Der Kaninchen Polyklonal Anti-TNFSF18-Antikörper wurde für WB, ELISA und ICC validiert. Er ist geeignet, TNFSF18 in Proben von Human und Maus zu detektieren.
Produktnummer ABIN6990563
Kurzübersicht für TNFSF18 Antikörper (ABIN6990563)
TNFSF18
Reaktivität: Human
WB
Wirt: Kaninchen
Polyclonal
unconjugated
Applikationshinweise
GITRL antibody can be used for the detection of GITRL by Western blot at 1 μ,g/mL. Antibody can also be used for immunocytochemistry starting at 10 μ,g/mL.
Antibody validated: Immunocytochemistry in human samples. All other applications and species not yet tested.
Beschränkungen
Nur für Forschungszwecke einsetzbar
Format
Liquid
Konzentration
1 mg/mL
Buffer
GITRL Antibody is supplied in PBS containing 0.02 % 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
-20 °C,4 °C
Informationen zur Lagerung
GITRL antibody can be stored at 4°C for three months and -20°C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
Target
TNFSF18
(Tumor Necrosis Factor (Ligand) Superfamily, Member 18 (TNFSF18))
Andere Bezeichnung
GITRL
Hintergrund
GITRL Antibody: The tumor necrosis factor (TNF) and TNF receptor (TNFR) gene superfamilies regulate numerous biological functions including cell proliferation, differentiation, and survival through regulating the activation of the transcription factor NF-κ,B and various mitogen-activated protein kinases. The glucocorticoid-induced tumor necrosis factor receptor (GITR) is an emerging member of this family that is expressed on CD4+ CD25+ regulatory T cells and appears to have crucial immune regulation functions. Its ligand GITRL is expressed in endothelial and antigen-presenting cells and can activate NF-κ,B, induce both pro- and anti-apoptotic effects, inhibit the suppressive activity of regulatory T cells, and co-stimulate responder T cells through GITR. Dominant negative forms of NIK and TRAF2 expressed in transfected 293 cells substantially inhibited NF-κ,B activation, suggesting that the GITRL-GITR pathway involves both NIK and TRAF2.