CXCL10 Antikörper

Produktnummer ABIN2664899

Produktdetails anti-CXCL10 Antikörper

Target: CXCL10 (Chemokine (C-X-C Motif) Ligand 10 (CXCL10))

Reaktivität: Human, Maus

Wirt: Maus

Klonalität: Monoklonal

Konjugat: Dieser CXCL10 Antikörper ist unkonjugiert

Applikation: Flow Cytometry (FACS)

Aufreinigung: The antibody was purified by affinity chromatography.

Klon: J036G3

Isotyp: IgG2a kappa

Anwendungsinformationen

Applikationshinweise: Optimal working dilution should be determined by the investigator.

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Konzentration: 0.5 mg/mL

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

Konservierungsmittel: Sodium azide

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

Lagerung: 4 °C

Informationen zur Lagerung: The antibody solution should be stored undiluted between 2°C and 8°C.

Details zu CXCL10

Target: CXCL10 (Chemokine (C-X-C Motif) Ligand 10 (CXCL10))

Andere Bezeichnung: CXCL10 (CXCL10 Produkte)

Hintergrund: CXCL10 is an ELR-negative chemokine structurally and functionally related to CXCL9 and CXCL11. CXCL10, CXCL9, and CXCL11 are produced and secreted by monocytes, macrophages, fibroblasts, and epithelial cells upon stimulation with proinflammatory cytokines, especially IFNγ. CXCL10 chemoattracts CD4, CD8, and NK and NKT cells through the binding to its receptor CXCR3, which is shared with CXCL9 and CXCL11. In addition, CXCL10 inhibits neovascularization in tumors and in wound healing in vivo. Also, CXCL10 has anti-proliferative effects on endothelial cells in vitro, and angiostatic and antitumor effects in vivo. It has been suggested that the anti-proliferative effect of CXCL10 in endothelial cells is CXCR3-independent and that it is mediated through GAG interaction. CXCL10 also possesses antimicrobial activity against E. coli and L. monocytogenes, and both the spore and bacillus forms of B. anthracis. CXCL10 expression is strongly upregulated in many human inflammatory diseases, including rheumatoid arthritis, type I diabetes, multiple sclerosis, atherosclerosis, allograft rejection, and others.