ADAR Antibody, FITC conjugated

Datasheet
Code CSB-PA001324LC01HU
Size US$299
Uniprot No. P55265
Protocols ELISA Protocol
Immunogen Recombinant Human Double-stranded RNA-specific adenosine deaminase protein (367-471AA)
Raised in Rabbit
Species Reactivity Human
Tested Applications ELISA
Relevance 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.
Form Liquid
Conjugate FITC
Storage Buffer Preservative: 0.03% Proclin 300
Constituents: 50% Glycerol, 0.01M PBS, pH 7.4
Purification Method >95%, Protein G purified
Isotype IgG
Clonality Polyclonal
Alias Double-stranded RNA-specific adenosine deaminase (DRADA) (EC 3.5.4.37) (136 kDa double-stranded RNA-binding protein) (p136) (Interferon-inducible protein 4) (IFI-4) (K88DSRBP), ADAR, ADAR1 DSRAD G1P1 IFI4
Immunogen Species Human
Research Area Microbiology
Target Names ADAR
Storage Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
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Function Catalyzes the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) referred to as A-to-I RNA editing
Involvement in disease Dyschromatosis symmetrica hereditaria (DSH); Aicardi-Goutieres syndrome 6 (AGS6)
Subcellular Location Isoform 1: Cytoplasm, Nucleus, Note=Shuttles between the cytoplasm and nucleus (PubMed:7565688, PubMed:24753571), Nuclear import is mediated by TNPO1 (PubMed:24753571), SUBCELLULAR LOCATION: Isoform 5: Cytoplasm, Nucleus, Nucleus, nucleolus
Tissue Specificity 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 high
Database Links

HGNC: 225

OMIM: 127400

KEGG: hsa:103

STRING: 9606.ENSP00000357459

UniGene: Hs.12341

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