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Cleavage of C5 requires complement fragment C3b which binds C5 and renders it susceptible to cleavage by the C4b,2a complex. Includes former EC 3.4.21.44. Complement component C2a is in peptidase family S1 (trypsin family). Links to other databases: BRENDA, EXPASY, KEGG, MEROPS, Metacyc, PDB, CAS registry number: 56626-15-4. References 1. Kerr, M.A. The second component of human complement. Methods Enzymol. 80 (1980) 54-64. [PMID: 7043188]. 2. Müller-Eberhard, H.J. Molecular organization and function of the complement system. Annu. Rev. Biochem. 57 (1988) 321-347. [PMID: 3052276]. ...
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TY - JOUR. T1 - Transcriptional transactivation functions localized to the glucocorticoid receptor N terminus are necessary for steroid induction of lymphocyte apoptosis. AU - Dieken, E. S.. AU - Miesfeld, R. L.. PY - 1992/1/1. Y1 - 1992/1/1. N2 - Genetic studies have suggested that transcriptional regulation of specific target genes (by either induction or repression) is the molecular basis of glucocorticoid-mediated lymphocyte apoptosis. To examine the role of transcriptional regulation more directly, we developed a complementation assay utilizing stable transfection of wild-type (wt) and mutant (nt(i)) glucocorticoid receptor (GR) cDNA constructs into a GR-deficient S49 murine cell line (7r). Our data confirm that the level of functional GR is rate limiting for S49 apoptosis and moreover that the GR amino terminus (N terminus), which has been deleted from the nt(i) GR, is absolutely required for complementation in this system. Surprisingly, we found that at physiological levels of receptor, ...
In severe preeclampsia, heightened activation of downstream complement protein C5 leads to excess generation of C5a and C5b-9.13-16 C5a propagates a potent proinflammatory response,13,24-26 whereas C5b-9 incorporates into cell membranes, including villous trophoblast,27 and contributes to platelet activation, procoagulant effects, and lytic cell death.28-31 In addition, C5a stimulates monocytes to release soluble fms-like tyrosine kinase 1,32 which sequesters vascular endothelial growth factor and PlGF, contributing to hypertension and glomerular endotheliosis.33,34. Our results introduce the novel finding that complement activation products C3a, C5a, and C5b-9 are excreted in urine in association with severe preeclampsia. Although urinary excretion of C3a, C5a, and C5b-9 was exaggerated in cases with severe preeclampsia compared with healthy controls, excretion of C5b-9 distinguished most clearly between severe preeclampsia and chronic hypertension. As a biomarker of disease, urinary C5b-9 was ...
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This Standard of the American Society for Testing and Materials is issued under the fixed designation D 2427; the number immediately following the designation indicates the year of original adoption or, in the case of revision, the year of last revision. A number in parentheses indicates the year of last reapproval. ...
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We prospectively studied 14 consecutive septic shock patients with a pulmonary artery catheter in place. For 3 days after admission, hemodynamic variables, and plasma levels of lactate, thrombin-antithrombin complexes (TAT), tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI) and plasmin-α2-antiplasmin complexes and TNFα, IL-6 and complement activation product C3a were measured 6-hourly. ...
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The putative role of the N-terminal region of rhodopsin-like 7 transmembrane biogenic amine receptors in agonist-induced signaling has not yet been clarified despite recent advances in 7 transmembrane receptor structural biology. Given the existence of N-terminal nonsynonymous polymorphisms (R6G;E42G) within the HTR2B gene in a drug-abusing population, we assessed whether these polymorphisms affect 5-hydroxytryptamine 2B (5-HT2B) receptor in vitro pharmacologic and coupling properties in transfected COS-7 cells. Modification of the 5-HT2B receptor N terminus by the R6G;E42G polymorphisms increases such agonist signaling pathways as inositol phosphate accumulation as assessed by either classic or operational models. The N-terminal R6G;E42G mutations of the 5-HT2B receptor also increase cell proliferation and slow its desensitization kinetics compared with the wild-type receptor, further supporting a role for the N terminus in transduction efficacy. Furthermore, by coexpressing a tethered wild-type 5-HT2B
Activation of complement C5 generates the potent anaphylatoxin C5a and leads to pathogen lysis, inflammation and cell damage. The therapeutic potential of C5 inhibition has been demonstrated by eculizumab, one of the worlds most expensive drugs. However, the mechanism of C5 activation by C5 convertases remains elusive, thus limiting development of therapeutics. Here we identify and characterize a new protein family of tick-derived C5 inhibitors. Structures of C5 in complex with the new inhibitors, the phase I and phase II inhibitor OmCI, or an eculizumab Fab reveal three distinct binding sites on C5 that all prevent activation of C5. The positions of the inhibitor-binding sites and the ability of all three C5-inhibitor complexes to competitively inhibit the C5 convertase conflict with earlier steric-inhibition models, thus suggesting that a priming event is needed for activation.
APD350Hu01, Active Interleukin 17 Receptor C (IL17RC), Homo sapiens (Human), Active protein, IL17-RL, IL17R-C, IL17Rhom, Interleukin-17 receptor homolog, Interleukin-17 receptor-like protein, ZcytoR14, Designed by Cloud-Clone Corp.
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TY - JOUR. T1 - An anti-inflammatory function for the complement anaphylatoxin C5a-binding protein, C5L2. AU - Gerard, Norma P.. AU - Lu, Bao. AU - Liu, Pixu. AU - Craig, Stewart. AU - Fujiwara, Yuko. AU - Okinaga, Shoji. AU - Gerard, Craig. PY - 2005/12/2. Y1 - 2005/12/2. N2 - C5L2 is an enigmatic serpentine receptor that is co-expressed with the C5a receptor on many cells including polymorphonuclear neutrophils. The apparent absence of coupling of C5L2 with G proteins suggests that this receptor may modulate the biological activity of C5a, perhaps by acting as a decoy receptor. Alternatively, C5L2 may affect C5a function through formation of a heteromeric complex with the C5aR, or it may utilize a G protein-independent signaling pathway. Here we show that in mice bearing a targeted deletion of C5L2, the biological activity of C5a/C5adesArg is enhanced both in vivo and in vitro. The biological role of C5L2 thus appears to be limiting to the pro-inflammatory response to the anaphylatoxin. ...
The structure of the human C5aR antagonist, C5a-A8, reveals a three-helix bundle conformation similar to that observed for human C5a-desArg, whereas murine C5a and C5a-desArg both form the canonical four-helix bundle. These conformational differences are discussed in light of the differential C5aR activation properties observed for the human and murine complement anaphylatoxins across species. Complement is an ancient part of the innate immune system that plays a pivotal role in protection against invading pathogens and helps to clear apoptotic and necrotic cells. Upon complement activation, a cascade of proteolytic events generates the complement effectors, including the anaphylatoxins C3a and C5a. Signalling through their cognate G-protein coupled receptors, C3aR and C5aR, leads to a wide range of biological events promoting inflammation at the site of complement activation. The function of anaphylatoxins is regulated by circulating carboxypeptidases that remove their C-terminal arginine ...
Now, they may soon add a new risk factor to the list: activation of the complement system. The complement system is usually implicated in immune responses, but now theres a role for it in cardiovascular disease. In a new research report appearing in the January 2011 print issue of the FASEB Journal (http://www.fasebj.org), scientists from Europe and the United States show that anaphylatoxin C5a, a protein released when complement is activated, contributes to atherosclerotic disease. C5a causes plaques to break free from where they would be anchored to ultimately cause blockages elsewhere in the body. This new discovery not only shows that C5a is a new marker for identifying risk for heart attack and stroke, but it also establishes C5a as a new therapeutic target for preventing these problems.. "Given the huge impact of cardiovascular disease in general, and atherosclerosis in particular, on public health, we feel that unraveling mechanisms involved in the development and progression of the ...
Background: Elevated interleukin-6 (IL-6) and complement activation are associated with detrimental effects of inflammation in coronary artery disease (CAD). The complement anaphylatoxins C5a and C3a interact with their receptors; the highly inflammatory C5aR1, and the C5aR2 and C3aR. We evaluated the effect of the IL-6 receptor (IL-6R)-antagonist tocilizumab on the expression of the anaphylatoxin receptors in whole blood from non-ST-elevation myocardial infarction (NSTEMI) patients. Separately, anaphylatoxin receptor expression in peripheral blood mononuclear cells (PBMC) from patients with different entities of CAD was investigated. Materials and Methods: NSTEMI patients were randomized to one dose of tocilizumab (n = 28) or placebo (n = 32) and observed for 6 months. Whole blood samples drawn at inclusion, at day 2, 3 and after 6 months were used for mRNA isolation. Plasma was prepared for analysis of complement activation measured as sC5b-9 by ELISA. Furthermore, patients with different CAD ...
Innate immunity is the first line of defense in human beings against pathogen infection; monocytes/macrophages are the primary cells of the innate immune system. Recently, macrophages/monocytes have been discovered to participate in LPS clearance, and the clearance efficiency determines the magnitude of the inflammatory response and subsequent organ injury. Previously, we reported that artesunate (AS) protected sepsis mice against heat-killed E. coli challenge. Herein, we further confirmed that AS protected cecal ligation/puncture (CLP) sepsis mice. Its protection on sepsis mice was related to not only reduction of pro-inflammatory cytokines and serum LPS levels but also improvement of liver function. Based on the fact that AS did not directly bind and neutralize LPS, we hypothesized that the reduction of serum LPS level might be related to enhancement of LPS internalization and subsequent detoxification. Our results showed that AS increased FITC-LPS internalization by peritoneal macrophage and liver
Patzelt, J.; Mueller, K. A. L.; Breuning, S.; Karathanos, A.; Schleicher, R.; Seizer, P.; Gawaz, M.; Langer, H. F.; Geisler, T. ...
The role of complement activation products in sepsis and in complications such as MOF is a debatable issue. There is fairly good evidence to suggest that, in the absence of complement such as in complement-depleted animals (14) or in C3 or C4 mutant mice lacking this critical complement component (18, 19), animals are highly susceptible to the early and lethal effects of experimental sepsis. These observations reinforce the long-standing concept that the complement system functions as a critical protective pathway via products such as C3b and iC3b. Evidence also exists that, during sepsis, extensive activation of the complement system occurs resulting in loss of homeostasis, which may in some manner compromise survival. Intravenous infusion of C5a into dogs generated a shock syndrome characterized by portal blood pooling and an associated decrease in venous return, cardiac output, and arterial pressure (20). In experimental sepsis caused by massive i.v. infusion of live, Gram-negative bacteria ...
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C5a / C5a des Arg antibody [2942] (complement component 5) for IA, WB. Anti-C5a / C5a des Arg mAb (GTX11877) is tested in Human samples. 100% Ab-Assurance.
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Purpose : Age-related macular degeneration (AMD) is the major cause of impaired vision in developed countries. The first indication of this disease is the formation of basal deposits (BD) between the retinal pigment epithelium (RPE) and the Bruchs membrane. We recently demonstrated the roles of complement C3a and extracellular matrix (ECM) turnover in an in vitro model for deposit formation in inherited macular degeneration using primary mouse RPE cells. For this study we tested the hypothesis that C3a can cause the formation of BD in vitro by human RPE cells. Methods : Human fetal RPE cells were isolated from the eyes of 14-18 week old fetuses and grown on transwells for 2 weeks when homogeneous pigmentation was observed. RPE cultures were treated with different doses of recombinant human C3a protein every 72 hours for 1, 2 or 4 weeks. The formation of BD was characterized by transmission electron microscopy and immunofluorescence. The presence of complement components, ECM proteins and other ...
Results : CNV resulted in an increase in splenic IL-17-producing γδT- and Th17-cells; yet in the CNV eye, only elevated levels of γδT-cells could be observed. Administration of anti-C5 or anti-C5a-blocking antibodies to reduce levels of C5a production in the eye, blunted the CNV-induced production of splenic Th17- and γδT-cells, reduced CNV size (anti-C5: 3666 ± 359.9 pixels; anti-C5a: 3453 ± 253.8) when compared to control (12B4: 5572 ± 630.6; p ≤ 0.01) and eliminated ocular γδT-cell infiltration. In ARPE-19 cell monolayers, IL-17 triggered a pro-inflammatory state; and T-cell proliferation was elevated in response to ocular proteins Conclusions : Taken together, we demonstrated that CNV lesions trigger a systemic immune response, augmenting local ocular inflammation via the infiltration of IL-17-producing γδT-cells, which are presumably recruited to the eye in a C5a-dependent manner. Finally, understanding complement-mediated pathological mechanisms will aid in the development ...
Activation of the complement cascade is clearly implicated in the pathology of multiple sclerosis (MS). However, the extent and nature of its involvement in specific athological processes remains uncertain. We describe a detailed immunohistochemical study to localise a strategically selected set of complement proteins, activation products and regulators in brain and spinal cord tissue of 17 patients with progressive MS, examining 35 different plaques, and 16 control donors, including 9 with CNS disease. Plaques were consistently positive for complement proteins (C3, factor B, C1q), activation products (C3b, iC3b, C4d, TCC) and regulators (factor H, C1-inhibitor, clusterin), suggesting continuing local complement synthesis, activation and regulation despite no other evidence of on-going inflammation. Complement immunolabelling was most apparent in plaque and peri-plaque areas but also present in normal appearing white matter and cortical areas to a greater extent than in control tissue. Cellular ...
Recombinant Human C1 Esterase Inhibitor/ conestat alfa].. The ongoing pediatric study is an open label Phase II clinical trial assessing safety, immunogenicity and efficacy in children 2-13 years of age with C1INH deficiency. Eight children were treated on demand for 28 HAE attacks at 50 IU/kg body weight (up to a maximum of 4200 IU). Efficacy endpoints were time to onset of relief and to minimal symptoms, assessed by the patient (assisted by their parent), using a visual analogue scale (VAS) and by physicians using an Investigator Score. Median time to beginning of relief was 60 minutes as determined by the patients and the investigators. Using the VAS, 93% of patients had onset of relief within 2 hours. No related serious adverse events, including hypersensitivity reactions, were reported.. "We believe the additional body of pediatric clinical data in children under 13 years of age are in line with the excellent data in adolescents (13-18 years of age) and adult HAE patients treated with ...
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Esophageal carcinoma is a common malignancy worldwide, with a low 5‑year survival rate. As the majority of cases are diagnosed at an advanced stage, there is an urgent need for an effective biomarker for early diagnosis of esophageal cancer patients. Surface‑enhanced laser desorption ionization time‑of‑flight mass spectrometry (SELDI‑TOF‑MS) was applied to detect the serum protein expression in esophageal cancer patients using ProteinChip software, and the results were analyzed and screened using Biomarker Patterns and SPSS16.0 software. The ELISA method was conducted to determine the concentration of anaphylatoxin C3a, which is one of the complement proteins, in the serum of esophageal cancer patients and non‑esophageal cancer participants. A total of 144 effective differential expression protein peaks in the window of 1‑10 kDa were obtained ( ...