Mouse CD40 Ligand / TNFSF5 Protein, His Tag (active trimer) (MALS verified)

Source : 

Mouse CD40 Ligand, His Tag (active trimer) (MALS verified) (CDL-M5248) is expressed from human 293 cells (HEK293). It contains AA Gly 115 - Leu 260 (Accession # P27548-1).

 

Molecule : CD40 Ligand

 

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

 

Format : Powder

 

Category : Immune Checkpoint Proteins

 

Accession : N/A

 

Storage : -20℃

 

Shipping condition : Powder,RT

 

Molecular Weight : 16.8 kDa

 

Characteristics :

This protein carries a polyhistidine tag at the N-terminus. The protein has a calculated MW of 16.8 kDa. The protein migrates as 21-25 kDa under reducing (R) condition (SDS-PAGE).

 

Endotoxin Level : Less than 1.0 EU per μg by the LAL method.

 

Buffer : PBS, pH7.4

 

Description :

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.

 

References :

(1) Schönbeck U, Libby P, 2001, Cell. Mol. Life Sci. 58 (1): 4–43.
(2) Furman M.I. et al., 2004, J. Am. Coll. Cardiol. 43: 2319-25.
(3) Spriggs, M.K. et al., 1992, J. Exp. Med. 176:1543.
(4) Fanslow, W.C. et al., 1994, Seminars in Immunology 6:267.