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Rabbit anti-Human ADAR Polyclonal Antibody

The antibody against ADAR was raised in rabbit using the Synthesized peptide derived from the C-terminal region of Human ADAR1. as the immunogen. This antibody exists as a non-conjugated isotype IgG. The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen. This antibody has been validated on IHC, ELISA.

ADC-36655A

The antibody against ADAR was raised in rabbit using the Synthesized peptide derived from the C-terminal region of Human ADAR1. as the immunogen. This antibody exists as a non-conjugated isotype IgG. The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen. This antibody has been validated on IHC, ELISA.

$167.00

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Specifications


Cat.No ADC-36655A ClonalityPolyclonal
Host SpeciesRabbitTarget NameADAR
FormLiquidSpecies ReactivityHuman, Mouse, Rat
IsotypeIgGStorage Buffer0.5% BSA and 0.02% sodium azide., Liquid in PBS containing 50% glycerol
Purification MethodThe antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.ConjugateNon-conjugated
ApplicationELISA, IHCStorageUpon receipt

Immunogen Information


Immunogen DescriptionSynthesized peptide derived from the C-terminal region of Human ADAR1.Target SpeciesHuman
Immunogen SequenceComplete sequences for the immunogen, target protein, and peptides are available upon request.Uniprot IDP55265
Background Information
  • Uniprot Id

    P55265

  • Target Species

    Human

  • Target Name

    ADAR

  • Target Full Name

    Double-stranded RNA-specific adenosine deaminase

  • Target Function

    Catalyzes the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) referred to as A-to-I RNA editing. 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.

  • Target Involvement

    Dyschromatosis symmetrica hereditaria (DSH); Aicardi-Goutieres syndrome 6 (AGS6)

  • Target Subcellular Location

    [Isoform 1]: Cytoplasm. Nucleus.; [Isoform 5]: Cytoplasm. Nucleus. Nucleus, nucleolus.

  • Target Tissue Specificity

    Ubiquitously expressed, highest levels were found in brain and lung. 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 ag

  • Target Research Area

    Epigenetics and Nuclear Signaling, Transcription

  • Target Synonyms

    136 kDa double-stranded RNA-binding protein; 136kDa double stranded RNA binding protein; Adar 1; ADAR; Adar1; Adenosine deaminase acting on RNA 1 A; Adenosine deaminase RNA specific 1; Adenosine deaminase RNA specific; Adenosine deaminase that act on RNA; AGS6; AV242451; Double stranded RNA specific adenosine deaminase; Double-stranded RNA-specific adenosine deaminase; Double-stranded RNA-specific editase Adar; DRADA; Dsh; Dsrad; DSRAD_HUMAN; dsRNA adenosine deaminase; EC 3.5.4.-; G1P1; IFI 4; IFI-4; IFI4; Ifi4 protein; Interferon induced protein 4; Interferon inducible protein 4; Interferon-inducible protein 4; K88DSRBP; mZaADAR; P136; Pre-mRNA adenosine deaminase; RNA adenosine deaminase 1; RNA-editing deaminase 1; RNA-editing enzyme 1

  • Target Background

    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.

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