GDF-15 Antibody [G11L21]

Catalog No.: F4427

    Application: Reactivity:

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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
    1:100-1:1000
    1:50-1:500
    Application
    WB, IP, IF, ELISA
    Source
    Mouse Monoclonal Antibody
    Reactivity
    Human, Mouse, Rat
    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
    40 kDa (GDF-15 precursor), 30 kDa (mature GDF-15)

    Datasheet & SDS

    生物学的記述

    Specificity
    GDF-15 Antibody [G11L21] detects endogenous levels of total GDF-15 protein.
    Clone
    G11L21
    Synonym(s)
    Growth/differentiation factor 15; GDF-15; Macrophage inhibitory cytokine 1; MIC-1; NSAID-activated gene 1 protein (NAG-1); NSAID-regulated gene 1 protein (NRG-1); Placental TGF-beta; GDF15; MIC1; PDF; PLAB; PTGFB
    Background
    GDF-15 (Growth/Differentiation Factor 15, also known as MIC-1) is a stress-inducible cytokine and divergent member of the TGF-β superfamily, synthesized as an inactive precursor that is proteolytically cleaved at a furin-like RXXR site to produce a mature, disulfide-linked dimer via a conserved cysteine knot motif. GDF-15 is secreted in its mature form and signals predominantly through the GFRAL receptor in the hindbrain, activating MAPK/ERK and SMAD pathways independently of canonical TGF-β receptors. GDF-15 is markedly upregulated in response to cellular stress, inflammation, mitochondrial dysfunction, and tissue injury, serving as a sensitive biomarker for perioperative risk, organ damage, and postoperative complications, often outperforming traditional markers like CRP or BNP. It modulates immune responses by restraining macrophage activity, protects tissue integrity through ERK/Akt signaling and mitochondrial stabilization, and exerts metabolic effects such as appetite suppression and weight loss relevant to bariatric surgery. Elevated GDF-15 indicates immune dysfunction in sepsis and contributes to cancer cachexia through p53-dependent transcriptional mechanisms.
    References

    技術サポート

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