DATASHEET
Host:
Rabbit
Target Protein:
ADAR1
Immunogen Range:
151-250/1226
Clonality:
Polyclonal
Isotype:
IgG
Entrez Gene:
103
Swiss Prot:
P55265
Source:
KLH conjugated synthetic peptide derived from human ADAR1
Purification:
Purified by Protein A.
Storage Buffer:
Aqueous buffered solution containing 0.01M TBS (pH 7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
Storage:
Store at -20°C. Aliquot into multiple vials to avoid repeated freeze-thaw cycles.
Background:
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.
Conjugation:
ALEXA FLUOR® 350
Excitation/ Emission:
346nm/442nm
Size:
100ul
Concentration:
1ug/ul
Applications:
WB(1:300-5000)
IF(IHC-P)(1:50-200)
IF(IHC-F)(1:50-200)
IF(ICC)(1:50-200)
135
Human
For research use only. Not intended for diagnostic or therapeutic use.