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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
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 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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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
Aspergillus fumigatus conidial metalloprotease Mep1p cleaves host major complement components C3, C4, and C5.
Furthermore, Apigenin reduced the proliferation of human NPC cells triggered by C5a through negative regulation of C5aR/PCAF/STAT3 axis. These might provide a new insight into the function of Apigenin in cancer treatment, and also provide a potential strategy for treating human NPC through inhibition of C5aR expression on cancer cells
Study identified that peripheral mRNA expression levels of two complement genes (C5, SERPING1) made unique contributions to the variance in superior frontal cortical thickness. Vertex-wise maps of the association between gene expression levels and thickness across the cortex suggested that this relationship was especially strong with SERPING1 in the superior frontal region.
these data demonstrate that Mesenchymal Stem Cells inhibit the activation of pathogenic C5 via up-regulation of FH, which improves our understanding of the immunomodulatory mechanisms of MSCs in the treatment of lupus nephritis.
recombinant C5a potentiated TNFalpha-induced NF-kappaB activation in renal tubular epithelial cells
tumoral C5a is an independent adverse prognostic biomarker for clinical outcome of Clear Cell Renal Cell Carcinoma patients after nephectomy.
C5a synergises with P. aeruginosa LPS in both PD-L1 expression and the production of IL-10 and TGF-beta.
these results not only confirm the critical role of C5b-9 in complement-mediated hemolysis and but also highlight the critical role of C5b-9 in inflammasome activation.
Mean cerebrospinal fluid C5 levels increased in patients with depression and schizophrenia.
elevated in the cerebrospinal fluid of preterm newborns
Up-regulation of granulocyte and monocyte CD11b during plasma separation was C5-dependent.
This study provides the preclinical rationale for the combined blockade of PD-1/PD-L1 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 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 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/p-p21 expression via activation of PI3K/AKT signaling.
this study shows that C5 acts in the control of serum triglycerides and cholesterol, liver cholesterol deposition, liver homeostasis and C5 promotes a pro-inflammatory liver environment in our mouse model of alcoholic liver disease
a library of 61 peptides based on the C-terminus of C5a was assayed for the ability to selectively modulate C5aR2 function.
Studies indicate that the complement response lie the active fragments, C3a and C5a, acting through their specific receptors, C3aR, C5aR1 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.
Complement C5 but not C3 is expendable for tissue factor activation by cofactor-independent antiphospholipid antibodies.
We present evidence that mice deficient in C5aR or treated with AON-D21 are poor hematopoietic stem/progenitor cells mobilizers, thereby establishing a critical role for the C5a/C5adesArg-C5aR axis in the mobilization process.
C5 and C5aR 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.
C5 contributes effectively to liver steatosis and inflammation in non-alcoholic fatty liver disease pathogenesis
C5a in vitro caused activation (phosphorylation) of MAPKs and Akt 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 in heart.
data suggest a novel role for the anaphylatoxin C5a as a master switch of the delicate pHi balance in neutrophils resulting in profound inflammatory and metabolic changes that contribute to hyperlactatemia during sepsis.
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 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 expression through p38 MAPK activation in acute liver failure.in mice.
We induced anti-myeloperoxidase 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-producing gamma-delta T-cells, which are presumably recruited to the eye in a C5a-dependent manner.
Identify complement 5a as the major C3 activation product that was involved in macrophage polarization and DOCA-salt-induced vascular injury.
Data (including data from studies in knockout mice) suggest that C5aR/C5aR (complement C5a/anaphylatoxin C5a Receptor) signaling pathway is involved in neurocognitive injury in uninfected pups induced by malaria in pregnancy.
Carboxypeptidase B2 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, which may be evaluated for potential therapeutic exploitation in ALI/ARDS.
In mice, loss of C5 or injection of a C5a-receptor antagonist significantly reduced the level of fibrosis of chronic pancreatitis.
C5a signaling increases the expression of the chemokine monocyte chemoattractant protein-1 in hepatic metastases of colon cancer
Properdin provides protection from Citrobacter rodentium-induced intestinal inflammation in a C5a/IL-6-dependent manner.
C5a produced during lung injury binds to C5aR in alveolar macrophages, initiates downstream signaling that promotes autophagy.
Loss of C5a is associated with atherosclerotic plaques.
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