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Human Monoclonal C3B Primary Antibody pour IHC (fro), WB - ABIN2477797
Hallström, Nordström, Tan, Manolov, Lambris, Isenman, Zipfel, Blom, Riesbeck: Immune evasion of Moraxella catarrhalis involves ubiquitous surface protein A-dependent C3d binding. dans Journal of immunology (Baltimore, Md. : 1950) 2011
Evasion of C3b deposition at division septa and lateral amplification underneath the capsule requires localization of the FH-binding protein PspC at division sites.
Clinical Manifestation of Patients With Atypical Hemolytic Uremic Syndrome With the C3 p.I1157T Variation in the Kinki Region of Japan.
In our meta-analysis, C3 genetic polymorphisms unveiled a positive effect on the risk of advanced age-related macular degeneration, especially in Caucasians
Case Report: recurrent proliferative glomerulonephritis with persistent isolated C3 deposition.
A phage Ab against C3b that inhibited the alternative complement pathway, but not the classical pathway, was described in 2009. Studies using this Ab in a variety of assays have now demonstrated that it acts primarily by inhibiting tickover, thereby confirming that tickover really exists.
Anti-HLA class I and class II C3d-binding donor-specific antibodies carried a twofold and 1.5-fold increased risk of kidney graft loss, respectively.
Study shows no significant association of the C3 gene with uveitis, suggesting C3 confers either no or limited risk for uveitis susceptibility.
Here we have shown for the first time, that ligand- or insulin-mediated activation of PPARgamma in human hepatoma cell line HepG2 causes the downregulation of C3 gene expression and protein secretion
Single Nucleotide Polymorphism rs11569514 in C3 and haplotypes of C3 variants were associated with schizophrenia in a Han Chinese population.
alphaXbeta2 uses the alphaX alphaI domain to bind iC3b on its C3c moiety at one of two sites.
findings revealed a significant association between variant p.R102G in complement component C3 gene with exudative age-related macular degeneration in the Tunisian population
SNPs within the complement genes may contribute to IA, the first step to type 1 diabetes, with at least one SNP in C3 significantly associated with clinically diagnosed type 1 diabetes.
An increase in serum C4, as well as a decrease in C3, was an important outcome determinant for patients with immunoglobulin A nephropathy.
rituximab was not effective in few cases of complement-mediated C3 glomerulonephritis and dense deposit disease . Despite promising results in immunoglobulin-associated and idiopathic Membranoproliferative glomerulonephritis, current evidence on this treatment remains weak, and controlled and prospective data are urgently needed.
C3F polymorphism is associated with viral infections and protection from rejection after liver transplantation.
Pra1 targets C3 by cleaving C3 at a unique site. This inhibited effector function of the activation fragments. The newly formed C3a-like peptide lacked the C-terminal arginine residue needed for C3a-receptor binding and activation. Pra1 also bound to C3a and C3b generated by human convertases and blocked their effector functions, C3a binding to human C3a receptor, C3 antifungal activity, and C3b deposition.
data provide the first evidence that T17M rhodopsin mutant disrupts C3 secretion via the induction of ROS and the suppression of TWIST1.
The complement activation factors Bb, C3a, C5a, and MAC were increased significantly in early-onset severe pre-eclampsia (EOSPE) (all P<.01) and late-onset severe pre-eclampsia (LOSPE). (P value: .027, <.001, .001, and <.001, respectively) compared with E/L-control. C1q and C4d were increased significantly in LOSPE (P value: .003 and .014, respectively) compared with L-control.
High C3 was significantly associated with incidence of diabetes after risk factor adjustments
This study enclosed strong synergistic association of risk genotypes of C3 and CFH Y402H with AMD. We also revealed synergistic influence of CCL2-2518 and the at-risk genotype of the C3 in AMD with an estimated AP = 50.9% (adjusted AP = 24.7%). Present findings show that CCL2-2518 polymorphism is not an innocent bystander in AMD susceptibility when combined with the at-risk genotype of C3 (R102G).
Complement component C3 plays a central role in the activation of complement system. Its activation is required for both classical and alternative complement activation pathways. People with C3 deficiency are susceptible to bacterial infection.
C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1
, C3a anaphylatoxin
, acylation-stimulating protein cleavage product
, complement C3
, complement component C3
, complement component C3a
, complement component C3b