iLite C5a Assay Ready Cells

$1,555.00

The iLite® C5a Assay Ready Cells can be used for the quantification of C5a activity, and for determination of inhibitory activity against either C5a itself or against the C5a receptor in test samples, including human serum. The Eagle Biosciences iLite® C5a Assay Ready Cells are for research use only.

iLite C5a Assay Ready Cells

iLite C5a Assay Ready Cells are Developed and Manufactured by Svar Life Science

The Eagle Biosciences iLite C5a Assay Ready Cells are intended for:

    • Quantification of C5a activity
    • Determination of inhibitory activity against either C5a itself or against the C5a receptor in test samples

Content: 250 µL of Assay Ready Cells suspended in cryoprotective medium from Gibco
Receipt and Storage: Upon receipt confirm that adequate dry-ice is present, and the cells are frozen. Immediately transfer to -80°C storage. Cells should be stored at -80°C (do not store at any other temperature) and are stable as supplied until the expiry date shown. Cells should be used within 30 min of thawing and should be diluted immediately after thawing.
For Research Use Only


Key benefits of iLite Assays

  • Highly specific reporter gene cell lines
  • Very sensitive cell line responses (10 fold inductions)
  • Assay Ready Cells – ready-to-use from the freezer, without culturing of cells
  • Assays within a workday (typically 4-7 hour assays)
  • Normalization gene, which eliminates unwanted matrix effects

Product Description

iLite C5a Assay Ready Cells are human HEK293[1] cells (ATCC# CRL-1573) which have been genetically engineered and optimized to be responsive to human complement component 5a (C5a), resulting in a proportional expression of Firefly Luciferase. Normalization of cell counts, and serum matrix effects is obtained by a second reporter gene, a Renilla Luciferase reporter gene construct, under control of a constitutive promotor.

[1] The HEK-293 cell line has been used under a license obtained from AdVec Inc.


Related Products

Complement C4d ELISA Assay Kit
Terminal Complement Complex (TCC) ELISA Assay Kit

Additional Information

Background


C5a is a 74 amino acid small protein fragment of complement protein 5 (C5). C5 is cleaved to C5a and C5b by C5 convertase enzymes as a result of complement activation. Factors of the coagulation and fibrinolytic pathway are also able to cleave C5 to C5a. (1) C5a is a highly potent anaphylatoxin and chemoattracting peptide, with the ability to increase blood vessel permeability, stimulatation of cytokine release from myeloid cells, and expression of adhesion molecules on endothelial cells. (2)
Main pro-inflammatory effector functions are induced by C5a binding to a seven-transmembrane G-protein-coupled receptor, C5aR1 (CD88). Rapidly after cleavage of C5 into C5a and C5b, C5a is metabolized by carboxypeptidases which removes the C-terminal arginine and forms C5a-desArg, a less potent ligand of C5aR1. C5a can also bind to a second receptor, C5aR2 (C5L2 or GPR77), however the biological effects associated with C5a binding C5aR2 are less well understood, both anti-inflammatory and pro-inflammatory effects have been described in literature. The C5a receptors are expressed in a wide range of cells and tissues, and the effect of C5a activation is dependent on the location of the C5a receptors. (3, 4)
While the complement system is an important part of the innate immune defense against pathogens, research has shown that excessive complement activation including C5a-C5aR interaction plays a central role in several autoimmune and neurodegenerative disorders as well as in acute and chronic inflammatory conditions. Given the strong evidence of a pathogenic role for C5a-C5aR in many disorders both ligand and receptor are promising therapeutic targets. Clinical studies of pharmacologic candidates inhibiting C5a and C5aR1 are ongoing. (2,3,5)

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Please note: All documents above are for reference use only and should not be used in place of the documents included with this physical product. If digital copies are needed, please contact us.

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