Recombinant full length protein, corresponding to amino acids 1-403 of Human CD96
Abcam is committed to meeting high standards of ethical manufacturing and has decided to discontinue this product by June 2019 as it has been generated by the ascites method. We are sorry for any inconvenience this may cause.
Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
WB: Use at a concentration of 1-5 µg/ml.
This antibody has only been tested in WB against the recombinant fragment used as immunogen. We have no data on the detection of endogenous protein.
Not yet tested in other applications. Optimal dilutions/concentrations should be determined by the end user.
May be involved in adhesive interactions of activated T and NK cells during the late phase of the immune response. Promotes NK cell-target adhesion by interacting with PVR present on target cells. May function at a time after T and NK cells have penetrated the endothelium using integrins and selectins, when they are actively engaging diseased cells and moving within areas of inflammation.
Expressed on normal T-cell lines and clones, and some transformed T-cells, but no other cultured cell lines tested. It is expressed at very low levels on activated B-cells.
Defects in CD96 are a cause of C syndrome (CSYN) [MIM:211750]; also called Opitz trigonocephaly syndrome. This syndrome is characterized by trigonocephaly and associated anomalies, such as unusual facies, wide alveolar ridges, multiple buccal frenula, limb defects, visceral anomalies, redundant skin, psychomotor retardation and hypotonia. Note=A chromosomal aberration involving CD96 has been found in a patient with C syndrome. Translocation t(3;18)(q13.13;q12.1). CD96 gene was located at the 3q13.13 breakpoint. Precise structural analysis around the breakpoint showed that the gene was disrupted by the translocation in exon 5, probably leading to premature termination or loss of expression of CD96 protein. No gene was detected at the chromosome 18 breakpoint. Defects in CD96 are a cause of C-like syndrome (CLSYN) [MIM:605039]; also called Opitz trigonocephaly-like syndrome. The C-like syndrome seems to be a severe form of the C syndrome. It is controversial whether there is (1) a gradient of spectrum in the C syndrome, from the mild form (C syndrome) to the severe form (C-like syndrome), or (2) genetic heterogeneity among the patients with the C syndrome.