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C3F (show LPCAT3 Proteins) polymorphism is associated with viral infections and protection from rejection after liver transplantation.
Pra1 (show RABAC1 Proteins) 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 (show RABAC1 Proteins) 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 (show RHO Proteins) mutant disrupts C3 secretion via the induction of ROS (show ROS1 Proteins) and the suppression of TWIST1 (show TWIST1 Proteins).
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 Proteins) Y402H with AMD (show AMD1 Proteins). We also revealed synergistic influence of CCL2 (show CCL2 Proteins)-2518 and the at-risk genotype of the C3 in AMD (show AMD1 Proteins) with an estimated AP = 50.9% (adjusted AP = 24.7%). Present findings show that CCL2 (show CCL2 Proteins)-2518 polymorphism is not an innocent bystander (show SEPT1 Proteins) in AMD (show AMD1 Proteins) 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 Proteins) (exudative-and-geographic-atrophy) in an Iranian population.
BBB disruption is present in ACS (show PLA2G15 Proteins), and elevated levels of IL-6 (show IL6 Proteins) and C3 in CSF (show CSF2 Proteins) 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 and C5a, acting through their specific receptors, C3aR (show C3AR1 Proteins), C5aR1 (show C5AR1 Proteins) and C5aR2 to direct the cellular response to inflammation.
exposure of neural stem cells to neutrophil-synthesized concentrations of C1q and C3a promoted astrogliogenesis and cell migrationtion.
complement C3 or downstream complement activation fragments may play an important role in Abeta (show APP Proteins) plaque pathology.
C5 and C5aR (show C5AR1 Proteins) have critical roles in the development of C3 glomerulopathy.
Data show that months after irradiation (IR) complement component 3 (C3-/-) mice made fewer errors than WT mice in a reversal learning test indicating better learning capacity in C3-/- mice after IR.
Time-lapse video microscopy established the localization of the complement anaphylatoxin C3a and its receptor on enteric neural crest cells during their migration in the embryonic gut (show GUSB Proteins). C3a plays a role in regulating collective and directional cell migration, and in ganglia network organization during enteric nervous system ontogenesis. It regulates cell migration in a N-cadherin (show CDH2 Proteins)-dependent process.
Retinal C3 was expressed by microglia/macrophages located in the outer retina in AMD (show AMD1 Proteins) eyes. In rodent photo-oxidative damage, C3-expressing microglia/macrophages and complement activation were located in regions of lesion expansion in the outer retina over 2 months
Demonstrate local synthesis of complement proteins by both PDGFRbeta-positive pericytes and CD45 (show PTPRC Proteins)-positive cells in kidney fibrosis.
Wild-type C57BL/6 mice with pristane-induced lupus developed a strong IFN signature, which was absent in immunoglobulin-deficient (muMT), C3(-/-) , and CD18 (show ITGB2 Proteins)(-/-) mice. In vivo phagocytosis of dead cells was impaired in C3-deficient mice.
Study found that cancer-cell-derived C3 activates the C3a receptor in the choroid plexus epithelium to disrupt the blood-cerebrospinal fluid (CSF (show CSF2 Proteins)) barrier. This effect allows plasma components, including amphiregulin (show AREG Proteins), and other mitogens to enter the CSF (show CSF2 Proteins) and promote cancer cell growth.
We induced anti-myeloperoxidase (show MPO Proteins) vasculitis in mice and confirmed a role for complement activation by demonstrating protection in C3-deficient mice.
These data indicated that alpha7-nAChR (show CHRNA7 Proteins) caused the inhibition of ASPinduced activation of p38 (show CRK Proteins) kinase and NFkappa B to inhibit the production of MCP1 (show CCL2 Proteins) and keratinocytederived chemokine (show CCL1 Proteins).
Neural crest cells are coattracted via the complement fragment C3a and its receptor C3aR (show C3AR1 Proteins), revealing an unexpected role of complement proteins in early vertebrate development.
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
, acylation stimulating protein
, complement component 3d
, complement factor 3
, complement component 3
, complement C3 alpha chain
, complement component C3d