MegaCD40L™, Soluble (mouse) (rec.)

  • AG-40B-0020-C01010 µg INQ
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Product Data
Synonyms ACRP30headless:CD40L; ACRP30headless:CD154; ACRP30headless:TNFSF5; ADIPOQ-CD40L
Properties
Source/Host CHO cells
Sequence Mouse CD40L (aa 115-260) is fused at the N-terminus to mouse ACRP30headless (aa 18-111) and a FLAG®-tag.
Crossreactivity Human, Mouse
Specificity Binds to human and mouse CD40.
Biological Activity Induces B cells activation (as demonstrated by dose-dependent upregulation of CD86).
MW ~35-40kDa
Purity ≥95% (SDS-PAGE)
Endotoxin Content <0.1EU/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 P27548: CD40L (mouse)
Uniprot link Q60994: ACRP30 (mouse) (precursor)

FLAG is a registered trademark of Sigma-Aldrich Co.

Product Type Protein
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. 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.
Documents
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Product Description

MegaCD40L 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. MegaCD40L has 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.

Product References

  1. T cells dampen innate immune responses through inhibition of NLRP1 and NLRP3 inflammasomes: G. Guarda, et al.; Nature 460, 269 (2009)
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