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产品信息
PA5-62429
产品规格
种属反应
Human
宿主/亚型
Rabbit
/ IgG
分类
Polyclonal
类型
Antibody
抗原
偶联物
形式
Liquid
浓度
0.3 mg/mL
纯化类型
Antigen affinity chromatography
保存液
PBS, pH 7.2, with 40% glycerol
内含物
0.02% sodium azide
保存条件
Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.
运输条件
Wet ice
RRID
AB_2637681
产品详细信息
Immunogen sequence: ALLTHFLQPI YLKSVTLGYL FSQGHLTRAI CCRVTRDGSA FEDGLRHPFI VNHPKVGRVS IYDSKRQSGK TKETSVNWCL ADGYDLEILD GTRGTVDGPR NELSRVSKKN IFLLFKKLCS FRYRRDLLRL SYGEAKKAAR DY
Highest antigen sequence identity to the following orthologs: Mouse - 93%, Rat - 94%.
靶标信息
Adenosine Deaminase RNA Specific (ADAR) 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. ADAR 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. (Uniprot)
仅用于科研。不用于诊断过程。未经明确授权不得转售。
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生物信息学
蛋白别名: 136 kDa double-stranded RNA-binding protein; ADA; Adenosine Deaminase; adenosine deaminase acting on RNA 1-A; adenosine deaminase, RNA-specific; Double-stranded RNA-specific adenosine deaminase; DRADA; dsRNA adenosine deaminase; dsRNA adeonosine deaminase; IFI-4; interferon-induced protein 4; Interferon-inducible protein 4; K88DSRBP; p136
基因别名: ADAR; ADAR1; AGS6; DRADA; DSH; DSRAD; G1P1; IFI-4; IFI4; K88DSRBP; P136
UniProt ID: (Human) P55265
Entrez Gene ID: (Human) 103
osteoblast differentiation
in utero embryonic development
hematopoietic progenitor cell differentiation
somatic diversification of immune receptors via somatic mutation
adenosine to inosine editing
mRNA processing
response to virus
base conversion or substitution editing
erythrocyte differentiation
pre-miRNA processing
miRNA loading onto RISC involved in gene silencing by miRNA
response to interferon-alpha
negative regulation of apoptotic process
negative regulation of protein kinase activity by regulation of protein phosphorylation
positive regulation of viral genome replication
negative regulation of viral genome replication
innate immune response
defense response to virus
definitive hemopoiesis
type I interferon signaling pathway
negative regulation of type I interferon-mediated signaling pathway
hematopoietic stem cell homeostasis
cellular response to virus
negative regulation of RNA interference
