Work with LifeSpan to design a custom immunohistochemistry to address your specific biological question. Outsource the entire localization process without having to
worry about finding and characterizing target specific antibodies, sourcing and validating difficult-to-find tissues, and having the ability to interpret the resulting
immunostaining in relation to complex human pathologies.
Test your therapeutic antibodies in immunohistochemistry against a broad panel of normal frozen human tissue types in order to determine potential unintended binding.
Our non-GLP TCR services are designed on the FDA recommendation outlined in their "Points to Consider in the Manufacture and Testing of Monoclonal Antibody Products for Human Use".
(tested or 100% immunogen sequence identity)
Protein G purified
CD55 antibody was raised against human fibroblast cell line.
Recognizes the CD55 antigen, a 70kD glycoprotein also known as Decay Accelerating Factor (DAF). Distributed on erythrocytes and other circulating blood cells and also on cells in non-hemopoietic tissue particularly epithelium and endothelium. Found specifically at the fetal-maternal interfaces in placenta. CD55 has reduced expression on individuals with paroxysmal nocturnal hemoglobinuria. Has a functional binding affinity to erythrocytes of 8.7 x 107 M-1. The antigen is pronase and trypsin resistant and chymotrypsin sensitive. Recognizes the consensus region 3 of the DAF molecule, which contains the functional site, and the antibody blocks the function of DAF.
Flow Cytometry: Use 10 ul of the suggested working dilution to label 10^6 cells in 100 ul Method sheets are available on request.
0.09% Sodium Azide
Short term: 4°C. Long term: Store at -20°C. Avoid freeze-thaw cycles.
This protein recognizes C4b and C3b fragments that condense with cell-surface hydroxyl or amino groups when nascent C4b and C3b are locally generated during C4 and c3 activation. Interaction of daf with cell-associated C4b and C3b polypeptides interferes with their ability to catalyze the conversion of C2 and factor B to enzymatically active C2a and Bb and thereby prevents the formation of C4b2a and C3bBb, the amplification convertases of the complement cascade.