Datasheet

生物学的記述

Specificity	ADAR1 Antibody [E16C6] detects endogenous levels of total ADAR1 protein.
Background	ADAR1 (adenosine deaminase acting on RNA 1) is a double‑stranded RNA‑specific adenosine deaminase that belongs to the ADAR family and catalyzes the conversion of adenosine to inosine (A‑to‑I editing) in structured RNA regions, a process that is interpreted as an A‑to‑G change by the splicing and translational machinery and thereby diversifies transcript and protein isoforms without altering the genomic sequence. It exists as two major isoforms, ADAR1L (p150) and ADAR1S (p110), generated from alternative promoters and translation start sites, with ADAR1S localized constitutively in the nucleus and ADAR1L being inducible by interferon and present in both the nucleus and the cytoplasm, where it can engage overlapping but non‑identical substrate pools. ADAR1‑mediated editing modulates sequence recognition by RNA‑binding proteins and non‑coding RNAs, including microRNAs, and thereby influences alternative splicing, mRNA stability, translational efficiency, and the targeting of regulatory RNAs. ADAR1 functions as a key suppressor of aberrant interferon responses by editing endogenous double‑stranded RNAs so that they are not recognized as foreign by cytoplasmic RNA sensors such as MDA5 and RIG‑I; loss or inhibition of ADAR1 leads to accumulation of unedited or hyperedited substrates that trigger type‑I and type‑II interferon signaling and inflammation. ADAR1 is also essential for their maintenance in the fetal liver and adult bone marrow, and ADAR1 deficiency in these cells causes global upregulation of interferon‑stimulated genes and rapid apoptosis.

Specificity

ADAR1 Antibody [E16C6] detects endogenous levels of total ADAR1 protein.

Background

ADAR1 (adenosine deaminase acting on RNA 1) is a double‑stranded RNA‑specific adenosine deaminase that belongs to the ADAR family and catalyzes the conversion of adenosine to inosine (A‑to‑I editing) in structured RNA regions, a process that is interpreted as an A‑to‑G change by the splicing and translational machinery and thereby diversifies transcript and protein isoforms without altering the genomic sequence. It exists as two major isoforms, ADAR1L (p150) and ADAR1S (p110), generated from alternative promoters and translation start sites, with ADAR1S localized constitutively in the nucleus and ADAR1L being inducible by interferon and present in both the nucleus and the cytoplasm, where it can engage overlapping but non‑identical substrate pools. ADAR1‑mediated editing modulates sequence recognition by RNA‑binding proteins and non‑coding RNAs, including microRNAs, and thereby influences alternative splicing, mRNA stability, translational efficiency, and the targeting of regulatory RNAs. ADAR1 functions as a key suppressor of aberrant interferon responses by editing endogenous double‑stranded RNAs so that they are not recognized as foreign by cytoplasmic RNA sensors such as MDA5 and RIG‑I; loss or inhibition of ADAR1 leads to accumulation of unedited or hyperedited substrates that trigger type‑I and type‑II interferon signaling and inflammation. ADAR1 is also essential for their maintenance in the fetal liver and adult bone marrow, and ADAR1 deficiency in these cells causes global upregulation of interferon‑stimulated genes and rapid apoptosis.

使用情報

Application

WB

Dilution

WB

1:1000

Reactivity

Human, Monkey

Source

Rabbit Monoclonal Antibody

MW

110 kDa, 150 kDa

Storage Buffer

PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage
(from the date of receipt)

-20°C (avoid freeze-thaw cycles), 2 years

プロトコール

References

https://pubmed.ncbi.nlm.nih.gov/19060901/
https://pubmed.ncbi.nlm.nih.gov/25456137/

Application Data

WB

Validated by Selleck

Lane 1: HepG2, Lane 2: Vero