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Human CFP ELISA Kit for Sandwich ELISA - ABIN415275
Inoshita, Ohsawa, Kusaba, Ishii, Onda, Horikoshi, Ohi, Tomino: Complement in patients receiving maintenance hemodialysis: functional screening and quantitative analysis. in BMC nephrology 2010
studies demonstrate an essential role of properdin oligomerization in vivo while our monomers enable detailed structural insight paving the way for novel modulators of complement.
can directly interact with neutrophil myeloperoxidase (show MPO ELISA Kits) resulting in activation of alternative pathway of complement
Our data show that physiological forms of human properdin bind directly to human platelets after activation by strong agonists in the absence of C3
Factor h (show CFH ELISA Kits) and properdin recognize different epitopes on renal tubular epithelial heparan sulfate.
Properdin released from human polymorphonuclear cells does not bind to zymosan or E. coli, but when incubated in properdin-depleted serum this form of properdin binds efficiently to both substrates in a strictly complement C3 (show C3 ELISA Kits)-dependent manner.
Properdin and SC5b-9 may be novel biomarkers for future risk of type 2 diabetes in this high-risk population and warrant further investigation.
Immune human serum that contained bactericidal Abs directed against the 2C (show C4BPA ELISA Kits)7 lipooligosaccharide epitope (show C4BPA ELISA Kits)required functional properdin to kill C4BP-binding strains, but not C4BP-nonbinding strains.
report a large Finnish family with a novel mutation in the properdin gene. The mutation is located in exon 9 and changes guanine to adenine at nucleotide 1164 (c.1164G>A) that causes tryptophan to change to a premature stop codon (W388X).
tubular HS as a novel docking platform for alternative pathway activation via properdin, which might play a role in proteinuric renal damage.
levels of properdin are not associated with childhood wheezing and atopy
We induced anti-myeloperoxidase vasculitis in mice and showed that neither MASP-2- nor properdin-deficient mice were protected, suggesting that alternative pathway activation does not require properdin or the lectin pathway.
The results show that Properdin (show CFB ELISA Kits) plays a key role in allergen-induced airway inflammation and represents a potential therapeutic target for human asthma.
Authors conclude that properdin (show CFB ELISA Kits) controls the strength of immune responses by affecting humoral as well as cellular phenotypes during acute bacterial infection and ensuing inflammation.
Properdin (show CFB ELISA Kits) deficiency exacerbated renal injury in mice lacking complement factor H (show CFH ELISA Kits).
deficiency of properdin (show CFB ELISA Kits) in mice with factor H (show CFH ELISA Kits) mutation exacerbates C3 glomerulonephritis
Murine antigonococcal antiserum required functional properdin (show CFB ELISA Kits) to kill C4BP-binding strains, but not C4BP-nonbinding strains.
properdin (show CFB ELISA Kits) may be added to the list of complement proteins which influence lipid metabolism, energy storage and insulin (show INS ELISA Kits) resistance, and further support the hypothesis of a dual role of complement in adipose tissue
At the initial phase of local, zymosan-induced inflammation, properdin (show CFB ELISA Kits)-deficient and wild-type mice showed bone erosion, proteoglycan (show Vcan ELISA Kits) loss and cell infiltration.
Properdin (show CFB ELISA Kits) localizes to mast cells, has the ability to directly associate with Escherichia coli DH5alpha, and plays a significant role in the outcome of polymicrobial sepsis.
properdin (show CFB ELISA Kits) deficiency attenuates zymosan-induced shock and exacerbates LPS (show TLR4 ELISA Kits)-induced shock.
This gene encodes a plasma glycoprotein that positively regulates the alternative complement pathway of the innate immune system. This protein binds to many microbial surfaces and apoptotic cells and stabilizes the C3- and C5-convertase enzyme complexes in a feedback loop that ultimately leads to formation of the membrane attack complex and lysis of the target cell. Mutations in this gene result in two forms of properdin deficiency, which results in high susceptibility to meningococcal infections. Multiple alternatively spliced variants, encoding the same protein, have been identified.
complement factor P
, properdin P factor, complement
, properdin factor, complement
, Properdin P factor, complement