Product Details
| Alternative Name: | Apo-2L, TNFSF 10, CD253 |
| |
| Clone: | 2E5 |
| |
| Host: | Mouse |
| |
| Isotype: | IgG1 |
| |
| Immunogen: | Recombinant human soluble TRAIL (aa 95-281). |
| |
| UniProt ID: | P50591 |
| |
| GenBank ID: | U57059 |
| |
| Gene/Protein Identifier: | 8743 (Entrez GeneID) |
| |
| Species reactivity: | Human
|
| |
| Crossreactivity: | Does not cross-react with mouse TRAIL. |
| |
| Applications: | Flow Cytometry, FUNC
|
| |
| Application Notes: | Functional Application (excellent): neutralizes human TRAIL mediated killing in a concentration range of 0.5-1.5µg/ml.
Only detects the native protein. Does not work in WB, ICC, IHC or other applications where fixation is necessary. |
| |
| Purity Detail: | Protein A-affinity purified. Sterile filtered. |
| |
| Formulation: | Liquid. In PBS, pH 7.4. Contains no preservatives. |
| |
| Shipping: | Blue Ice Not Frozen |
| |
| Short Term Storage: | +4°C |
| |
| Long Term Storage: | +4°C |
| |
| Regulatory Status: | RUO - Research Use Only |
| |
Figure 1: Apoptosis induced in Jurkat T leukemia cells by
KillerTRAIL
TM (Prod. No.
ALX-201-073) is completely blocked by mouse MAb to TRAIL (human) (2E5) (Prod. No.
ALX-804-296) in a concentration range of 0.5-1.5µg/ml. Concentration of MAb 2E5 required for inhibition may vary depending of the cell type studied and the concentration of soluble recombinant human TRAIL used. The neutralizing activity of MAb 2E5 has been confirmed with various sources of soluble recombinant human TRAIL including
KillerTRAIL
TM.
Method: Jurkat cells (5x10
4) were treated with
KillerTRAIL
TM (300ng/ml) in the presence or absence of the MAb to TRAIL (human) (2E5) or a control IgG1 mouse monoclonal antibody. After 16 hours apoptosis was evaluated by forward/sideward scatter (FSC/SSC) combined with propidium iodide (PI) staining analyzed by flow cytometry."
Figure 2: MAb to TRAIL (human) (2E5) (Prod. No.
ALX-804-296) can be used to detect surface human TRAIL in transiently transfected 293T cells in flow cytometry as well on untransfected cells expressing endogenous surface TRAIL.
Method: 293T cells (10cm dishes) were transfeced with 0, 1, or 15µg plasmid coding for full length human TRAIL for 24 hours using a standard calcium phosphate transfection method. All dishes were cotransfected with 1µg plasmid coding for EGFPas a cotransfection marker. Viable cells (FSC/SSC region R1), that were GFP-positive (transfected) (FL1 region R3) were analyzed with respect to surface expression of human TRAIL. Cells were stained with MAb to TRAIL (human) (2E5) as well as with an isotype-matched control (control IgG1) at 10µg/ml. Binding of the primary MAbs is detected using RPE conjugated goat anti-mouse IgG (FL2)."
Figure: Neutralizing effect of MAb to TRAIL (human) (2E5) on TRAIL-induced apoptosis (TRAIL, Soluble (human) (recombinant) Set (Prod. No.
ALX-850-018); containing Enhancer for Ligands)."
Please mouse over
Product Literature References
Characterization of BV6-Induced Sensitization to the NK Cell Killing of Pediatric Rhabdomyosarcoma Spheroids: V. Särchen, et al.; Cells
12, 906 (2023),
Abstract;
Pediatric multicellular tumor spheroid models illustrate a therapeutic potential by combining BH3 mimetics with Natural Killer (NK) cell-based immunotherapy: V. Särchen, et al.; Cell Death Discov.
8, 11 (2022),
Abstract;
A Bak-dependent mitochondrial amplification step contributes to Smac mimetic/glucocorticoid-induced necroptosis: K. Rohde, et al.; Cell Death Differ.
24, 83 (2017),
Abstract;
Inhibition of B-Raf/MEK/ERK signaling suppresses DR5 expression and impairs response of cancer cells to DR5-mediated apoptosis and T cell-induced killing: Y.T. Oh, et al.; Oncogene
35, 459 (2016),
Application(s): Functional Studies,
Abstract;
IFN{alpha}-stimulated neutrophils and monocytes release a soluble form of TNF-related apoptosis-inducing ligand (TRAIL/Apo-2 ligand) displaying apoptotic activity on leukemic cells: C. Tecchio, et al.; Blood
103, 3837 (2004),
Abstract;
TRAIL (Apo2L) suppresses growth of primary human leukemia and myelodysplasia progenitors: M. Plasilova, et al.; Leukemia
16, 67 (2002),
Abstract;
Related Products
