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GILZ (F2U9K) Rabbit Monoclonal Antibody #25841

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  • WB
  • IP
  • F

    Product Specifications

    REACTIVITY H M
    SENSITIVITY Endogenous
    MW (kDa) 15-25
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • F-Flow Cytometry 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:200
    Flow Cytometry (Fixed/Permeabilized) 1:400 - 1:1600

    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

    GILZ (F2U9K) Rabbit Monoclonal Antibody recognizes endogenous levels of total GILZ protein. This antibody is not recommended for flow cytometry with mouse samples.

    Species Reactivity:

    Human, Mouse

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human GILZ protein.

    Background

    Glucocorticoids (GCs) are drugs with potent anti-inflammatory and immunosuppressive effects. GCs act by inhibiting the function of macrophages and antigen-presenting cells (1,2), and their varied biological effects are controlled by several well-characterized pathways (3-5). Identifying proteins that are transcriptionally regulated downstream of GC treatment is of significant research interest. Glucocorticoid-induced leucine zipper (GILZ), also known as TSC22 domain family member 3 (TSC22D3), is a protein primarily expressed under glucocorticoid receptor (GR) transcriptional control. GILZ was first identified in a screen for genes mediating GC-induced apoptosis (3). GILZ has subsequently been shown to regulate apoptosis, proliferation, and differentiation, in addition to signaling pathways associated with host immunity and inflammation (4,5). One mechanism by which GCs induce immunosuppression is through regulation of the T cell response (1,5). GILZ interferes with the function of AP-1 and NF-κB in T lymphocytes and macrophages (2,4). GILZ also inhibits NF-κB by directly binding to the p65 subunit, preventing its interaction with specific gene regulatory elements (3). Recent research has focused on the role of GILZ in stress response and tumor biology (6-8). GILZ expression is associated with poor prognosis in patients with acute myeloid leukemia (AML) and is being investigated as a prognostic biomarker (7). Furthermore, combined therapy targeting GILZ alongside PD-L1 checkpoint blockade has been shown as an effective method to prevent immune escape in glioblastomas (8).

    Alternate Names

    delta sleep inducing peptide, immunoreactor; Delta sleep-inducing peptide immunoreactor; DIP; DKFZp313A1123; DSIP-immunoreactive leucine zipper protein; DSIP-immunoreactive peptide; DSIPI; GILZ; Glucocorticoid-induced leucine zipper protein; hDIP; Protein DIP; T22D3; TSC-22 related protein; TSC-22-like protein; TSC-22-related protein; TSC-22R; TSC22 domain family member 3; TSC22 domain family protein 3; TSC22 domain family, member 3; TSC22D3

    For Research Use Only. Not for Use in Diagnostic Procedures.
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