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CXCL9 antibody (Alexa Fluor 647)

This anti-CXCL9 antibody is a Armenian Hamster Monoclonal antibody detecting CXCL9 in FACS. Suitable for Mouse.
Catalog No. ABIN2657882

Quick Overview for CXCL9 antibody (Alexa Fluor 647) (ABIN2657882)

Target

See all CXCL9 Antibodies
CXCL9 (gamma-Interferon-Induced Monokine (CXCL9))

Reactivity

  • 78
  • 23
  • 20
  • 16
  • 3
  • 2
  • 1
Mouse

Host

  • 59
  • 26
  • 2
  • 1
  • 1
Armenian Hamster

Clonality

  • 64
  • 25
Monoclonal

Conjugate

  • 43
  • 11
  • 8
  • 4
  • 4
  • 2
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
This CXCL9 antibody is conjugated to Alexa Fluor 647

Application

  • 68
  • 37
  • 29
  • 15
  • 13
  • 13
  • 11
  • 9
  • 7
  • 5
  • 3
  • 3
  • 3
  • 3
  • 2
  • 2
  • 1
Flow Cytometry (FACS)

Clone

MIG-2F5-5
  • Purification

    The antibody was purified by affinity chromatography, and conjugated with Alexa Fluor® 647 under optimal conditions.

    Isotype

    IgG, IgG kappa
  • Application Notes

    Optimal working dilution should be determined by the investigator.

    Restrictions

    For Research Use only
  • Concentration

    0.5 mg/mL

    Buffer

    Phosphate-buffered solution, pH 7.2, containing 0.09 % sodium azide.

    Preservative

    Sodium azide

    Precaution of Use

    This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

    Handling Advice

    Protect from prolonged exposure to light. Do not freeze.

    Storage

    4 °C

    Storage Comment

    The antibody solution should be stored undiluted between 2°C and 8°C
  • Target

    CXCL9 (gamma-Interferon-Induced Monokine (CXCL9))

    Alternative Name

    CXCL9

    Background

    MIG, also known as mig-1, CXCL9, is a member of the alpha subfamily of inflammatory chemokine. It is inducible in macrophages, hepatocytes, and endothelial cells by IFN-γ, but not by TNF-α or bacterial lipopolysacchrides (LPS). Mig functions as a chemotactic factor for resting memory and activated T cells, both CD4+ and CD8+, and natural killer cells. Furthermore, it was reported that Mig induced both calcium signals and chemotaxis in activated B cells and that B cell activation induced expression of mouse CXCR3. MIG and CXCR3 may be important not only to recruit T cells to peripheral inflammatory sites, but also in some cases to maximize interactions among activated T cells, B cells, and dendritic cells within lymphoid organs to provide optimal humoral responses to pathogens.
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