoma and Hodgkin's lymphoma
- The CTD of POLR2A and ADAR2 function together to enforce the order of events that allows editing to precede splicing, and they furthermore suggest a new role for the CTD as a coordinator of two interdependent pre-mRNA processing events.
- Reference values of serum adenosine deaminase (ADA) in normal pregnancy may provide important database for making clinical decisions in pregnancies complicated by conditions where cellular immunity has been altered.
- 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