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Human Monoclonal C3B Primary Antibody for 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. in Journal of immunology (Baltimore, Md. : 1950) 2011
Pra1 (show RABAC1 Antibodies) targets C3 by cleaving C3 at a unique site. This inhibited effector function of the activation fragments. The newly formed C3a (show C3 Antibodies)-like peptide lacked the C-terminal arginine residue needed for C3a (show C3 Antibodies)-receptor binding and activation. Pra1 (show RABAC1 Antibodies) also bound to C3a (show C3 Antibodies) and C3b generated by human convertases and blocked their effector functions, C3a (show C3 Antibodies) binding to human C3a (show C3 Antibodies) receptor, C3 antifungal activity, and C3b deposition.
data provide the first evidence that T17M rhodopsin (show RHO Antibodies) mutant disrupts C3 secretion via the induction of ROS (show ROS1 Antibodies) and the suppression of TWIST1 (show TWIST1 Antibodies).
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.
This study enclosed strong synergistic association of risk genotypes of C3 and CFH (show CFH Antibodies) Y402H with AMD (show AMD1 Antibodies). We also revealed synergistic influence of CCL2 (show CCL2 Antibodies)-2518 and the at-risk genotype of the C3 in AMD (show AMD1 Antibodies) with an estimated AP = 50.9% (adjusted AP = 24.7%). Present findings show that CCL2 (show CCL2 Antibodies)-2518 polymorphism is not an innocent bystander (show SEPT1 Antibodies) in AMD (show AMD1 Antibodies) susceptibility when combined with the at-risk genotype of C3 (R102G).
Our study shows C3 to be a relatively strong susceptibility gene for advanced-type-AMD (show AMD1 Antibodies) (exudative-and-geographic-atrophy) in an Iranian population.
BBB (show ALMS1 Antibodies) disruption is present in ACS (show PLA2G15 Antibodies), and elevated levels of IL-6 (show IL6 Antibodies) and C3 in CSF (show CSF2 Antibodies) in diffuse NPSLE
This study uncovers the origin of the effect of ionic strength on C3d-CR2 interaction and deepens the understanding of the molecular mechanism of their interaction, which is valuable for the design of vaccines and small molecule inhibitors.
Studies indicate that the complement response lie the active fragments, C3a (show C3 Antibodies) and C5a, acting through their specific receptors, C3aR (show C3AR1 Antibodies), C5aR1 (show C5AR1 Antibodies) and C5aR2 to direct the cellular response to inflammation.
exposure of neural stem cells to neutrophil-synthesized concentrations of C1q and C3a (show C3 Antibodies) promoted astrogliogenesis and cell migrationtion.
THP (show UMOD Antibodies) appears to participate directly in complement inactivation by its ability to act as a cofactor for C3b degradation.
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