TEAD1 Antibody [H6K12]

Catalog No.: F4878

    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
    1:10 - 1:100
    1:1000
    1:2000
    Application
    WB, IP, IHC, ChIP
    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
    48 kDa 50,70, 52 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
    TEAD1 Antibody [H6K12] detects endogenous levels of total TEAD1 protein.
    Clone
    H6K12
    Synonym(s)
    TCF13; TEF1; TEAD1; Transcriptional enhancer factor TEF-1; NTEF-1; Protein GT-IIC; TEA domain family member 1; Transcription factor 13; TEAD-1; TCF-13
    Background
    TEAD1 is a member of the TEA domain (TEAD) family of transcription factors (TEAD1-4), which serve as key downstream effectors of the evolutionarily conserved Hippo signaling pathway that controls organ size, cell proliferation, and tumor suppression by regulating YAP/TAZ activity. Its N-terminal TEA DNA-binding domain (TEAD) adopts a three-helix bundle homeodomain fold, with key structural features including an L1 loop essential for cooperative binding to tandem M-CAT DNA sites, unstructured regions (e.g., residues 1–11, 24–31), and a hydrophobic core of 12 residues (e.g., Ile-13, Leu-21); chemical shift perturbations identify helix H3, L2 loop, and the back surface as the primary DNA-binding interface. TEAD1 primarily drives gene expression for cell proliferation and anti-apoptosis upon nuclear translocation of unphosphorylated YAP, forming YAP/TEAD1 complexes that bind TEA/ATTS consensus sequences to activate pro-growth genes, with critical roles in cardiac, skeletal, and smooth muscle development. In the Hippo-off state, YAP escapes LATS1/2 phosphorylation and 14-3-3 sequestration to enable this activity, while Hippo-on signaling inactivates it; TEAD1’s tissue-specific expression underscores its developmental importance. Dysregulated TEAD1 activity contributes to oncogenesis, as seen in YAP-driven hepatocellular carcinoma where dominant-negative TEAD1 suppresses tumorigenesis.
    References

    技術サポート

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