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SSH1 Antibody [K8K10]

Cat.No.: F1247

    Application: Reactivity:

    Usage Information

    Dilution
    1:1000
    1:100
    Application
    WB, IP
    Reactivity
    Human, Mouse, Rat
    Source
    Rabbit Monoclonal Antibody
    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
    140 kDa

    Datasheet & SDS

    Biological Description

    Specificity
    SSH1 Antibody [K8K10] detects endogenous levels of total SSH1 protein.
    Clone
    K8K10
    Synonym(s)
    Protein phosphatase Slingshot homolog 1; SSH-like protein 1 (SSH-1L; hSSH-1L); SSH1; KIAA1298; SSH1L
    Background
    Slingshot homolog 1 (SSH1) is a dual-specificity protein phosphatase that is central to actin cytoskeleton dynamics by dephosphorylating cofilin at Ser3, thereby reactivating its F-actin severing and depolymerizing functions essential for lamellipodia protrusion, filopodia formation, cell migration, cytokinesis, and neuronal morphogenesis. SSH1 features an N-terminal regulatory domain with actin-binding motifs that allosterically stimulate phosphatase activity 14-fold upon F-actin engagement, a central catalytic phosphatase domain (Cys-X5-Arg/Ser motif, with Asp487 for phosphate coordination and Arg502 for stabilization) flanked by unstructured loops for LIMK1 substrate access, and a C-terminal F-actin binding domain (including Trp1001, Lys1023) that promotes SSH1 stabilization and actin bundling independent of its phosphatase activity. In resting cells, SSH1 is cytosolic and autoinhibited via 14-3-3 binding to phospho-Ser978, but upon Rho GTPase signaling (ROCK/PAK via LIMK/TESK-mediated cofilin phosphorylation) or integrin/FAK activation, SSH1 is dephosphorylated and translocated to the membrane, where F-actin docking exposes its active site. This enables rapid cofilin reactivation (kcat/Km ~10^6 M^-1 s^-1), generating free barbed ends for Arp2/3 nucleation, recycling G-actin for treadmilling, and balancing LIMK-mediated inactivation in a Rho/ROCK-LIMK-cofilin-SSH1 feedback circuit that regulates epithelial-to-mesenchymal transition, cancer invasion (where upregulated SSH1 correlates with metastasis in HCC and breast tumors via WNT/β-catenin crosstalk), neurodegeneration (impaired Tau clearance via SQSTM1 flux defects), and vascular permeability.
    References
    • https://pubmed.ncbi.nlm.nih.gov/36637427/
    • https://pubmed.ncbi.nlm.nih.gov/25187968/

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