NKG2D/CD314 Antibody (tesnatilimab) [HRP]
Novus Biologicals, part of Bio-Techne | Catalog # NBP3-28109H
Recombinant Monoclonal Antibody
Conjugate
Catalog #
Key Product Details
Species Reactivity
Human
Applications
ELISA, Flow Cytometry, Functional
Label
HRP
Antibody Source
Recombinant Monoclonal Human IgG4 Clone # tesnatilimab
Concentration
Please see the vial label for concentration. If unlisted please contact technical services.
Product Specifications
Immunogen
NKG2D / CD314
Clonality
Monoclonal
Host
Human
Isotype
IgG4
Applications for NKG2D/CD314 Antibody (tesnatilimab) [HRP]
Application
Recommended Usage
ELISA
Optimal dilutions of this antibody should be experimentally determined.
Flow Cytometry
Optimal dilutions of this antibody should be experimentally determined.
Functional
Optimal dilutions of this antibody should be experimentally determined.
Application Notes
Optimal dilution of this antibody should be experimentally determined.
Formulation, Preparation, and Storage
Purification
Protein A purified
Formulation
PBS
Preservative
No Preservative
Concentration
Please see the vial label for concentration. If unlisted please contact technical services.
Shipping
The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.
Stability & Storage
Store at 4C in the dark.
Background: NKG2D/CD314
In general, NKG2D signaling has dual functions, playing a role in both immune surveillance and immune escape (4,6). Detection of viruses or pathogens and corresponding cytokine production induces NKG2D-ligand expression on dendritic cells and macrophages as well as NKG2D receptor upregulation on NK cells to initiate an immune response (1,2,4,6). Similarly, NKG2D-ligand expression on tumor cells is upregulated in cancers such as liver cancer, ovarian cancer, colon cancer, and leukemia, and the NKG2D/NKG2D-ligand signaling axis functions in preventing progression and metastasis (1,4,6). By contrast, NKG2D signaling also mediates tumor escape through ligand shedding via proteases from the matrix metalloproteinase (MMP) and a disintegrin and metalloprotease (ADAM) families and transforming growth factor (TGF)-beta inhibition of T cell and NK cell function (4). A number of therapeutic strategies targeting the NKG2D receptor-ligand pathway have been developed for cancer immunotherapies including upregulating NKG2D expression on immune cells via soluble cytokines, modulating ligand expression with histone deacetylase (HDAC) inhibitors, or inhibiting ligand shedding molecules like ADAMs and MMPs (1,4,6). Alternatively, in instances of autoimmune diseases or inflammation, NKG2D blocking strategies are of interest (6).
References
1. Wang, J., Li, C. D., & Sun, L. (2020). Recent Advances in Molecular Mechanisms of the NKG2D Pathway in Hepatocellular Carcinoma. Biomolecules, 10(2), 301. https://doi.org/10.3390/biom10020301
2. Stojanovic, A., Correia, M. P., & Cerwenka, A. (2018). The NKG2D/NKG2DL Axis in the Crosstalk Between Lymphoid and Myeloid Cells in Health and Disease. Frontiers in immunology, 9, 827. https://doi.org/10.3389/fimmu.2018.00827
3. Wensveen, F. M., Jelencic, V., & Polic, B. (2018). NKG2D: A Master Regulator of Immune Cell Responsiveness. Frontiers in immunology, 9, 441. https://doi.org/10.3389/fimmu.2018.00441
4. Liu, H., Wang, S., Xin, J., Wang, J., Yao, C., & Zhang, Z. (2019). Role of NKG2D and its ligands in cancer immunotherapy. American journal of cancer research, 9(10), 2064-2078.
5. Uniprot (P26718)
6. Lanier L. L. (2015). NKG2D Receptor and Its Ligands in Host Defense. Cancer immunology research, 3(6), 575-582. https://doi.org/10.1158/2326-6066.CIR-15-0098
Long Name
Natural Killer G2D
Alternate Names
CD314, D12S2489E, KLRK1
Gene Symbol
KLRK1
Additional NKG2D/CD314 Products
Product Documents for NKG2D/CD314 Antibody (tesnatilimab) [HRP]
Product Specific Notices for NKG2D/CD314 Antibody (tesnatilimab) [HRP]
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.
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