CD137L/4-1BBL/TNFSF9
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Introduction To CD137L/4-1BBL/TNFSF9
Drug targets a biomolecule that can directly bind to drugs and then react. Generally, the target refers to a protein, which is related to the cause of disease. The focus of the target began with focusing on tumors, and then began to spread to various fields. CD137L/4-1BBL/TNFSF9 protein is a common target in medicine.
CD137L, also known as 4-1 BBL or tumor necrosis daughter superfamily member 9 (TNFSF9), is a transmembrane protein that is mainly expressed on the surface of APCS, such as macrophages, dendritic cells, and B cells.CD137L Is a ligand for CD137, and this ligand – receptor interaction plays an important co-stimulatory role in the immune system.
Function of Target CD137L/4-1BBL/TNFSF9
CD137 on the surface of T cells would react with CD137L on APCs and then destimulate the two cells already producing the response. CD137 induced differentiation and growth of T cells and APCS with increased secretion of cytokines. CD137 preempts CD8 + T cells, preventing CD8 + T cell-induced AICD. The expression level of CD137 in cells is also affected by different TCR affinities, and the different intensity and type of stimulation can also alter CD137L expression. Signaling between the appearance of CD137 / CD137L may also mitigate the effects of T cells in producing an immune response, prevent T cell activation and proliferation, and reduce cytokine production. When CD137 is not expressed on the surface of T cells, T cells and myeloid cells will overproliferate. This may be because the signal transmitted by CD137 itself causes some kind of regulatory molecule by DCs, or possibly due to the inhibitory signal from CD137L to T cells. In addition, the costimulatory effect of CD137L contributes to the formation of long-term immune memory, which has important implications for preventing tumor recurrence and continuous control of tumor growth.
CD137 / CD137L co-stimulatory signaling is one of the main drivers of type 1 cell-mediated immune responses, involving a variety of autoimmune diseases, including systemic lupus erythematosus (SLE) rheumatoid arthritis (RA) type 1 diabetes mellitus (TID) ankylosing spondylitis.
Gene Pathway of Target CD137L/4-1BBL/TNFSF9
After CD137L binds to CD137, they aggregate TRAF proteins, such as TRAF 1 and TRAF 2, which eventually activate the NF-ᴋB signaling pathway and promote cell activation, proliferation, and survival. The binding of CD137L also activates the MAPK signaling pathway, which further enhances the effector function of T cells. Ultimately leading to IL-2 and IFN- γ secretion, and the upregulation of the anti-apoptotic molecules Bcl-xL and Bfl-1 all contribute to the protection of T cells from apoptosis.
Fig 1: CD137L Gene Pathway. (Reference documentation: Zeng Q, Zhou Y, Schwarz H. CD137L-DCs, Potent Immune-Stimulators-History, Characteristics, and Perspectives. Front Immunol. 2019 Oct 2;10:2216. )
Alpha Lifetech Can Provide
| Catalog Number | Product Name | Product Sizes |
|---|---|---|
| ALP64688 | 50ug,100ug,500ug | |
| ALP64683 | 50ug,100ug,500ug | |
| ALP64586 | 50ug,100ug,500ug | |
Reference
[1] Wu J, Wang Y, Yang Y, Liu F, Jiang Z, Jiang Z. TNFSF9 promotes metastasis of pancreatic cancer by regulating M2 polarization of macrophages through Src/FAK/p-Akt/IL-1β signaling. Int Immunopharmacol. 2022 Jan;102:108429.
[2] Zeng Q, Zhou Y, Schwarz H. CD137L-DCs, Potent Immune-Stimulators-History, Characteristics, and Perspectives. Front Immunol. 2019 Oct 2;10:2216.
[3] Wei H, Chen L, Li Q, Liang X, Wang K, Zhang Y, Li Y, Liu Y, Xu G. CD137L-macrophage induce lymphatic endothelial cells autophagy to promote lymphangiogenesis in renal fibrosis. Int J Biol Sci. 2022 Jan 1;18(3):1171-1187.
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2018-07-16
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