NP_001020278.1
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NCBI GenBank Nucleotide #
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UniProt Primary Accession #
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UniProt Secondary Accession #
UniProt Related Accession #
Molecular Weight
103,642 Da
NCBI Official Full Name
double-stranded RNA-specific adenosine deaminase isoform d
NCBI Official Synonym Full Names
adenosine deaminase, RNA specific
NCBI Official Synonym Symbols
DSH; AGS6; G1P1; IFI4; P136; ADAR1; DRADA; DSRAD; IFI-4; K88DSRBP [Similar Products]
NCBI Protein Information
double-stranded RNA-specific adenosine deaminase
UniProt Protein Name
Double-stranded RNA-specific adenosine deaminase
UniProt Synonym Protein Names
136 kDa double-stranded RNA-binding protein; p136; Interferon-inducible protein 4; IFI-4; K88DSRBP
UniProt Synonym Gene Names
NCBI Summary for ADAR
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. [provided by RefSeq, Jul 2010]
UniProt Comments for ADAR
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.
Research Articles on ADAR
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Pathways associated with ADAR recombinant protein
Diseases associated with ADAR recombinant protein
Organs/Tissues associated with ADAR recombinant protein
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