Render Target: STATIC
Render Timestamp: 2024-10-11T09:37:18.569Z
Commit: 56767fe525c928647c8401233a175d0d607d385d
XML generation date: 2024-09-30 01:57:19.922
Product last modified at: 2024-09-30T08:01:06.525Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

SSX1/3 (E9P5M) Rabbit mAb (Amino-terminal Antigen) #42734

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 25
    Source/Isotype Rabbit IgG
    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, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    SSX1/3 (E9P5M) Rabbit mAb recognizes endogenous levels of total SSX1 and SSX3 protein. This antibody does not react with SSX2, SSX4, or the SS18/SSX fusion protein. This antibody cross-reacts with an 82 kDa protein of unknown origin.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro11 of human SSX1 protein.

    Background

    The SS18-SSX fusion proteins are a result of in-frame fusions that fuse the SS18 gene on chromosome 18 with X chromosome genes SSX1, SSX2, and to a lesser extent SSX4 (1). Human synovial sarcoma (SS) accounts for 8-10% of all soft tissue malignancies and 95% of these malignancies express the recurrent translocation of the SS18 gene on chromosome 18 (1). The N-terminal SNH domain (SYT N-terminal homology domain) of the SS18 protein interacts with SWI/SNF chromatin remodeling complexes via the N terminal region of BRM and BRG1 subunits (2). Studies of the SS18-SSX fusion in SS suggest that endogenous SS18 competes with the mutant SS18-SSX fusion for occupancy in the SWI/SNF complexes resulting in the displacement of the SNF5 (BAF47) subunit. Displacement of the SNF5 subunit results in altered function of the SWI/SNF complex that leads to deregulated expression of genes such as Sox2 in SS (1).

    While the SSX family of proteins is well characterized in SS, little is known outside of this context. The conserved N-terminus of the SSX family contains a KRAB domain which seems to function as a transcriptional repressor (3).
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