ADARB1 Antibody

Catalog Number:

33838

Amount:

100μg

Price:

$319

Swiss-Prot No:

Swiss-Prot: P78563
NCBI Gene ID: 104

Form of Antibody:

Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

Storage/Stability:

Immunogen:

Synthesized peptide derived from internal of human ADARB1.

Purification:

The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.

Specificity/Sensitivity:

The antibody detects endogenous levels of total ADARB1 protein.

Applications:

WB

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 GRIK2) and serotonin (HTR2C), GABA receptor (GABRA3) and potassium voltage-gated channel (KCNA1). Site-specific RNA editing of transcripts encoding these proteins results in amino acid substitutions which consequently alter their functional activities. Edits GRIA2 at both the Q/R and R/G sites efficiently but converts the adenosine in hotspot1 much less efficiently. Can exert a proviral effect towards human immunodeficiency virus type 1 (HIV-1) and enhances its replication via both an editing-dependent and editing-independent mechanism. The former involves editing of adenosines in the 5'UTR while the latter occurs via suppression of EIF2AK2/PKR activation and function. Can inhibit cell proliferation and migration and can stimulate exocytosis.

Mittaz L., Genomics 41:210-217(1997).
Lai F., Mol. Cell. Biol. 17:2413-2424(1997).
Villard L., Somat. Cell Mol. Genet. 23:135-145(1997).

References:

appl_detail:

Western blotting: 1:500~1:3000

Datasheet PDF