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Western blot(SDS PAGE) analysis of extracts from HepG2 cells.Using ADAR1 Rabbit mAb [8897] at dilution of 1:1000 incubated at 4℃ over night.
Protein names :ADAR,ADAR1,DSRAD,G1P1,IFI4,DSRAD_HUMAN,Double-stranded RNA-specific adenosine deaminase
UniProtID :P55265
MASS(da) :136,066
MW(kDa) :110, 150 kDa
Form :Liquid
Purification :Protein A purification
Host :Rabbit
Isotype :IgG
sensitivity :Endogenous
Reactivity :Human
Specificity :Antibody is produced by immunizing animals with a synthetic peptide at the sequence of Human ADAR1
Storage :Antibody store in 10 mM PBS, 0.5mg/ml BSA, 50% glycerol. Shipped at 4°C. Store at-20°C or -80°C. Products are valid for one natural year of receipt.Avoid repeated freeze / thaw cycles.
WB Positive detected :HepG2 cells
Function : 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 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..
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 higher in the most aggressive tumors..
Subcellular locationi :[Isoform 1]: Cytoplasm. Nucleus.
IMPORTANT: For western blots, incubate membrane with diluted primary antibody in 1% w/v BSA, 1X TBST at 4°C overnight.