CXCL9 anticorps (Alexa Fluor 647)

N° du produit ABIN2657882

Cet anticorps anti-CXCL9 est un anticorps Hamster arménien Monoclonal détectant CXCL9 dans FACS. Adapté pour Souris.

Aperçu rapide pour CXCL9 anticorps (Alexa Fluor 647) (ABIN2657882)

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

Reactivité: Souris

Hôte: Hamster arménien

Clonalité: Monoclonal

Conjugué: Cet anticorp CXCL9 est conjugé à/à la Alexa Fluor 647

Application: Flow Cytometry (FACS)

Clone: MIG-2F5-5

Détail du produit anti-CXCL9 anticorps (Alexa Fluor 647)

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

Isotype: IgG, IgG kappa

Information d'application

Indications d'application: Optimal working dilution should be determined by the investigator.

Restrictions: For Research Use only

Stockage

Concentration: 0.5 mg/mL

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

Agent conservateur: Sodium azide

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

Conseil sur la manipulation: Protect from prolonged exposure to light. Do not freeze.

Stock: 4 °C

Stockage commentaire: The antibody solution should be stored undiluted between 2°C and 8°C

Détails sur CXCL9

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

Autre désignation: CXCL9

Sujet: 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.