CTLA-4 IgG Fusion Protein

Produktnummer ABIN1177344

Dieses -Protein wird in exprimiert und wurde in 4+ Publikationen erwähnt.

Kurzübersicht für CTLA-4 IgG Fusion Protein (ABIN1177344)

Target: CTLA-4 IgG Fusion

Spezies: Maus

Wirt: Bitte anfragen

Applikation: Blocking Reagent (BR)

Produktdetails

Marke: BD Pharmingen™

Aufreinigung: Purified from tissue culture supernatant or ascites by affinity chromatography

Sterilität: 0.2 μm filtered

Endotoxin-Niveau: Endotoxin level is ≤0.01 ng/μg of protein.

Anwendungsinformationen

Applikationshinweise: This fusion protein has been tested by LAL assay for endotoxin level, by SDS-PAGE to assure purity, and by an in vitro T-cell proliferation assay to assure blocking activity.

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Format: Liquid

Konzentration: 0.5 mg/mL

Buffer: No azide/low endotoxin: Aqueous buffered solution containing no preservative, 0.2μm filtered.

Konservierungsmittel: Azide free

Lagerung: 4 °C

Informationen zur Lagerung: This preparation contains no preservatives, thus it should be handled under aseptic conditions. The monoclonal antibody was purified from tissue culture supernatant or ascites by affinity chromatography. Avoid multiple freeze-thaws of product. The fusion protein solution should be stored at -20°C until the vial is opened. Thawed aliquots may be stored for at least 1 week at 4°C.

Referenzen

Carreno, Collins: "The B7 family of ligands and its receptors: new pathways for costimulation and inhibition of immune responses." in: Annual review of immunology, Vol. 20, pp. 29-53, (2002) (PubMed).

Tivol, Boyd, McKeon, Borriello, Nickerson, Strom, Sharpe: "CTLA4Ig prevents lymphoproliferation and fatal multiorgan tissue destruction in CTLA-4-deficient mice." in: Journal of immunology (Baltimore, Md. : 1950), Vol. 158, Issue 11, pp. 5091-4, (1997) (PubMed).

Lenschow, Walunas, Bluestone: "CD28/B7 system of T cell costimulation." in: Annual review of immunology, Vol. 14, pp. 233-58, (1996) (PubMed).

Steurer, Nickerson, Steele, Steiger, Zheng, Strom: "Ex vivo coating of islet cell allografts with murine CTLA4/Fc promotes graft tolerance." in: Journal of immunology (Baltimore, Md. : 1950), Vol. 155, Issue 3, pp. 1165-74, (1995) (PubMed).

Antigendetails

Target: CTLA-4 IgG Fusion

Substanzklasse: Antibody

Hintergrund: The Non-Cytolytic Mouse CTLA-4 - IgG Fusion Protein is composed of the extracellular domain of mouse CTLA-4 (CD152) fused to a mutant Fc region of mouse IgG2a, which is unable to bind to the C1q complement or to Fc receptors. This chimeric protein binds to CTLA-4's ligands B7-1 (CD80) and B7-2 (CD86) on mouse antigen-presenting cells and blocks their binding to both CTLA-4 and CD28. CTLA-4 (also known as CD152) is a cell-surface Ig-superfamily glycoprotein closely related to the CD28 costimulatory receptor. CTLA-4 is expressed on activated T lymphocytes 2-3 days after stimulation through the T-cell receptor. Whereas CD28 delivers a costimulatory signal required for T-cell activation, CTLA-4 is a negative regulator of cell-mediated immune responses. CTLA-4 IgG Fusion Protein has been shown to prevent allograft rejection and induce donor-specific tolerance, inhibit in vitro responses of splenocytes to ConA, inhibit the spontaneous in vitro and in vivo lymphoproliferation in CTLA-4-deficient mice, and limit superantigen-induced T-cell proliferation, anergy, and secretion of IL-2, IFN-gamma, and IL-4, but not TNF-alpha or IL-10. Inhibition of ConA-induced proliferation of splenic T lymphocytes by Non-Cytolytic Mouse CTLA-4 - IgG Fusion Protein. C57BL/6 splenocytes were cultured for three days, either with no stimulation or with 4 µg ConA per 10^6 cells, as indicated. The indicated concentrations of either Non-Cytolytic Mouse CTLA-4 - IgG Fusion Protein or a control fusion protein were added to ConA-stimulated cells. Cell proliferation was quantitated by the MTT fluorometric assay. The CTLA-4 fusion protein inhibited ConA-induced cell proliferation in a dose-dependent manner, whereas the control fusion protein had little effect.