SOX10 Antibody [E22E2]

Catalog No.: F4814

    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
    1:1000-1:10000
    1:30
    1:1000
    Application
    WB, IP, IHC
    Source
    Rabbit Monoclonal Antibody
    Reactivity
    Mouse, Rat, Human
    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 Observed MW
    270 kDa 314 kDa
    *なぜ予測分子量と実際の分子量が異なるのか?
    下記の原因により、実際の分子量が予測と異なる:タンパク質の翻訳後修飾(リン酸化/糖鎖付加),スプライシングバリアント,イソフォーム,相対的な電荷,ポリマー。

    Datasheet & SDS

    生物学的記述

    Specificity
    SOX10 Antibody [E22E2] detects endogenous levels of total SOX10 protein.
    Clone
    E22E2
    Synonym(s)
    Transcription factor SOX-10
    Background
    SOX10, a SOX E-group transcription factor, is a master regulator of neural crest cell fate, orchestrating their specification, survival, migration, and differentiation into melanocytes, Schwann cells, and oligodendrocytes via DNA binding and coactivator recruitment. It consists of a central HMG-box DNA-binding domain that bends DNA at specific motifs, an N-terminal dimerization domain, dual transactivation domains (acidic K2/TAM and potent C-terminal TA/TAC), and regulatory phosphorylation and acetylation sites that fine-tune its activity. SOX10 primarily acts by occupying enhancers and promoters as a monomer and synergizing with lineage-defining transcription factors, such as Pax3→Mitf for melanocytes, Krox20→Egr2 for Schwann cells, and Olig1/2→Myrf for oligodendrocytes, to trigger stage-specific gene expression cascades, enforced through self-regulatory and partner-dependent mechanisms. This ensures proper formation of neural crest-derived glial cells in both the peripheral and central nervous systems, as well as the development of the inner ear, enteric nervous system, and oligodendroglial maturation. Loss of SOX10 disrupts neural crest cell development, while mutations cause disorders like Waardenburg syndrome, PCWH, and increase melanoma risk; its overexpression in tumors promotes stemness and cancer progression, all modulated by intricate auto-regulation and partner interactions.
    References

    技術サポート

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