Render Target: STATIC
Render Timestamp: 2024-12-12T11:05:47.081Z
Commit: 611277b6de3cd1bb065350b6ef8d63df412b7185
XML generation date: 2024-08-01 15:25:37.061
Product last modified at: 2024-09-26T12:15:35.121Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Siva-1 Antibody #12532

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 19
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    Siva-1 Antibody recognizes endogenous levels of total Siva-1 protein. This antibody does not cross-react with Siva-2. This antibody cross-reacts with a protein of unknown origin at ~70 kDa.

    Species Reactivity:

    Human

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro71 of human Siva-1 protein. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    First identified as a pro-apoptotic protein that binds the cytoplasmic tail of the TNF receptor superfamily member CD27 (1), Siva-1 also binds several other TNFR family members including glucocorticoid-induced tumor necrosis factor receptor (GITR) and OX40 (1-3), as well as anti-apoptotic Bcl-2 family members Bcl-xL and Bcl-2 (4,5). Siva-1 is composed of a central death domain homology region, a C-terminal box-B-like ring finger followed by a zinc finger-like domain, and a unique N-terminal amphipathic helical region (SAH) (1,4). Studies have demonstrated that Siva-1 has the ability to induce cell death via both the extrinsic and intrinsic apoptotic pathways (1-8). The SAH domain of Siva-1 is responsible for the inhibition of the pro-survival activities of Bcl-xL and Bcl-2, leading to caspase-mediated cell death (4,5,8). Siva-1 plays a role in T cell signaling and homeostasis by inhibiting NF-κB activity, also resulting in apoptotic cell death (7,9). An alternative splice variant of Siva-1, Siva-2, lacks part of the SAH and death domains and is less effective at inducing apoptosis (1,2,5,8). Studies in xenografts have shown that down-regulation of Siva-1 inhibits tumorigenesis in response to p53 activation (10). Down-regulation of Siva-1 may also play a role in tumor metastasis through its regulation of the epithelial-mesenchymal transition (EMT) and cell migration (11). Overexpression of Siva-1 is implicated in several pathological conditions including acute ischemic injury (12) and Coxsackievirus infection (13).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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