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ADAR1 Antibody
Rabbit mAb
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC, FC, ICC |
|---|---|
| Primary Accession | P55265 |
| Clonality | Monoclonal |
| Other Names | ADAR; Adar1; AGS6; DRADA; Dsh; Dsrad; IFI4; P136; |
| Isotype | Rabbit IgG |
| Host | Rabbit |
| Calculated MW | 136066 Da |
| Dilution | WB 1:500~1:2000 IHC 1:50~1:200 ICC/IF 1:50~1:200 FC 1:50 |
|---|---|
| Purification | Affinity-chromatography |
| Immunogen | A synthesized peptide derived from human ADAR1 |
| Description | Converts multiple adenosines to inosines and creates I/U mismatched base pairs in double-helical RNA substrates without apparent sequence specificity. |
| Storage Condition and Buffer | Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at +4°C short term. Store at -20°C long term. Avoid freeze / thaw cycle. |
| Name | ADAR |
|---|---|
| Synonyms | ADAR1, DSRAD, G1P1, IFI4 |
| Function | Catalyzes the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) referred to as A-to-I RNA editing (PubMed:12618436, PubMed:7565688, PubMed:7972084). This may affect gene expression and function in a number of ways that include mRNA translation by changing codons and hence the amino acid sequence of proteins since the translational machinery read the inosine as a guanosine; pre-mRNA splicing by altering splice site recognition sequences; RNA stability by changing sequences involved in nuclease recognition; genetic stability in the case of RNA virus genomes by changing sequences during viral RNA replication; and RNA structure- dependent activities such as microRNA production or targeting or protein-RNA interactions. Can edit both viral and cellular RNAs and can edit RNAs at multiple sites (hyper-editing) or at specific sites (site- specific editing). Its cellular RNA substrates include: bladder cancer- associated protein (BLCAP), neurotransmitter receptors for glutamate (GRIA2) and serotonin (HTR2C) and GABA receptor (GABRA3). Site-specific RNA editing of transcripts encoding these proteins results in amino acid substitutions which consequently alters their functional activities. Exhibits low-level editing at the GRIA2 Q/R site, but edits efficiently at the R/G site and HOTSPOT1. Its viral RNA substrates include: hepatitis C virus (HCV), vesicular stomatitis virus (VSV), measles virus (MV), hepatitis delta virus (HDV), and human immunodeficiency virus type 1 (HIV-1). Exhibits either a proviral (HDV, MV, VSV and HIV-1) or an antiviral effect (HCV) and this can be editing-dependent (HDV and HCV), editing-independent (VSV and MV) or both (HIV-1). Impairs HCV replication via RNA editing at multiple sites. Enhances the replication of MV, VSV and HIV-1 through an editing-independent mechanism via suppression of EIF2AK2/PKR activation and function. Stimulates both the release and infectivity of HIV-1 viral particles by an editing-dependent mechanism where it associates with viral RNAs and edits adenosines in the 5'UTR and the Rev and Tat coding sequence. Can enhance viral replication of HDV via A-to-I editing at a site designated as amber/W, thereby changing an UAG amber stop codon to an UIG tryptophan (W) codon that permits synthesis of the large delta antigen (L-HDAg) which has a key role in the assembly of viral particles. However, high levels of ADAR1 inhibit HDV replication. |
| Cellular Location | [Isoform 1]: Cytoplasm. Nucleus. Note=Shuttles between the cytoplasm and nucleus (PubMed:24753571, PubMed:7565688). Nuclear import is mediated by TNPO1 (PubMed:24753571). |
| Tissue Location | Ubiquitously expressed, highest levels were found in brain and lung (PubMed:7972084). Isoform 5 is expressed at higher levels in astrocytomas as compared to normal brain tissue and expression increases strikingly with the severity of the tumor, being higher in the most aggressive tumors. |
Research Areas
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Application Protocols
Provided below are standard protocols that you may find useful for product applications.
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$ 350.00
$ 175.00
Cat# AP91966
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