Render Target: STATIC
Render Timestamp: 2024-12-26T11:12:54.712Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-09-30 01:57:48.384
Product last modified at: 2024-12-17T19:00:51.528Z
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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.

TIM-3 (E9K5D) Rabbit mAb #75743

Filter:
  • IF
  • F

    Supporting Data

    REACTIVITY M
    SENSITIVITY Endogenous
    MW (kDa)
    Source/Isotype Rabbit IgG
    Application Key:
    • IF-Immunofluorescence 
    • F-Flow Cytometry 
    Species Cross-Reactivity Key:
    • M-Mouse 

    Product Information

    Product Usage Information

    Application Dilution
    Immunofluorescence (Frozen) 1:100 - 1:400
    Immunofluorescence (Immunocytochemistry) 1:100 - 1:400
    Flow Cytometry (Fixed/Permeabilized) 1:200 - 1:800
    Flow Cytometry (Live) 1:200 - 1:800

    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

    TIM-3 (E9K5D) Rabbit mAb recognizes endogenous levels of total TIM-3 protein.

    Species Reactivity:

    Mouse

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with mouse TIM-3 recombinant protein.

    Background

    T cell Ig- and mucin-domain-containing molecules (TIMs) are a family of transmembrane proteins expressed by various immune cells. TIM-3 is an inhibitory molecule that is induced following T cell activation (1-3 ). TIM-3 is expressed by exhausted T cells in the settings of chronic infection and cancer (4,5), and tumor-infiltrating T cells that coexpress PD-1 and TIM-3 exhibit the most severe exhausted phenotype (5). Tumor-infiltrating dendritic cells (DCs) also express TIM-3. TIM-3 expression on DCs was found to suppress innate immunity by reducing the immunogenicity of nucleic acids released by dying tumor cells (6). Research studies show that heterodimerization of TIM-3 with CEACAM-1 is critical for the inhibitory function of TIM-3, and co-blockade of TIM-3 and CEACAM-1 enhanced anti-tumor responses in a mouse model of colorectal cancer (7). In addition, blockade of TIM-3 in mouse models of autoimmunity enhanced the severity of disease (1). Finally, binding of Galectin-9 to TIM-3 expressed by Th1 cells induces T cell death (8).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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