CD95 (APO-1/Fas) Mouse anti-Canine, Human, APC, Clone: DX2, eBioscience
Mouse Monoclonal Antibody
Manufacturer: Invitrogen 17095941
Description: The DX2 monoclonal antibody reacts with human CD95 (Fas, Apo-1), a 40-50 kDa member of the TNFR superfamily. CD95 is expressed by a broad range of hematopoietic and non-hematopoietic cells including monocytes, neutrophils, lymphocytes and fibroblasts. Interaction of CD95 on mature lymphocytes with its ligand (FasL) induces apoptosis and is thought to be important in peripheral tolerance. DX2 does not block binding of EOS9.1, another antibody specific for human CD95. The DX2 monoclonal is reported to recognize dog/canine CD95. Applications Reported: This DX2 antibody has been reported for use in flow cytometric analysis. Applications Tested: This DX2 antibody has been pre-titrated and tested by flow cytometric analysis of normal human peripheral blood cells. This can be used at 5 µL (0.125 µg) per test. A test is defined as the amount (µg) of antibody that will stain a cell sample in a final volume of 100 µL. Cell number should be determined empirically but can range from 10^5 to 10^8 cells/test. Excitation: 633-647 nm; Emission: 660 nm; Laser: Red Laser. Filtration: 0.2 µm post-manufacturing filtered.CD95 (Fas, APO-1), a 46 kDa transmembrane glycoprotein, is a cell death receptor of the TNFR superfamily. Stimulation of CD95 results in aggregation of its intracellular death domains, formation of the death-inducing signaling complex (DISC) and activation of caspases. In type I cells caspase 3 is activated by high amounts of caspase 8 generated at the DISC, in type II cells low concentration of caspase 8 activates pathway leading to the release of cytochrome c from mitochondria and activation of caspase 3 by cytochom c. Besides its roles in induction of apoptosis, Fas also triggers pro-inflammatory cytokine responses.
|PBS with 0.1% gelatin, 0.2% BSA and 0.09% sodium azide; pH 7.2|
|ALPS1A, APO-1, APT1, Apo-1 Fas, CD95, FAS1, FASTM, TNFRSF6|
|4° C, store in dark, DO NOT FREEZE!|
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