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Human Monoclonal C5 Primary Antibody for BP, ELISA - ABIN257905
Kola, Baensch, Bautsch, Klos, Köhl: Analysis of the C5a anaphylatoxin core domain using a C5a phage library selected on differentiated U937 cells. in Molecular immunology 1999
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Human Monoclonal C5 Primary Antibody for IA, WB - ABIN2191948
Kola, Baensch, Bautsch, Hennecke, Klos, Casaretto, Köhl: Epitope mapping of a C5a neutralizing mAb using a combined approach of phage display, synthetic peptides and site-directed mutagenesis. in Immunotechnology : an international journal of immunological engineering 1997
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Human Monoclonal C5 Primary Antibody for IA - ABIN2191947
Mollnes, Brekke, Fung, Fure, Christiansen, Bergseth, Videm, Lappegård, Köhl, Lambris: Essential role of the C5a receptor in E coli-induced oxidative burst and phagocytosis revealed by a novel lepirudin-based human whole blood model of inflammation. in Blood 2002
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Human Monoclonal C5 Primary Antibody for IA, WB - ABIN2191951
Mollnes, Klos, Tschopp: Identification of a human C5 beta-chain epitope exposed in the native complement component but concealed in the SC5b-9 complex. in Scandinavian journal of immunology 1988
Human Monoclonal C5 Primary Antibody for Func, ELISA - ABIN2477815
Ades, Waldmann, Polk, Coflesky: Referral patterns and exercise response in the rehabilitation of female coronary patients aged greater than or equal to 62 years. in The American journal of cardiology 1992
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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.
C5a/C5aR pathway promotes gastric cancer pathogenesis by suppressing p21 (show CDKN1A Antibodies)/p-p21 (show CDKN1A Antibodies) expression via activation of PI3K (show PIK3CA Antibodies)/AKT (show AKT1 Antibodies) signaling.
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.
Data show the expression of a neoepitope which was exposed on complement C5 (C5) after binding to eculizumab in vivo.
data indicate that properdin enhances platelet/granulocyte aggregates (PGAs) formation via increased production of C5a, and that inhibition of properdin function has therapeutic potential to limit thromboinflammation in diseases characterized by increased PGA formation
Increased C5a expression is associated with increased inflammation in cystic fibrosis (show S100A8 Antibodies).
In an arterial thrombosis model, plasminogen activator administration increased C5a levels. Overall, these findings suggest plasmin bridges thrombosis and the immune response by liberating C5a and inducing MAC assembly.
C5 rs2269067 GG genotype confers risk for proliferative diabetic retinopathy of type 2 diabetes in Chinese Han population (associated with an elevated C5 mRNA expression and an increased IL-6 (show IL6 Antibodies) production)
In mice that lost the ability to express complement C5, there was a lower frequency of metastasis, and males no longer had a higher frequency of metastasis than females.
C5a in vitro caused activation (phosphorylation) of MAPKs and Akt (show AKT1 Antibodies) in cardiomyocytes, which required availability of both C5a receptors. These data suggest that polymicrobial sepsis causes cardiac dysfunction that appears to be linked to activation of MAPKs and Akt (show AKT1 Antibodies) in heart.
n the complex but clinically relevant DH model the local and systemic inflammatory immune response features both, C5-dependent and C5-independent characteristics. Activation of caspase-3 (show CASP3 Antibodies) in lung tissue after DH was C5-dependent whereas local inflammation in lung tissue was C5-independent.
The C5a/C5aR pathway is essential for up-regulating SphK1 (show SPHK1 Antibodies) expression through p38 MAPK (show MAPK14 Antibodies) activation in acute liver failure.in mice.
We induced anti-myeloperoxidase (show MPO Antibodies) vasculitis in bone marrow chimaeric mice and found that circulating and not bone marrow-derived C5 was required for disease
Choroidal neovascularization lesions trigger a systemic immune response, augmenting local ocular inflammation via the infiltration of IL-17 (show IL17A Antibodies)-producing gamma-delta T-cells, which are presumably recruited to the eye in a C5a-dependent manner.
Data (including data from studies in knockout mice) suggest that C5aR/C5aR (show C5AR1 Antibodies) (complement C5a/anaphylatoxin C5a Receptor) signaling pathway is involved in neurocognitive injury in uninfected pups induced by malaria in pregnancy.
Carboxypeptidase B2 (show CPB2 Antibodies) deficiency reveals that complement C5a exacerbates infection in a murine polymicrobial sepsis model.
our results suggest that the detrimental effects of C5a in this model are partly mediated through CCR5 activation downstream of C5aR1 (show C5AR1 Antibodies), which may be evaluated for potential therapeutic exploitation in ALI/ARDS.
C5a signaling increases the expression of the chemokine (show CCL1 Antibodies) monocyte chemoattractant protein-1 (show CCL2 Antibodies) in hepatic metastases of colon cancer
The protein encoded by this gene is the fifth component of complement, which plays an important role in inflammatory and cell killing processes. This protein is comprised of alpha and beta polypeptide chains that are linked by a disulfide bridge. An activation peptide, C5a, which is an anaphylatoxin that possesses potent spasmogenic and chemotactic activity, is derived from the alpha polypeptide via cleavage with a convertase. The C5b macromolecular cleavage product can form a complex with the C6 complement component, and this complex is the basis for formation of the membrane attack complex, which includes additional complement components. Mutations in this gene cause complement component 5 deficiency, a disease where patients show a propensity for severe recurrent infections. Defects in this gene have also been linked to a susceptibility to liver fibrosis and to rheumatoid arthritis.
complement component 5
, similar to complement component C5-1
, C3 and PZP-like alpha-2-macroglobulin domain-containing protein 4
, C5a anaphylatoxin
, anaphylatoxin C5a analog
, complement C5
, complement component C5
, complement C5a anaphylatoxin