Anti-ADAR antibody (AA35686)

$287.00


Alternative names 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, DSRAD_HUMAN
Species Reactivity Human, Mouse, Rat
Applications IF/ICC, IP, IHC, WB
Host Rabbit
Class Polyclonal
Conjugated Unconjugated


Description

Product name Anti-ADAR antibody (AA35686)
Catalog number AA35686
Brand family Ango
Product type Primary Antibody
Antibody Alternative Names Double-stranded RNA-specific adenosine deaminase antibody, DRADA antibody, EC 3.5.4.37 antibody, 136 kDa double-stranded RNA-binding protein antibody, p136 antibody, Interferon-inducible protein 4 antibody, IFI-4 antibody, K88DSRBP antibody, ADAR antibody, ADAR1 antibody, DSRAD antibody, G1P1 antibody, IFI4 antibody, DSRAD_HUMAN antibody


Biological Information

Immunogen Recombinant protein of human ADAR
Concentration 1 mg/ml
Isotype IgG
Application Notes WB 1:500 - 1:2000 IHC 1:50 - 1:200 IF 1:50 - 1:100 IP 1:20 - 1:50
Purification method Purified by affinity chromatography


Target

Target Name ADAR
SwissProt ID Link P55265
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.
Subcellular Location Isoform 1: Cytoplasm. Nucleus. Shuttles between the cytoplasm and nucleus.; Isoform 5: Cytoplasm. Nucleus. Nucleus, nucleolus. Predominantly nuclear but can shuttle between nucleus and cytoplasm. TNPO1 can mediate its nuclear import whereas XPO1 can mediate its nuclear export.
Involvement in Disease Dyschromatosis symmetrica hereditaria: An autosomal dominant pigmentary genodermatosis characterized by a mixture of hyperpigmented and hypopigmented macules distributed on the face and the dorsal parts of the hands and feet, that appear in infancy or early childhood. The disease is caused by mutations affecting the gene represented in this entry. Aicardi-Goutieres syndrome 6: A form of Aicardi-Goutieres syndrome, a genetically heterogeneous disease characterized by cerebral atrophy, leukoencephalopathy, intracranial calcifications, chronic cerebrospinal fluid lymphocytosis, increased CSF alpha-interferon, and negative serologic investigations for common prenatal infection. Clinical features as thrombocytopenia, hepatosplenomegaly and elevated hepatic transaminases along with intermittent fever may erroneously suggest an infective process. Severe neurological dysfunctions manifest in infancy as progressive microcephaly, spasticity, dystonic posturing and profound psychomotor retardation. Death often occurs in early childhood. The disease is caused by mutations affecting the gene represented in this entry.
Post-Translational Modification Sumoylation reduces RNA-editing activity.
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 aggressive tumors.
Subunit Structure Homodimer. Homodimerization is essential for its catalytic activity. Isoform 5 can form heterodimers with ADARB1/ADAR2. Isoform 1 interacts with ILF2/NF45 and ILF3/NF90. Binding to ILF3/NF90 up-regulates ILF3-mediated gene expression. Isoform 5 (via DRBM 3 domain) interacts with TNPO1. Isoform 5 (via DRBM domains) interacts with XPO5. Isoform 1 and isoform 5 can interact with EIF2AK2/PKR and UPF1.
Sequence Similarities Contains 1 A to I editase domain. Contains 2 DRADA repeats. Contains 3 DRBM (double-stranded RNA-binding) domains.


Poduct Presentation

Form Liquid
Preservative 0.02% (w/v) sodium azide
Storage buffer PBS with 50% glycerol, pH 7.3


Storage and Shipping Information

Storage Store at -20 or -80 C. Avoid multiple freeze/thaw cycles.