ADAR1 Antibody [E16C6]

Catalog No.: F7867

    Application: Reactivity:
    • Lane 1: HepG2, Lane 2: Vero
    1/

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    代表番号: 045-509-1970|電子メール:sales@selleck.co.jp

    使用情報

    Dilution
    1:1000
    Application
    WB
    Source
    Rabbit Monoclonal Antibody
    Reactivity
    Human, Monkey
    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
    Predicted MW
    110 kDa, 150 kDa

    Datasheet & SDS

    生物学的記述

    Specificity
    ADAR1 Antibody [E16C6] detects endogenous levels of total ADAR1 protein.
    Clone
    E16C6
    Synonym(s)
    Double-strand adenosine deaminase; DRADA; 136 kDa double-stranded RNA-binding protein (p136); Interferon-inducible protein 4 (IFI-4); K88DSRBP; ADAR; ADAR1; DSRAD; G1P1; IFI4
    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.
    References

    技術サポート

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