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AdipoGen Life Sciences
CD40L (rat) (multimeric) (rec.)
Product Details | |
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Synonyms | MultimericCD40L™; ACRP30headless:CD40L; ACRP30headless:CD154; ACRP30headless:TNFSF5; ADIPOQ-CD40L |
Product Type | Protein |
Properties | |
Source/Host | CHO cells |
Sequence | Rat CD40L (aa 115-260) is fused at the N-terminus to mouse ACRP30headless (aa 18-111) and a FLAG®-tag. |
Crossreactivity |
Human Mouse Rat |
Specificity | Binds to rat, human and mouse CD40. |
Biological Activity | Induces B cell activation (as demonstrated by dose-dependent upregulation of CD86). |
MW | ~35-40kDa |
Purity | ≥95% (SDS-PAGE) |
Endotoxin Content | <0.02EU/μg purified protein (LAL test; Lonza). |
Concentration | 0.1mg/ml after reconstitution. |
Reconstitution | Reconstitute with 100μl sterile water. |
Formulation | Lyophilized. Contains PBS. |
Other Product Data |
Uniprot link Q9Z2V2: CD40L (rat) FLAG is a registered trademark of Sigma-Aldrich Co. |
Shipping and Handling | |
Shipping | BLUE ICE |
Short Term Storage | +4°C |
Long Term Storage | -20°C |
Handling Advice |
After reconstitution, prepare aliquots and store at -20°C. Avoid freeze/thaw cycles. Centrifuge lyophilized vial before opening and reconstitution. PBS containing at least 0.1% BSA should be used for further dilutions. |
Use/Stability |
Stable for at least 6 months after receipt when stored at -20°C. Working aliquots are stable for up to 3 months when stored at -20°C. |
Documents | |
MSDS | Download PDF |
Product Specification Sheet | |
Datasheet | Download PDF |
MultimericCD40L™ is a high activity construct in which two trimeric CD40 ligands are artificially linked via the collagen domain of ACRP30. This construct very effectively simulates the natural membrane-assisted aggregation of CD40L in vivo. It provides a simple and equally potent alternative to CD40L+enhancer combinations. MultimericCD40L™ has been shown to suppress alum-induced IL-1β release and caspase-1 activation in a dose-, CD40- and time dependent manner, without affecting BMDM (Bone marrow-derived macrophages) viability. It also effectively suppressed the inflammasome function triggered by NLRP3 activators. The secretion of caspase-1 independent inflammatory mediators has been shown to be unaltered or even enhanced.