Anti-ADAR1 antibody
Specifications
| Product Cat#: | AB-07-2292 |
| Product type: | Primary antibody |
| Antigen: | ADAR1 |
| Immunogen: | A synthetic peptide derived from human ADAR1. The exact amino-acid sequence is proprietary. |
| Species immunized: | Rabbit |
| Isotype: | IgG |
| Applications: | Western Blot (1:500-1:2500); ELISA (1:20000) |
| Reactivity: | Human, Mouse, Rat |
| Clonality (clone number): | Polyclonal |
| Form: | Liquid |
| Buffer: | PBS (without Mg2+ and Ca2+ ), pH 7.4, 150 mM NaCl, 0.02% sodium azide and 50% glycerol. |
| Concentration: | 1 mg/ml |
| Purity: | Antigen affinity chromatography |
| Storage: | Aliquot and freeze at -20°C. Avoid multiple freeze/thaw cycles. |
| Alternative names: | 136 kDa double-stranded RNA binding protein; ADAR1; DRADA; DSH; DSRAD; EC 3.5.4.-; IFI-4 protein; IFI4; P136; Double-stranded RNA-specific adenosine deaminase, interferon-inducible protein 4 |
Target information
Catalyzes the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) referred to as A-to-I RNA editing (PubMed:7972084, PubMed:7565688, PubMed:12618436). 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; 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.
Provider
Erpantech Laboratory
