PRMT5 Antibody [M17F9]

Catalog No.: F7112

    Application: Reactivity:
    • Lane 1: Hela, Lane 2: C2C12, Lane 3: H-4-II-E, Lane 4: 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
    1:50
    1:400-1:1600
    Application
    WB, IP, IHC
    Source
    Rabbit Monoclonal Antibody
    Reactivity
    Human, Mouse, Rat, 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
    73 kDa

    Datasheet & SDS

    生物学的記述

    Specificity
    PRMT5 Antibody [M17F9] detects endogenous levels of total PRMT5 protein.
    Clone
    M17F9
    Synonym(s)
    Protein arginine N-methyltransferase 5; PRMT5; 72 kDa ICln-binding protein; Jak-binding protein 1; Shk1 kinase-binding protein 1 homolog (SKB1 homolog; SKB1Hs); HRMT1L5; IBP72; JBP1; SKB1
    Background
    PRMT5 (protein arginine methyltransferase 5) is a type II arginine methyltransferase that forms a stable complex with the methyltransferase cofactor WD repeat domain 77 (WDR77/MEP50) and is widely expressed in mammalian cells, where it catalyzes symmetric dimethylation of arginine residues on histones and multiple non‑histone substrates. PRMT5 is incorporated into chromatin remodeling complexes such as SWI/SNF and NuRD and methylates histones H3 and H4, which modulates chromatin compaction and transcriptional repression at specific loci, including genes involved in differentiation and cell‑cycle control. PRMT5 also methylates RNA‑processing factors and transcriptional regulators, thereby influencing pre‑mRNA splicing, export, and the activity of key signaling effectors, and contributes to the regulation of pathways such as p53‑dependent stress responses, translation initiation via eIF4E, and EGFR/Akt/GSK3β signaling in cancer cells. PRMT5 activity is required for G1‑to‑S phase progression, and loss or inhibition of PRMT5 triggers cell‑cycle arrest and reduces expression of cyclins and other growth‑promoting factors, whereas PRMT5 upregulation or aberrant activity is linked to enhanced proliferation and survival in multiple tumors. PRMT5‑dependent methylation modulates interferon and inflammatory signaling in T cells, and PRMT5 inhibition has been shown to blunt interferon‑stimulated gene expression and STAT1 activation, linking it to immune‑cell activation and inflammatory disease.
    References

    技術サポート

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