- Tel: 858.663.9055
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Email: info@nsjbio.com
- Tel: 858.663.9055
- Email: info@nsjbio.com
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Properdin antibody recognizes Complement factor properdin, also called Complement Factor P, a secreted plasma glycoprotein encoded by the CFP gene located on chromosome Xp11.4. Properdin is the only known positive regulator of the complement system and plays an essential role in stabilizing the alternative pathway C3 and C5 convertases. By extending the half-life of these convertases, properdin promotes complement activation, pathogen opsonization, and membrane attack complex formation. It is produced primarily by neutrophils, monocytes, dendritic cells, and selected T cell subsets, and can also be detected in serum, extracellular fluids, and complement-rich microenvironments. Properdin exists in plasma as cyclic dimers, trimers, and tetramers, with functional oligomerization contributing to its ability to initiate and amplify complement activation.
Properdin participates in several pathways that bridge innate and adaptive immune responses. Through its convertase-stabilizing functions, it enhances clearance of bacteria, apoptotic cells, and immune complexes. Properdin can also bind directly to microbial surfaces, damaged host tissues, and selected glycosaminoglycans, allowing it to act as a pattern-recognition molecule. This direct surface binding supports complement activation even in the absence of antibodies. Properdin further influences inflammatory signaling by regulating complement-derived anaphylatoxins, shaping leukocyte recruitment, and contributing to cytokine-driven immune responses. It often co-localizes with components of the alternative pathway, including Factor B and Factor D, within immune synapses and inflammation-associated extracellular matrices.
Deficiency or dysfunction of properdin is associated with heightened susceptibility to severe bacterial infections, particularly meningococcal disease. Properdin deficiency is inherited in an X-linked pattern and is characterized by impaired complement amplification, reduced opsonization efficiency, and diminished terminal pathway activation. In contrast, excessive or misdirected properdin activity contributes to inflammatory and complement-mediated tissue injury. Elevated properdin levels have been found in conditions including sepsis, autoimmune disease, chronic inflammatory disorders, and complement-driven renal diseases such as atypical hemolytic uremic syndrome. Properdin also participates in interactions between complement and coagulation pathways, linking innate immunity with thromboinflammatory responses.
At the subcellular level, properdin is stored in neutrophil secondary granules and released upon activation, where it co-localizes with other complement-regulating components. Monocytes and dendritic cells secrete properdin in response to inflammatory cues, contributing to localized complement activation within tissues. Developmentally, properdin expression increases as innate immune competence matures, becoming more prominent in childhood as complement function reaches full activity. Isoform diversity and glycosylation patterns can influence secretion, stability, and surface binding properties, contributing to its context-dependent biological effects.
This Properdin antibody is suitable for detecting Complement factor properdin in research addressing complement activation, innate immunity, inflammatory responses, host-pathogen interactions, and complement-mediated disease models. It supports studies examining alternative pathway regulation, immune cell activation, and complement involvement in tissue injury. NSJ Bioreagents provides this reagent within its immunology and complement biology antibody portfolio.
Optimal dilution of the Properdin antibody should be determined by the researcher.
Amino acids MVEGQGEKNVTFWGRPLPRCEELQGQKLVVEEKR were used as the immunogen for the Properdin antibody.
After reconstitution, the Properdin antibody can be stored for up to one month at 4oC. For long-term, aliquot and store at -20oC. Avoid repeated freezing and thawing.
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