Flow cytometric analysis of CD257 expression on U-937 cells. Cells from the Daudi (Human Burkitt's lymphoma lymphoblast, left) / U-937 (Human histiocytic lymphoma monocyte, right) labelling SDT Alexa Fluor® 488 Mouse Anti-Human CD257 Antibody at 5 μl/test / (red line histogram) compared with Alexa Fluor® 488 Mouse IgG2a, κ (black line histogram) isotype control. Flow cytometry and data analysis were performed using Agilent NovoCyte Quanteon and FlowJo™ software.
Negative control: Daudi
Alexa Fluor® 488 Mouse Anti-Human CD257 Antibody (S-3021)
Alexa Fluor® 488 Mouse Anti-Human CD257 Antibody (S-3021)
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Product Details
Product Details
Product Specification
| Host | Mouse |
| Antigen | CD257 |
| Synonyms | Tumor necrosis factor ligand superfamily member 13B; B lymphocyte stimulator (BLyS); B-cell-activating factor; Dendritic cell-derived TNF-like molecule; TNF- and APOL-related leukocyte expressed ligand 1 (TALL-1); BAFF; BLYS; TALL1; TNFSF20; ZTNF4; TNFSF13B |
| Location | Cell membrane |
| Accession | Q9Y275 |
| Clone Number | S-3021 |
| Antibody Type | Mouse mAb |
| Isotype | IgG2a,k |
| Isotype Control | S0B8029 |
| Application | FCM |
| Reactivity | Hu |
| Positive Sample | U-937 |
| Purification | Protein A |
| Concentration | 0.2 mg/ml |
| Conjugation | Alexa Fluor® 488 |
| Physical Appearance | Liquid |
| Storage Buffer | PBS, 1% BSA, 0.09% sodium azide |
| Stability & Storage | 12 months from date of receipt / reconstitution, 2 to 8 °C as supplied |
Dilution
| application | dilution | species |
| FCM | 5μl per million cells in 100μl volume | Hu |
Background
CD257, is a 285-aa type-II transmembrane glycoprotein of the TNF ligand superfamily produced by monocytes, dendritic cells, macrophages and activated T cells that can be cleaved to a soluble homotrimeric cytokine which, via engagement of three receptors—BAFF-R, TACI and BCMA—delivers survival and maturation signals to B cells, orchestrates T-cell co-stimulation, and drives class-switching and antibody production through NF-κB and PI3K/AKT pathways, while excess BAFF triggers B-cell hyperplasia and autoantibody formation, linking its overexpression to systemic lupus erythematosus, Sjögren syndrome, rheumatoid arthritis and multiple myeloma, and making BAFF antagonism (e.g., belimumab) a validated therapeutic strategy.
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