CD40 Ligand (CD40L) Lentivirus

Catalog #
78931
$995 *
Size: 2 x 500 µl
Qty
*US Pricing only. For international pricing, please contact your local distributor.
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Description

CD40 Ligand (CD40L) Lentivirus are replication incompetent, HIV-based, VSV-G pseudotyped lentiviral particles ready to transduce nearly all types of mammalian cells, including primary and non-dividing cells. These viruses result in expression of human CD40L (NM_000074.3) driven by an EF1a promoter, and a puromycin selection marker (Figure 1).

Figure 1. Schematic of the lenti-vector used to generate CD40 Ligand (CD40L) Lentivirus.

Synonyms
Tumor necrosis factor receptor superfamily member 5, B-cell surface antigen CD40, Bp50, CD40L receptor, CDw40, TNFRSF5
Product Info
Storage and Usage
Citations
Supplied As
Two vials (500 µl x 2) of lentivirus at a titer ≥107 TU/ml. The titer will vary with each lot; the exact value is provided with each shipment. 
Formulation

The lentivirus particles were produced in HEK293T cells in medium containing 90% DMEM + 10% FBS. Virus particles can be packaged in custom formulations by special request, for an additional fee.   

UniProt #
P25942
Background

CD40L (CD40 ligand), also known as TNFSF5 (tumor necrosis factor receptor superfamily 5) and CD154, is a type II membrane glycoprotein that exists in cells in a membrane bound (mCD40L) and a soluble (sCD40L) form. It is found at high levels in activated CD4+ T cells, and at lower levels in Th1, Th2, Th17 and Tregs. Expression can also be induced in NK cells, CD8+ T cells, basophils, and others. CD40 and CD40L are stimulatory immune checkpoints, and their signaling is mediated by different TRAF (TNF receptor associated factor), in a cell and stimuli-dependent mode. For example, it mediates the activation of the NF-κB (nuclear factor kappa-B) pathway. The role of CD40 and CD40L as immune checkpoints makes them highly attractive targets in cancer therapy, and several clinical trials using anti-CD40 or anti-CD40L agonist antibodies or trying to increase their expression are underway, targeting both hematological and solid tumors. The inhibition of CD40:CD40L interaction is also clinically relevant, and clinical trials have been focusing on treatment options for lupus, rheumatoid arthritis and ALS (amyotrophic lateral sclerosis). Further studies and development of refined therapies will continue to benefit the cancer therapy field and patients suffering from autoimmune disorders.

References

Annis A., et al., 2004 J. Amer. Chem. Soc. 126(4): 15495-15503. 
Yan, T., et al., 2001 J. Cellular Biochem. 83(2): 320-325. 
Tang T., et al., 2021 Pharmacol The 219:107709.