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Human Monoclonal C5 Primary Antibody für 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 für 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 für 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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Mouse (Murine) Polyclonal C5 Primary Antibody für IF (p), IHC (p) - ABIN727875
Miyabe, Miyabe, Murooka, Kim, Newton, Kim, Haribabu, Luscinskas, Mempel, Luster: Complement C5a Receptor is the Key Initiator of Neutrophil Adhesion Igniting Immune Complex-induced Arthritis. in Science immunology 2017
Human Monoclonal C5 Primary Antibody für 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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Human Monoclonal C5 Primary Antibody für 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
Diagnosis and therapeutic management of neonatal hemochromatosis (zeige HFE Antikörper) cannot only be based on C5b9 expression in liver samples as it is not specific of this disease.
C5a-C5aR enriched clear cell renal cell carcinoma (zeige MOK Antikörper) patients significantly had a poorer overall survival and recurrence free survival after nephrectomy.
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 (zeige CDKN1A Antikörper)/p-p21 (zeige CDKN1A Antikörper) expression via activation of PI3K (zeige PIK3CA Antikörper)/AKT (zeige AKT1 Antikörper) signaling.
Studies indicate that the complement response lie the active fragments, C3a (zeige C3 Antikörper) and C5a, acting through their specific receptors, C3aR (zeige C3AR1 Antikörper), C5aR1 (zeige C5AR1 Antikörper) 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 (zeige S100A8 Antikörper).
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 (zeige AKT1 Antikörper) 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 (zeige AKT1 Antikörper) 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 (zeige CASP3 Antikörper) 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 (zeige SPHK1 Antikörper) expression through p38 MAPK (zeige MAPK14 Antikörper) activation in acute liver failure.in mice.
We induced anti-myeloperoxidase (zeige MPO Antikörper) 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 (zeige IL17A Antikörper)-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 (zeige C5AR1 Antikörper) (complement C5a/anaphylatoxin C5a Receptor) signaling pathway is involved in neurocognitive injury in uninfected pups induced by malaria in pregnancy.
Carboxypeptidase B2 (zeige CPB2 Antikörper) 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 (zeige C5AR1 Antikörper), which may be evaluated for potential therapeutic exploitation in ALI/ARDS.
C5a signaling increases the expression of the chemokine (zeige CCL1 Antikörper) monocyte chemoattractant protein-1 (zeige CCL2 Antikörper) 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