Recombinant Human CD154/CD40 Ligand/TNFSF5/TRAP protein ,C- His Tag

Recombinant Human CD154/CD40 Ligand/TNFSF5/TRAP protein ,C- His Tag

>90% as determined by SDS-PAGE

Please contact with the lab for this information.

A DNA sequence encoding the human CD40LG(Glu108-Leu261) was fused with the C-terminal His Tag

P29965

E.coli

Homo sapiens (Human)

17.05kDa

Supplied as solution form in PBS or lyophilized from PBS .

In general, proteins are provided as lyophilized powder/frozen liquid. They are shipped out with dry ice/blue ice unless customers require otherwise.

Use a manual defrost freezer and avoid repeated freeze thaw cycles.
Store at 2 to 8 °C for one week .
Store at -20 to -80 °C for twelve months from the date of receipt.

Reconstitute in sterile water for a stock solution.A copy of datasheet will be provided with the products, please refer to it for details.

CD40 ligand is also known as CD40L, CD154, TNFSF5 and T-cell antigen Gp39, is a single-pass type I I membrane protein which belongs to the TNF superfamily of molecules. CD40 ligand is expressed predominantly on activated CD4+ T lymphocytes, and also found in other types of cells, including platelets, mast cells, macrophages, basophils, NK cells, B lymphocytes, as well as non-haematopoietic cells (smooth muscle cells, endothelial cells, and epithelial cells). Although all monomeric, dimeric and trimeric forms of soluble CD40 ligand can bind to CD40, the trimeric form of soluble CD40 ligand has the most potent biological activity through oligomerization of cell surface CD40, a common feature of TNF receptor family members. CD40 ligand binds to CD40 on antigen-presenting cells (APC), which leads to many effects depending on the target cell type. In general, CD40 ligand plays the role of a costimulatory molecule and induces activation in APC in association with T cell receptor stimulation by MHC molecules on the APC. In total CD40 ligand has three binding partners: CD40, α5β1 integrin and αIIbβ3. CD40 ligand regulates B cell function by engaging CD40 on the B cell surface. A defect in this gene results in an inability to undergo immunoglobulin class switch and is associated with hyper IgM syndrome.

CD40LG,CD154,CD40L,HIGM1,IGM,IMD3,T-BAM,TNFSF5,TRAP,gp39

Miura, Yoshihisa, Misaka, Yamaki, Kojima, Toyokawa, Ogawa, Shimura, Yamamoto, Kasahara, Takeishi, Kitazume (2020) Amyloid precursor protein 770 is specifically expressed and released from platelets The Journal of biological chemistry ()

For research use only .

Platelets not only play an essential role in hemostasis after vascular injury, but are also involved in the development of coronary artery disease (CAD) and cerebrovascular lesions. Patients with CAD and cerebral ischemia are recommended to undergo antiplatelet therapy, but they have an increased incidence of major bleeding complications. Both assessment of the platelet activation status and response to antiplatelet therapy in each patient are highly desired. Amyloid β-precursor protein (APP) 770 is expressed in vascular endothelial cells, and its extracellular region, a soluble form of APP770 (sAPP770, also called nexin-2), is proteolytically cleaved for shedding. Abundant sAPP770 is also released from activated platelets. In this study, we used peripheral blood samples from patients with CAD and control subjects and evaluated sAPP770 as a specific biomarker for platelet activation. First, the plasma levels of sAPP770 correlated well with those of the soluble form CD40 ligand (CD40L), an established biomarker for platelet activation. Additionally, flow cytometry analysis using peripheral blood cells showed that CD40L expression is upregulated in activated T cells, while APP770 expression is negligible in all blood cell types except platelets. Following stimulation with collagen or ADP, aggregating platelets immediately released sAPP770. Finally, patients with dual antiplatelet therapy showed significantly lower levels of plasma sAPP770 than those with no therapy. Taken together, our data show that plasma sAPP770 could be a promising biomarker for platelet activation. Published under license by The American Society for Biochemistry and Molecular Biology, Inc.

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