Transfected Stable Cell Lines
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Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
Cat.No. | Product Name | Price |
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CLOE-1582 | Human CD40LG HEK293 Cell Lysate | Inquiry |
CLOE-2089 | Rat Cd40lg (Fc) HEK293 Cell Lysate | Inquiry |
CLOE-2758 | Mouse Cd40lg (Fc) HEK293 Cell Lysate | Inquiry |
CSC-DC002751 | Panoply™ Human CD40LG Knockdown Stable Cell Line | Inquiry |
CSC-RO0090 | Human CD40LG Stable Cell Line-HEK293T | Inquiry |
CSC-RO01395 | Mouse Cd40lg Stable Cell Line - NIH/3T3 | Inquiry |
CSC-RO0500 | Monkey CD40LG Stable Cell Line - CHO-K1 | Inquiry |
CSC-RO0508 | Human CD40LG Stable Cell Line - CHO-K1 | Inquiry |
CSC-RO0555 | Monkey CD40LG Stable Cell Line - HEK293T | Inquiry |
CSC-RO0592 | Mouse Cd40lg Stable Cell Line - NIH_3T3 | Inquiry |
CSC-SC002751 | Panoply™ Human CD40LG Over-expressing Stable Cell Line | Inquiry |
Cat.No. | Product Name | Price |
---|---|---|
CLOE-1582 | Human CD40LG HEK293 Cell Lysate | Inquiry |
CLOE-2089 | Rat Cd40lg (Fc) HEK293 Cell Lysate | Inquiry |
CLOE-2758 | Mouse Cd40lg (Fc) HEK293 Cell Lysate | Inquiry |
CSC-DC002751 | Panoply™ Human CD40LG Knockdown Stable Cell Line | Inquiry |
CSC-RO0090 | Human CD40LG Stable Cell Line-HEK293T | Inquiry |
CSC-RO01395 | Mouse Cd40lg Stable Cell Line - NIH/3T3 | Inquiry |
CSC-RO0500 | Monkey CD40LG Stable Cell Line - CHO-K1 | Inquiry |
CSC-RO0508 | Human CD40LG Stable Cell Line - CHO-K1 | Inquiry |
CSC-RO0555 | Monkey CD40LG Stable Cell Line - HEK293T | Inquiry |
CSC-RO0592 | Mouse Cd40lg Stable Cell Line - NIH_3T3 | Inquiry |
CSC-SC002751 | Panoply™ Human CD40LG Over-expressing Stable Cell Line | Inquiry |
Cat.No. | Product Name | Price |
---|---|---|
CLOE-1582 | Human CD40LG HEK293 Cell Lysate | Inquiry |
CLOE-2089 | Rat Cd40lg (Fc) HEK293 Cell Lysate | Inquiry |
CLOE-2758 | Mouse Cd40lg (Fc) HEK293 Cell Lysate | Inquiry |
CSC-DC002751 | Panoply™ Human CD40LG Knockdown Stable Cell Line | Inquiry |
CSC-RO0090 | Human CD40LG Stable Cell Line-HEK293T | Inquiry |
CSC-RO01395 | Mouse Cd40lg Stable Cell Line - NIH/3T3 | Inquiry |
CSC-RO0500 | Monkey CD40LG Stable Cell Line - CHO-K1 | Inquiry |
CSC-RO0508 | Human CD40LG Stable Cell Line - CHO-K1 | Inquiry |
CSC-RO0555 | Monkey CD40LG Stable Cell Line - HEK293T | Inquiry |
CSC-RO0592 | Mouse Cd40lg Stable Cell Line - NIH_3T3 | Inquiry |
CSC-SC002751 | Panoply™ Human CD40LG Over-expressing Stable Cell Line | Inquiry |
Cat.No. | Product Name | Price |
---|---|---|
CLOE-1582 | Human CD40LG HEK293 Cell Lysate | Inquiry |
CLOE-2089 | Rat Cd40lg (Fc) HEK293 Cell Lysate | Inquiry |
CLOE-2758 | Mouse Cd40lg (Fc) HEK293 Cell Lysate | Inquiry |
CSC-DC002751 | Panoply™ Human CD40LG Knockdown Stable Cell Line | Inquiry |
CSC-RO0090 | Human CD40LG Stable Cell Line-HEK293T | Inquiry |
CSC-RO01395 | Mouse Cd40lg Stable Cell Line - NIH/3T3 | Inquiry |
CSC-RO0500 | Monkey CD40LG Stable Cell Line - CHO-K1 | Inquiry |
CSC-RO0508 | Human CD40LG Stable Cell Line - CHO-K1 | Inquiry |
CSC-RO0555 | Monkey CD40LG Stable Cell Line - HEK293T | Inquiry |
CSC-RO0592 | Mouse Cd40lg Stable Cell Line - NIH_3T3 | Inquiry |
CSC-SC002751 | Panoply™ Human CD40LG Over-expressing Stable Cell Line | Inquiry |
Cat.No. | Product Name | Price |
---|---|---|
CLOE-1582 | Human CD40LG HEK293 Cell Lysate | Inquiry |
CLOE-2089 | Rat Cd40lg (Fc) HEK293 Cell Lysate | Inquiry |
CLOE-2758 | Mouse Cd40lg (Fc) HEK293 Cell Lysate | Inquiry |
CSC-DC002751 | Panoply™ Human CD40LG Knockdown Stable Cell Line | Inquiry |
CSC-RO0090 | Human CD40LG Stable Cell Line-HEK293T | Inquiry |
CSC-RO01395 | Mouse Cd40lg Stable Cell Line - NIH/3T3 | Inquiry |
CSC-RO0500 | Monkey CD40LG Stable Cell Line - CHO-K1 | Inquiry |
CSC-RO0508 | Human CD40LG Stable Cell Line - CHO-K1 | Inquiry |
CSC-RO0555 | Monkey CD40LG Stable Cell Line - HEK293T | Inquiry |
CSC-RO0592 | Mouse Cd40lg Stable Cell Line - NIH_3T3 | Inquiry |
CSC-SC002751 | Panoply™ Human CD40LG Over-expressing Stable Cell Line | Inquiry |
The CD40LG gene, encoding CD40 ligand (CD40L), plays a critical role in the immune system. Mostly generated on activated CD4+ T cells, it functions as a ligand for the CD40 receptor shown on the surface of B cells and antigen-presenting cells (APCs). Especially in B cell activation, immunoglobulin class flipping, and the development of adaptive immunity, the interplay between CD40L and CD40 determines the modulation of immunological responses.
A protein-coding gene, CD40LG generates a 39 kDa transmembrane protein. Usually existing in a trimeric form, CD40L is a member of the tumor necrosis factor (TNF) superfamily. It is crucial in humoral and cellular immunological responses. In T cells, CD40L modulates costimulation, therefore improving T-cell proliferation and cytokine synthesis—including IL-4 and IL-10—in concert with TCR/CD3 ligation and CD28 costimulation. Along with activating kinases like MAPK8 and PAK2 in T-cells, this activation triggers the NF-kB signaling cascade.
CD40L binds to CD40 in the presence of IL-4 to provide signals that set off several immunological reactions including IgE synthesis and B-cell growth. This link also underlies immunoglobulin class switching, a technique enabling B cells to produce various types of antibodies fit for combat of various illnesses.
Activation of immune cells depends critically on the CD40L-CD40 interaction. On B cells and APCs, CD40L binding to CD40 attracts TNF receptor-associated factors (TRAFs), therefore activating many intracellular signaling pathways. This controls immune cell development, differentiation, and survival using NF-kB, MAPK, PI3K-AKT, and JAK3-STAT signaling cascade. CD40L-CD40 signaling affects endothelial, smooth muscle, and fibroblast cells, thus influencing cell adhesion, inflammation, and vascular homeostasis.
Defects or mutations in the CD40LG gene could lead to Hyper-IgM syndrome, an immunodeficiency disorder defined by the inability to complete immunoglobulin class switching. Because their levels of IgM are high and their other immunoglobulin classes are low, affected individuals are consequently more prone to infections. A decreased adaptive immunological response resulting from CD40L loss follows from reduced T-cell activation and B-cell dysfunction.
Figure 1. The targeting of CD40/CD40L pathway: CD40/CD40L checkpoint molecules processing and interaction. (Tang T, et al., 2021)
Apart from Hyper-IgM syndrome, mutations in CD40LG have also been related to various immunological defects, including CD40L deficiency, which may lead to numerous autoimmune and inflammatory diseases. Active CD40L-CD40 pathway activation has been related, for example, to the pathophysiology of autoimmune diseases like rheumatoid arthritis, Crohn's disease, and systemic lupus erythematosus (SLE).
CD40L and CD40 have become interesting targets for treatments in both cancer immunotherapy and autoimmune illnesses because of their essential importance in immune regulation.
In cancer therapy, CD40L agonists under research are meant to boost anti-tumor immunity. Turning on CD40 on APCs helps CD40L agonists enhance the presentation of tumor antigens and increase T-cell responses to tumors. Treatments based on CD40L aim to generate a pro-inflammatory immune response that accelerates cancer cell destruction.
Although encouraging, CD40L agonists have to be carefully balanced against negative effects, especially since the CD40-CD40L interaction may cause inflammatory reactions. Though no such medication has been licensed, research points to CD40-targeted cancer immunotherapy as a possible use.
Under investigation as treatments for autoimmune diseases and conditions needing immune suppression are CD40L antagonists. Overactive CD40L-CD40 signaling has been linked to diseases like psoriasis, rheumatoid arthritis, and SLE. Through its blockage of the CD40-CD40L interaction, CD40L antagonists aim to reduce the overactive immune response linked with certain illnesses.
Early clinical findings suggest their possible usefulness in treating disorders including organ transplantation, systemic lupus erythematosus (SLE), and other autoimmune diseases; monoclonal antibodies targeted against CD40L are under continued investigation.
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