CD95 (FAS), Human Antibody from MILTENYI BIOTEC B.V. & Co. KG

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Antigenic SpecificityCD95 (FAS), Human
CloneREA738
Host SpeciesRecombinant Human
Reactive Specieshuman, nonhuman primate
IsotypeIgG1
Formatbiotin conjugate
Size100 tests in 200 µL
Concentration1:50
ApplicationsFlow cytometry
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DescriptionCD95 (FAS) Antibody, anti-human, Biotin, REAfinity™. Clone REA738 recognizes the human CD95 antigen, also known as Fas and Apo-1, which is a member of the tumor necrosis factor receptor superfamily (TNFR) and is found on the surface of many normal and neoplastically transformed cells. Its ligand, CD95L (FasL/Apo-1L), is able to induce apoptosis in CD95-expressing cells upon binding. CD95 and CD95L are up-regulated on lymphocytes upon activation and are known to play a key role in the regulation of an inflammatory response: Juxtocrine ``fratricide'' of neighbouring lymphocytes via mutual CD95 and CD95L expression helps to terminate immune responses, while apoptosis of pro-inflammatory cells via CD95 helps maintain immune privilege in sites such as the eye, where CD95L is found to be expressed in the retina and cornea. Cross-linking of CD95 receptors by DX2 monoclonal antibody has been described to induce apoptosis in certain target cells. | Additional information: Clone REA738 displays negligible binding to Fc receptors.
Immunogenn/a
Other NamesFAS, ALPS1A, APO-1, Apt1, FAS1, FASTM, Tnfrsf6
Gene, Accession #Gene ID: 355
Catalog #130-113-002
Price$275
Order / More InfoCD95 (FAS), Human Antibody from MILTENYI BIOTEC B.V. & Co. KG
Product Specific ReferencesGriffith, T. et al. (1995) Fas ligand-induced apoptosis as a mechanism of immune privilege. Science 270: 1189-1192. | Lynch, D. et al. (1995) Fas and FasL in the homeostatic regulation of immune responses. Immunol. Today 16: 569-574. | Pitcher, C. J. et al. (2002) Development and homeostasis of T cell memory in rhesus macaque. J Immunol 168: 29-43.
MILTENYI BIOTEC B.V. & Co. KG
MILTENYI BIOTEC B.V. & Co. KG
MILTENYI BIOTEC B.V. & Co. KG
Friedrich-Ebert-Straße 68
51429 Bergisch Gladbach GERMANY
P: +49 2204 8306-0
F: +49 2204 85197

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