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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 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 - 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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Mouse (Murine) Polyclonal C5 Primary Antibody for 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 Polyclonal C5 Primary Antibody for FACS, IHC (p) - ABIN652518
Zhang, Huang, Jing, Fu, Yuan, Xia, Cai, Gan, Chen, Zou, Long, Wang, Wang, Xu: SAK-HV Triggered a Short-period Lipid-lowering Biotherapy Based on the Energy Model of Liver Proliferation via a Novel Pathway. in Theranostics 2018
recombinant C5a potentiated TNFalpha (show TNF Antibodies)-induced NF-kappaB (show NFKB1 Antibodies) activation in renal tubular epithelial cells
tumoral C5a is an independent adverse prognostic biomarker for clinical outcome of Clear Cell Renal Cell Carcinoma (show MOK Antibodies) patients after nephectomy.
C5a synergises with P. aeruginosa LPS (show IRF6 Antibodies) in both PD-L1 (show CD274 Antibodies) expression and the production of IL-10 (show IL10 Antibodies) and TGF-beta (show TGFB1 Antibodies).
Up-regulation of granulocyte and monocyte CD11b (show ITGAM Antibodies) during plasma separation was C5-dependent.
This study provides the preclinical rationale for the combined blockade of PD-1 (show PDCD1 Antibodies)/PD-L1 (show CD274 Antibodies) and C5a to restore antitumor immune responses, inhibit tumor cell growth, and improve outcomes of patients with lung cancer
Diagnosis and therapeutic management of neonatal hemochromatosis (show HFE Antibodies) 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 (show MOK Antibodies) 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 (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.
We present evidence that mice deficient in C5aR (show C5AR1 Antibodies) or treated with AON-D21 are poor hematopoietic stem/progenitor cells mobilizers, thereby establishing a critical role for the C5a/C5adesArg-C5aR (show C5AR1 Antibodies) axis in the mobilization process.
C5 and C5aR (show C5AR1 Antibodies) have critical roles in the development of C3 glomerulopathy.
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.
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