Complement Inactivator Proteins: Serum proteins that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host. The complement system is tightly regulated by inactivators that accelerate the decay of intermediates and certain cell surface receptors.Complement C3b Inactivator Proteins: Endogenous proteins that inhibit or inactivate COMPLEMENT C3B. They include COMPLEMENT FACTOR H and COMPLEMENT FACTOR I (C3b/C4b inactivator). They cleave or promote the cleavage of C3b into inactive fragments, and thus are important in the down-regulation of COMPLEMENT ACTIVATION and its cytolytic sequence.Complement C1 Inactivator Proteins: Serum proteins that inhibit, antagonize, or inactivate COMPLEMENT C1 or its subunits.Complement C3: A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase.Complement Activation: The sequential activation of serum COMPLEMENT PROTEINS to create the COMPLEMENT MEMBRANE ATTACK COMPLEX. Factors initiating complement activation include ANTIGEN-ANTIBODY COMPLEXES, microbial ANTIGENS, or cell surface POLYSACCHARIDES.Complement System Proteins: Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).Complement C4: A glycoprotein that is important in the activation of CLASSICAL COMPLEMENT PATHWAY. C4 is cleaved by the activated COMPLEMENT C1S into COMPLEMENT C4A and COMPLEMENT C4B.Complement C5: C5 plays a central role in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C5 is cleaved by C5 CONVERTASE into COMPLEMENT C5A and COMPLEMENT C5B. The smaller fragment C5a is an ANAPHYLATOXIN and mediator of inflammatory process. The major fragment C5b binds to the membrane initiating the spontaneous assembly of the late complement components, C5-C9, into the MEMBRANE ATTACK COMPLEX.Complement C3b: The larger fragment generated from the cleavage of COMPLEMENT C3 by C3 CONVERTASE. It is a constituent of the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb), and COMPLEMENT C5 CONVERTASES in both the classical (C4b2a3b) and the alternative (C3bBb3b) pathway. C3b participates in IMMUNE ADHERENCE REACTION and enhances PHAGOCYTOSIS. It can be inactivated (iC3b) or cleaved by various proteases to yield fragments such as COMPLEMENT C3C; COMPLEMENT C3D; C3e; C3f; and C3g.Complement Pathway, Alternative: Complement activation initiated by the interaction of microbial ANTIGENS with COMPLEMENT C3B. When COMPLEMENT FACTOR B binds to the membrane-bound C3b, COMPLEMENT FACTOR D cleaves it to form alternative C3 CONVERTASE (C3BBB) which, stabilized by COMPLEMENT FACTOR P, is able to cleave multiple COMPLEMENT C3 to form alternative C5 CONVERTASE (C3BBB3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.Receptors, Complement: Molecules on the surface of some B-lymphocytes and macrophages, that recognize and combine with the C3b, C3d, C1q, and C4b components of complement.Complement C2: A component of the CLASSICAL COMPLEMENT PATHWAY. C2 is cleaved by activated COMPLEMENT C1S into COMPLEMENT C2B and COMPLEMENT C2A. C2a, the COOH-terminal fragment containing a SERINE PROTEASE, combines with COMPLEMENT C4B to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE).Complement Pathway, Classical: Complement activation initiated by the binding of COMPLEMENT C1 to ANTIGEN-ANTIBODY COMPLEXES at the COMPLEMENT C1Q subunit. This leads to the sequential activation of COMPLEMENT C1R and COMPLEMENT C1S subunits. Activated C1s cleaves COMPLEMENT C4 and COMPLEMENT C2 forming the membrane-bound classical C3 CONVERTASE (C4B2A) and the subsequent C5 CONVERTASE (C4B2A3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.Complement Factor B: A glycine-rich, heat-labile serum glycoprotein that contains a component of the C3 CONVERTASE ALTERNATE PATHWAY (C3bBb). Bb, a serine protease, is generated when factor B is cleaved by COMPLEMENT FACTOR D into Ba and Bb.Properdin: A 53-kDa protein that is a positive regulator of the alternate pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It stabilizes the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb) and protects it from rapid inactivation, thus facilitating the cascade of COMPLEMENT ACTIVATION and the formation of MEMBRANE ATTACK COMPLEX. Individuals with mutation in the PFC gene exhibit properdin deficiency and have a high susceptibility to infections.Complement C1q: A subcomponent of complement C1, composed of six copies of three polypeptide chains (A, B, and C), each encoded by a separate gene (C1QA; C1QB; C1QC). This complex is arranged in nine subunits (six disulfide-linked dimers of A and B, and three disulfide-linked homodimers of C). C1q has binding sites for antibodies (the heavy chain of IMMUNOGLOBULIN G or IMMUNOGLOBULIN M). The interaction of C1q and immunoglobulin activates the two proenzymes COMPLEMENT C1R and COMPLEMENT C1S, thus initiating the cascade of COMPLEMENT ACTIVATION via the CLASSICAL COMPLEMENT PATHWAY.Complement C9: A 63-kDa serum glycoprotein encoded by gene C9. Monomeric C9 (mC9) binds the C5b-8 complex to form C5b-9 which catalyzes the polymerization of C9 forming C5b-p9 (MEMBRANE ATTACK COMPLEX) and transmembrane channels leading to lysis of the target cell. Patients with C9 deficiency suffer from recurrent bacterial infections.Complement Factor H: An important soluble regulator of the alternative pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It is a 139-kDa glycoprotein expressed by the liver and secreted into the blood. It binds to COMPLEMENT C3B and makes iC3b (inactivated complement 3b) susceptible to cleavage by COMPLEMENT FACTOR I. Complement factor H also inhibits the association of C3b with COMPLEMENT FACTOR B to form the C3bB proenzyme, and promotes the dissociation of Bb from the C3bBb complex (COMPLEMENT C3 CONVERTASE, ALTERNATIVE PATHWAY).Complement Activating Enzymes: Enzymes that activate one or more COMPLEMENT PROTEINS in the complement system leading to the formation of the COMPLEMENT MEMBRANE ATTACK COMPLEX, an important response in host defense. They are enzymes in the various COMPLEMENT ACTIVATION pathways.Complement Membrane Attack Complex: A product of COMPLEMENT ACTIVATION cascade, regardless of the pathways, that forms transmembrane channels causing disruption of the target CELL MEMBRANE and cell lysis. It is formed by the sequential assembly of terminal complement components (COMPLEMENT C5B; COMPLEMENT C6; COMPLEMENT C7; COMPLEMENT C8; and COMPLEMENT C9) into the target membrane. The resultant C5b-8-poly-C9 is the "membrane attack complex" or MAC.Complement C3-C5 Convertases: Serine proteases that cleave COMPLEMENT C3 into COMPLEMENT C3A and COMPLEMENT C3B, or cleave COMPLEMENT C5 into COMPLEMENT C5A and COMPLEMENT C5B. These include the different forms of C3/C5 convertases in the classical and the alternative pathways of COMPLEMENT ACTIVATION. Both cleavages take place at the C-terminal of an ARGININE residue.Complement Inactivating Agents: Compounds that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host.Complement C3a: The smaller fragment generated from the cleavage of complement C3 by C3 CONVERTASE. C3a, a 77-amino acid peptide, is a mediator of local inflammatory process. It induces smooth MUSCLE CONTRACTION, and HISTAMINE RELEASE from MAST CELLS and LEUKOCYTES. C3a is considered an anaphylatoxin along with COMPLEMENT C4A; COMPLEMENT C5A; and COMPLEMENT C5A, DES-ARGININE.Complement C5a: The minor fragment formed when C5 convertase cleaves C5 into C5a and COMPLEMENT C5B. C5a is a 74-amino-acid glycopeptide with a carboxy-terminal ARGININE that is crucial for its spasmogenic activity. Of all the complement-derived anaphylatoxins, C5a is the most potent in mediating immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE), smooth MUSCLE CONTRACTION; HISTAMINE RELEASE; and migration of LEUKOCYTES to site of INFLAMMATION.Complement C6: A 105-kDa serum glycoprotein with significant homology to the other late complement components, C7-C9. It is a polypeptide chain cross-linked by 32 disulfide bonds. C6 is the next complement component to bind to the membrane-bound COMPLEMENT C5B in the assembly of MEMBRANE ATTACK COMPLEX. It is encoded by gene C6.Receptors, Complement 3b: Molecular sites on or in some B-lymphocytes and macrophages that recognize and combine with COMPLEMENT C3B. The primary structure of these receptors reveal that they contain transmembrane and cytoplasmic domains, with their extracellular portion composed entirely of thirty short consensus repeats each having 60 to 70 amino acids.Complement C1: The first complement component to act in the activation of CLASSICAL COMPLEMENT PATHWAY. It is a calcium-dependent trimolecular complex made up of three subcomponents: COMPLEMENT C1Q; COMPLEMENT C1R; and COMPLEMENT C1S at 1:2:2 ratios. When the intact C1 binds to at least two antibodies (involving C1q), C1r and C1s are sequentially activated, leading to subsequent steps in the cascade of COMPLEMENT ACTIVATION.Complement C4b: The large fragment formed when COMPLEMENT C4 is cleaved by COMPLEMENT C1S. The membrane-bound C4b binds COMPLEMENT C2A, a SERINE PROTEASE, to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE).Anaphylatoxins: Serum peptides derived from certain cleaved COMPLEMENT PROTEINS during COMPLEMENT ACTIVATION. They induce smooth MUSCLE CONTRACTION; mast cell HISTAMINE RELEASE; PLATELET AGGREGATION; and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from the strongest to the weakest is C5a, C3a, C4a, and C5a des-arginine.Complement C3d: A 302-amino-acid fragment in the alpha chain (672-1663) of C3b. It is generated when C3b is inactivated (iC3b) and its alpha chain is cleaved by COMPLEMENT FACTOR I into C3c, and C3dg (955-1303) in the presence COMPLEMENT FACTOR H. Serum proteases further degrade C3dg into C3d (1002-1303) and C3g (955-1001).Complement Fixation Tests: Serologic tests based on inactivation of complement by the antigen-antibody complex (stage 1). Binding of free complement can be visualized by addition of a second antigen-antibody system such as red cells and appropriate red cell antibody (hemolysin) requiring complement for its completion (stage 2). Failure of the red cells to lyse indicates that a specific antigen-antibody reaction has taken place in stage 1. If red cells lyse, free complement is present indicating no antigen-antibody reaction occurred in stage 1.Complement C7: A 93-kDa serum glycoprotein encoded by C7 gene. It is a polypeptide chain with 28 disulfide bridges. In the formation of MEMBRANE ATTACK COMPLEX; C7 is the next component to bind the C5b-6 complex forming a trimolecular complex C5b-7 which is lipophilic, resembles an integral membrane protein, and serves as an anchor for the late complement components, C8 and C9.Complement C8: A 150-kDa serum glycoprotein composed of three subunits with each encoded by a different gene (C8A; C8B; and C8G). This heterotrimer contains a disulfide-linked C8alpha-C8gamma heterodimer and a noncovalently associated C8beta chain. C8 is the next component to bind the C5-7 complex forming C5b-8 that binds COMPLEMENT C9 and acts as a catalyst in the polymerization of C9.Complement C3c: A 206-amino-acid fragment in the alpha chain (672-1663) of C3b. It is generated when C3b is inactivated (iC3b) and its alpha chain is cleaved by COMPLEMENT FACTOR I into C3c (749-954), and C3dg (955-1303) in the presence COMPLEMENT FACTOR H.Hemolysis: The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.Receptors, Complement 3d: Molecular sites on or in B-lymphocytes, follicular dendritic cells, lymphoid cells, and epithelial cells that recognize and combine with COMPLEMENT C3D. Human complement receptor 2 (CR2) serves as a receptor for both C3dg and the gp350/220 glycoprotein of HERPESVIRUS 4, HUMAN, and binds the monoclonal antibody OKB7, which blocks binding of both ligands to the receptor.Complement Hemolytic Activity Assay: A screening assay for circulating COMPLEMENT PROTEINS. Diluted SERUM samples are added to antibody-coated ERYTHROCYTES and the percentage of cell lysis is measured. The values are expressed by the so called CH50, in HEMOLYTIC COMPLEMENT units per milliliter, which is the dilution of serum required to lyse 50 percent of the erythrocytes in the assay.Complement C4a: The smaller fragment formed when complement C4 is cleaved by COMPLEMENT C1S. It is an anaphylatoxin that causes symptoms of immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE) but its activity is weaker than that of COMPLEMENT C3A or COMPLEMENT C5A.Lysine Carboxypeptidase: A metallocarboxypeptidase that removes C-terminal basic amino acid from peptides and proteins, with preference shown for lysine over arginine. It is a plasma zinc enzyme that inactivates bradykinin and anaphylatoxins.Complement Factor D: A serum protein which is important in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY. This enzyme cleaves the COMPLEMENT C3B-bound COMPLEMENT FACTOR B to form C3bBb which is ALTERNATIVE PATHWAY C3 CONVERTASE.Beta-Globulins: Serum proteins with an electrophoretic mobility that falls between ALPHA-GLOBULINS and GAMMA-GLOBULINS.Complement Factor I: A plasma serine proteinase that cleaves the alpha-chains of C3b and C4b in the presence of the cofactors COMPLEMENT FACTOR H and C4-binding protein, respectively. It is a 66-kDa glycoprotein that converts C3b to inactivated C3b (iC3b) followed by the release of two fragments, C3c (150-kDa) and C3dg (41-kDa). It was formerly called KAF, C3bINF, or enzyme 3b inactivator.Complement C4b-Binding Protein: A serum protein that regulates the CLASSICAL COMPLEMENT ACTIVATION PATHWAY. It binds as a cofactor to COMPLEMENT FACTOR I which then hydrolyzes the COMPLEMENT C4B in the CLASSICAL PATHWAY C3 CONVERTASE (C4bC2a).Complement C1s: A 77-kDa subcomponent of complement C1, encoded by gene C1S, is a SERINE PROTEASE existing as a proenzyme (homodimer) in the intact complement C1 complex. Upon the binding of COMPLEMENT C1Q to antibodies, the activated COMPLEMENT C1R cleaves C1s into two chains, A (heavy) and B (light, the serine protease), linked by disulfide bonds yielding the active C1s. The activated C1s, in turn, cleaves COMPLEMENT C2 and COMPLEMENT C4 to form C4b2a (CLASSICAL C3 CONVERTASE).Immunoelectrophoresis: A technique that combines protein electrophoresis and double immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct elliptical precipitin arc results for each protein detectable by the antisera.Cytochrome P-450 CYP2B1: A major cytochrome P-450 enzyme which is inducible by PHENOBARBITAL in both the LIVER and SMALL INTESTINE. It is active in the metabolism of compounds like pentoxyresorufin, TESTOSTERONE, and ANDROSTENEDIONE. This enzyme, encoded by CYP2B1 gene, also mediates the activation of CYCLOPHOSPHAMIDE and IFOSFAMIDE to MUTAGENS.Chloromercurinitrophenols: Mercuriphenols substituted with one or more chlorine atoms and one or more nitro groups. Some of these are sulfhydryl reagents which act as chromophoric probes in enzymes and other proteins.Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes IMMUNE COMPLEX DISEASES.Angioedema: Swelling involving the deep DERMIS, subcutaneous, or submucosal tissues, representing localized EDEMA. Angioedema often occurs in the face, lips, tongue, and larynx.Kinetics: The rate dynamics in chemical or physical systems.Complement C1r: A 80-kDa subcomponent of complement C1, existing as a SERINE PROTEASE proenzyme in the intact complement C1 complex. When COMPLEMENT C1Q is bound to antibodies, the changed tertiary structure causes autolytic activation of complement C1r which is cleaved into two chains, A (heavy) and B (light, the serine protease), connected by disulfide bonds. The activated C1r serine protease, in turn, activates COMPLEMENT C1S proenzyme by cleaving the Arg426-Ile427 bond. No fragment is released when either C1r or C1s is cleaved.Kaolin: The most common mineral of a group of hydrated aluminum silicates, approximately H2Al2Si2O8-H2O. It is prepared for pharmaceutical and medicinal purposes by levigating with water to remove sand, etc. (From Merck Index, 11th ed) The name is derived from Kao-ling (Chinese: "high ridge"), the original site. (From Grant & Hackh's Chemical Dictionary, 5th ed)Serum Globulins: All blood proteins except albumin ( = SERUM ALBUMIN, which is not a globulin) and FIBRINOGEN (which is not in the serum). The serum globulins are subdivided into ALPHA-GLOBULINS; BETA-GLOBULINS; and GAMMA-GLOBULINS on the basis of their electrophoretic mobilities. (From Dorland, 28th ed)Antigens, CD55: GPI-linked membrane proteins broadly distributed among hematopoietic and non-hematopoietic cells. CD55 prevents the assembly of C3 CONVERTASE or accelerates the disassembly of preformed convertase, thus blocking the formation of the membrane attack complex.Antigens, CD59: Small glycoproteins found on both hematopoietic and non-hematopoietic cells. CD59 restricts the cytolytic activity of homologous complement by binding to C8 and C9 and blocking the assembly of the membrane attack complex. (From Barclay et al., The Leukocyte Antigen FactsBook, 1993, p234)Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.Complement C5b: The larger fragment generated from the cleavage of C5 by C5 CONVERTASE that yields COMPLEMENT C5A and C5b (beta chain + alpha' chain, the residual alpha chain, bound by disulfide bond). C5b remains bound to the membrane and initiates the spontaneous assembly of the late complement components to form C5b-8-poly-C9, the MEMBRANE ATTACK COMPLEX.Hydroxybenzoate Ethers: Benzoate derivatives that contain one or more alkyl or aryl groups linked to the benzene ring structure by OXYGEN.

Capsular sialic acid limits C5a production on type III group B streptococci. (1/619)

The majority of type III group B streptococcus (GBS) human neonatal infections are caused by a genetically related subgroup called III-3. We have proposed that a bacterial enzyme, C5a-ase, contributes to the pathogenesis of neonatal infections with GBS by rapidly inactivating C5a, a potent pro-inflammatory molecule, but many III-3 strains do not express C5a-ase. The amount of C5a produced in serum following incubation with representative type III strains was quantitated in order to better understand the relationship between C5a production and C5a-ase expression. C5a production following incubation of bacteria with serum depleted of antibody to the bacterial surface was inversely proportional to the sialic acid content of the bacterial capsule, with the more heavily sialylated III-3 strains generating less C5a than the less-virulent, less-sialylated III-2 strains. The amount of C5a produced correlated significantly with C3 deposition on each bacterial strain. Repletion with type-specific antibody caused increased C3b deposition and C5a production through alternative pathway activation, but C5a was functionally inactivated by strains that expressed C5a-ase. The increased virulence of III-3 strains compared to that of III-2 strains results at least partially from the higher sialic acid content of III-3 strains, which inhibits both opsonophagocytic killing and C5a production in the absence of type-specific antibody. We propose that C5a-ase is not necessary for III-3 strains to cause invasive disease because the high sialic acid content of III-3 strains inhibits C5a production.  (+info)

Effects of a new C5a receptor antagonist on C5a- and endotoxin-induced neutropenia in the rat. (2/619)

A new C5a receptor antagonist, the cyclic peptide Phe-[Orn-Pro-D-cyclohexylalanine-Trp-Arg], (F-[OPdChaWR]), was tested for its ability to antagonize the neutropenic effects of both C5a and endotoxin in rats. Human recombinant C5a (2 microg kg(-1) i.v.) caused rapid neutropenia, characterized by an 83% decrease in circulating polymorphonuclear leukocytes (PMNs) at 5 min. Administration of F-[OPdChaWR] (0.3-3 mg kg(-1) i.v.), did not affect the levels of circulating PMNs but, when given 10 min prior to C5a, it inhibited the C5a-induced neutropenia by up to 70%. Administration of E. Coli lipopolysaccharide (LPS, 1 mg kg(-1) i.v.) also caused neutropenia with an 88% decrease in circulating PMNs after 30 min. When rats were pretreated with F-[OPdChaWR] (0.3 - 10 mg kg(-1) i.v.) 10 min prior to LPS, there was a dose-dependent antagonism of the neutropenia caused by LPS, with up to 69% reversal of neutropenia observed 30 min after LPS administration. These findings suggest that C5a receptor antagonists may have therapeutic potential in the many diseases known to involve either endotoxin or C5a.  (+info)

Endothelial targeting and enhanced antiinflammatory effects of complement inhibitors possessing sialyl Lewisx moieties. (3/619)

The complement inhibitor soluble complement receptor type 1 (sCR1) and a truncated form of sCR1, sCR1[desLHR-A], have been generated with expression of the selectin-reactive oligosaccharide moiety, sialyl Lewisx (sLex), as N-linked oligosaccharide adducts. These modified proteins, sCR1sLex and sCR1[desLHR-A]sLex, were assessed in the L-selectin- and P-selectin-dependent rat model of lung injury following systemic activation of complement by cobra venom factor and in the L-selectin-, P-selectin-, and E-selectin-dependent model of lung injury following intrapulmonary deposition of IgG immune complexes. In the cobra venom factor model, sCR1sLex and sCR1[desLHR-A]sLex caused substantially greater reductions in neutrophil accumulation and in albumin extravasation in lung when compared with the non-sLex-decorated forms. In this model, increased lung vascular binding of sCR1sLex and sCR1[desLHR-A]sLex occurred in a P-selectin-dependent manner, in contrast to the absence of any increased binding of sCR1 or sCR1[desLHR-A]. In the IgG immune complex model, sCR1[desLHR-A]sLex possessed greater protective effects relative to sCR1[desLHR-A], based on albumin extravasation and neutrophil accumulation. Enhanced protective effects correlated with greater lung vascular binding of sCR1[desLHR-A]sLex as compared with the non-sLex-decorated form. In TNF-alpha-activated HUVEC, substantial in vitro binding occurred with sCR1[desLHR-A]sLex (but not with sCR1[desLHR-A]). This endothelial cell binding was blocked by anti-E-selectin but not by anti-P-selectin. These data suggest that sLex-decorated complement inhibitors have enhanced antiinflammatory effects and appear to have enhanced ability to localize to the activated vascular endothelium.  (+info)

Inhibition of a membrane complement regulatory protein by a monoclonal antibody induces acute lethal shock in rats primed with lipopolysaccharide. (4/619)

Rats pretreated with traces of LPS developed acute fatal shock syndrome after i.v. administration of a mAb that inhibits the function of a membrane complement regulatory molecule. Such a shock was not observed after the administration of large amounts of LPS instead of the mAb following LPS pretreatment. The lethal response did not occur in rats depleted of either leukocytes or complement, and a C5a receptor antagonist was found to inhibit the reaction. Furthermore, LPS-treated rats did not suffer fatal shock following the injection of cobra venom factor, which activates complement in the fluid phase so extensively as to exhaust complement capacity. Therefore, complement activation on cell membranes is a requirement for this type of acute reaction.  (+info)

Epitope mapping of 10 monoclonal antibodies against the pig analogue of human membrane cofactor protein (MCP). (5/619)

Pig membrane cofactor protein (MCP; CD46) is a 50 000-60 000 MW glycoprotein that is expressed on a wide variety of cells, including erythrocytes. Pig MCP has cofactor activity for factor I-mediated cleavage of C3b and is an efficient regulator of the classical and alternative pathway of human and pig complement. A panel of 10 monoclonal antibodies (mAbs) was collected from two different laboratories; all of these mAbs were raised against pig leucocytes and all recognized the same complex banding pattern on sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) of erythrocyte membranes. All were shown to be reactive with pig MCP and were divided into four groups of mutually competitive antibodies based on competition studies for membrane-bound MCP and for soluble MCP, the latter by surface plasmon resonance (SPR) analysis. The antigenic properties of membrane-bound and soluble MCP were similar, although some interesting differences were revealed. None of the 10 mAbs were cross-reactive with human MCP and only one showed cross-reactivity with leucocytes from a panel of large mammals - a weak cross-reactivity with a subset of dog leucocytes. All antibodies in one of the epitope groups and some in a second epitope group were able to block the functional activity of pig MCP, as measured by inhibition of MCP-catalysed C3 degradation by factor I.  (+info)

Mechanisms of enhanced lung injury during sepsis. (6/619)

A major complication in sepsis is progressively impaired lung function and susceptibility to intrapulmonary infection. Why sepsis predisposes the lung to injury is not clear. In the current studies, rats were rendered septic by cecal ligation/puncture and evaluated for increased susceptibility to injury after a direct pulmonary insult (deposition of IgG immune complexes or airway instillation of lipopolysaccharide). By itself, cecal ligation/puncture did not produce evidence of lung injury. However, after a direct pulmonary insult, lung injury in septic animals was significantly enhanced. Enhanced lung injury was associated with increased accumulation of neutrophils in lung, enhanced production of CXC chemokines (but not tumor necrosis factor-alpha) in bronchoalveolar lavage fluids, and increased expression of lung vascular intercellular adhesion molecule-1 (ICAM-1). Complement depletion or treatment with anti-C5a abolished all evidence of enhanced lung injury in septic animals. When stimulated in vitro, bronchoalveolar lavage macrophages from septic animals had greatly enhanced CXC chemokine responses as compared with macrophages from sham-operated animals or from septic animals that had been complement depleted. These data indicate that the septic state causes priming of lung macrophages and suggest that enhanced lung injury in the septic state is complement dependent and related to increased production of CXC chemokines.  (+info)

Interaction between protein S and complement C4b-binding protein (C4BP). Affinity studies using chimeras containing c4bp beta-chain short consensus repeats. (7/619)

Human C4b-binding protein (C4BP) is a regulator of the complement system and plays an important role in the regulation of the anticoagulant protein C pathway. C4BP can bind anticoagulant protein S, resulting in a decreased cofactor function of protein S for activated protein C. C4BP is a multimeric protein containing several identical alpha-chains and a single beta-chain (C4BPbeta), each chain being composed of short consensus repeats (SCRs). Previous studies have localized the protein S binding site to the NH2-terminal SCR (SCR-1) of C4BPbeta. To further localize the protein S binding site, we constructed chimeras containing C4BPbeta SCR-1, SCR-2, SCR-3, SCR-1+2, SCR-1+3, and SCR-2+3 fused to tissue-type plasminogen activator. Binding assays of protein S with these chimeras indicated that SCR-2 contributes to the interaction of protein S with SCR-1, since the affinity of protein S for SCR-1+2 was up to 5-fold higher compared with SCR-1 and SCR-1+3. Using an assay that measures protein S cofactor activity, we showed that cofactor activity was decreased due to binding to constructs that contain SCR-1. SCR-1+2 inhibited more potently than SCR-1 and SCR-1+3. SCR-3 had no additional effect on SCR-1, and therefore the effect of SCR-2 was specific. In conclusion, beta-chain SCR-2 contributes to the interaction of C4BP with protein S.  (+info)

Consumption of C4b-binding protein (C4BP) during in vivo activation of the classical complement pathway. (8/619)

C4BP has a central role in regulating the classical complement (C') pathway, but it is still uncertain whether or not it is consumed during in vivo complement activation. Attempts to demonstrate changes in C4BP plasma levels in systemic lupus erythematosus and essential mixed cryoglobulinaemia have failed, probably due to up-regulation of this protein during the inflammatory reaction. We have studied one patient with severe post-transfusion complement-mediated anaphylaxis (CMA), and 67 patients with hereditary C1 inhibitor deficiency (hereditary angioedema (HAE)). The first of these two conditions is characterized by the absence of systemic inflammatory reaction and the second by acute and chronic activation of the C' classical pathway. C4BP, C4BP-C4b complex, and soluble terminal C' complex (sC5b-9) were measured in the patients' plasmas by ELISA techniques and C3a and C4a by radioimmunoassays. In CMA, 15 min after the transfusion, there was a massive C' activation, with increases in C4a, C3a, sC5b-9, C4BP-C4b complexes and decreases in C4, C3 and C4BP. All parameters reverted to preinfusion values within 24 h. Depletion of C4 was correlated with that of C4BP. In patients with HAE, the median value of C4BP (83% range 54-165) was significantly lower (P < 0.0001) than in normal controls (99% range 70-159), with no difference between patients in remission or during acute attacks. C4BP-C4b complexes could not be detected in HAE patients. The results of this study indicate that C4BP is consumed in vivo during acute, and possibly during chronic activation of the C' classical pathway, and that this protein, after interaction with C4b, not longer circulates in plasma.  (+info)

anti-Complement C4 beta-chain, mAb (52H10) is a monoclonal antibody that crossreacts with human protein. Works in ELISA, WB, IP. Important for Inflammation, Oxidative Stress, ROS, Immunology research.
A Novel Protocol Allowing Oral Delivery of a Protein Complement Inhibitor that Subsequently Targets to Inflamed Colon Mucosa and Ameliorates Murine Colitis. Elvington, M; Blichmann, P; Qiao, F; Scheiber, M; Wadsworth, C; et al. A novel protocol allowing oral delivery of a protein complement inhibitor that subsequently targets to inflamed colon mucosa and ameliorates murine colitis. Clinical and Experimental Immunology 177.2 (Aug 2014): 500-508. While there is evidence of a pathogenic role for complement in inflammatory bowel disease, there is also evidence for a protective role that relates to host defence and protection from endotoxaemia. There is thus concern regarding the use of systemic complement inhibition as a therapeutic strategy. Local delivery of a complement inhibitor to the colon by oral administration would ameliorate such concerns, but while formulations exist for oral delivery of low molecular weight drugs to the colon, they have not been used successfully for oral delivery of ...
article{5be1f4a6-d9f6-43e4-84be-f1c903a8b6fe, abstract = {C4b-binding protein (C4BP), an important inhibitor of complement activation, has a unique spider-like shape. It is composed of six to seven identical alpha-chains with or without a single beta-chain, the chains being linked by disulfide bridges in their C-terminal parts. To elucidate the structural requirements for the assembly of the alpha-chains, recombinant C4BP was expressed in HEK 293 cells. The expressed C4BP was found to contain six disulfide-linked alpha-chains. Pulse-chase analysis demonstrated that the recombinant C4BP was rapidly synthesized in the cells and the polymerized C4BP appeared in the medium after 40 min. The alpha-chains were polymerized in the endoplasmic reticulum (ER) already after 5 min chase. The polymerization process was unaffected by blockage of the transport from the ER to the Golgi mediated by brefeldin A or low temperature (10 degrees C). The C-terminal part of the alpha-chain (57 amino acids), containing ...
AMYNDAS is developing a novel peptidic complement inhibitor AMY-101, based on the third-generation compstatin analogue Cp40. AMY-101 is a selective inhibitor of complement activation in humans and in NHP. It binds to the complement component C3, the central functional hub that controls the upstream activation/amplification and downstream effector functions of complement. By binding to C3, AMY-101 inhibits the cleavage of native C3 to its active fragments C3a and C3b. As a consequence, the deposition of C3b, amplification via the alternative pathway and all downstream complement responses are prevented. AMY-101 is being developed to treat complement-mediated diseases, which are largely driven by aberrant C3 activation.. This first-in-human study of the C3-targeting complement inhibitor AMY-101 investigates the safety and PK/PD profile of AMY-101 in healthy male volunteers after Single Ascending Dose (SAD) and Multiple Doses (MD) using subcutaneous (SQ) or intravenous (IV) administration. The ...
La nostra investigació està dedicada a lestudi dels mecanismes moleculars de la mort i la proliferació cel·lular, ja que aquests estan involucrats en el desenvolupament de diferents patologies humanes.. ...
NEW HAVEN, Conn.--(BUSINESS WIRE)--Alexion Pharmaceuticals, Inc. (NASDAQ: ALXN) announced today that the pivotal Phase 3 study of ALXN1210, the Companys investigational long-acting C5 complement inhibitor, demonstrated non-inferiority to Soliris® (eculizumab) in complement inhibitor treatment-naïve patients with paroxysmal nocturnal hemoglobinuria (PNH) based on the co-primary endpoints of transfusion avoidance and normalization of lactate dehydrogenase (LDH) levels, a direct marker of complement-mediated hemolysis in PNH.
To provide insight into bacterial suppression of complement-mediated immunity, we present here structures of a bacterial complement inhibitory protein, both free and bound to its complement target. The 1.25-A structure of the complement component C3-inhibitory domain of Staphylococcus aureus extrace …
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2A55: Human C4b-binding Protein, Structural Basis for Interaction with Streptococcal M Protein, a Major Bacterial Virulence Factor
Author: Ashby, M. L. N. et al.; Genre: Journal Article; Published in Print: 2013-05-20; Title: SEDS: The Spitzer Extended Deep Survey. Survey design, photometry, and deep IRAC source counts
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Membrane cofactor protein (MCP) is a complement regulatory protein that is expressed on human cells and cell lines as two relatively broad species with Mr of 58,000-68,000 and 48,000-56,000. The structure of a previously reported cDNA clone indicated that MCP was a type 1 membrane glycoprotein and a member of the regulators of complement activation gene/protein cluster. However, it did not provide an explanation for the unusual phenotypic pattern of MCP. Therefore, in parallel with an analysis of the gene, additional cDNAs were cloned and characterized. Six different MCP cDNA classes were identified. All encode the same 5 untranslated signal peptide, four SCRs, transmembrane domain, and basic amino acid anchor. However, they differ in the length and composition of an extracellular serine/threonine/proline (STP)-rich area, a site of heavy O-glycosylation, and cytoplasmic tail. Analysis of the MCP gene demonstrated that the variation in cDNA structure was a result of alternative splicing. ...
Streptococcal inhibitor of complement (Sic) is a highly polymorphic extracellular protein made by serotype M1 group A Streptococcus strains that contributes to bacterial persistence in the mammalian upper respiratory tract. New variants of the Sic protein arise very rapidly by positive selection in human populations during M1 epidemics. The human antibody response to Sic was analyzed. Of 636 persons living in diverse localities, 43% had anti-Sic serum antibodies, but only 16.4% had anti-M1 protein serum antibody. Anti-Sic antibody was also present in nasal wash specimens in high frequency. Linear B cell epitope mapping showed that serum antibodies recognized epitopes located in structurally variable regions of Sic and the amino terminal hypervariable region of the M1 protein. Phage display analyses confirmed that the polymorphic regions of Sic are primary targets of host antibodies. These results support the hypothesis that selection of Sic variants occurs on mucosal surfaces by a mechanism that ...
Two-site ELISA method for the measurement of total Protein S (free or complexed with C4b-BP), in human citrated plasma. Assay designed with two conformational Murine monoclonal antibodies, calcium dependent, the first one for coating the microplate (immunocapture) and the second one, labeled with a Horse Radish Peroxidase (HRP) marker.
Decay-accelerating factor (DAF), extracted from the stroma of human erythrocytes, was purified to homogeneity and incorporated into the membrane of sheep red cell complement intermediates, where its functional properties were analyzed. Incorporation of DAF into the cell membranes was temperature dependent, took place on pronase- or trypsin-treated erythrocytes, and did not depend on prior deposition of antibody, C1 or C4. Serum lipoproteins (high and low density) effectively inhibited DAF incorporation, but had no effect on the activity of DAF after its association with the cell membrane. The incorporated DAF could not be removed from the red cell surface by repeated washings in the presence of high salt concentration but was solubilized when the stroma were extracted with 0.1% Nonidet P-40. The presence of DAF in the membrane of EA did not affect the deposition of C1 and C4, but as few as 10(2) DAF molecules per cell profoundly inhibited the assembly of C3 and C5 convertases of both the ...
Dendritic polyglycerol sulfate (dPGS) has originally been investigated as an anticoagulant to potentially substitute for the natural glycosaminoglycan heparin. Compared to unfractionated heparin, dPGS possesses lower anticoagulant activity but a much higher anticomplementary effect. Since coagulation, complement activation, and inflammation are often present in the pathophysiology of numerous diseases, dPGS polymers with both anticoagulant and anticomplementary activities represent promising candidates for the development of polymeric drugs of nanosized architecture. In this review, we describe the nanomedical applications of dPGS based on its anti-inflammatory activity. Furthermore, the application of dPGS as a carrier molecule for diagnostic molecules and therapeutic drugs is reviewed, based on the ability to target tumors and localize in tumor cells. Finally, the application of dPGS for inhibition of virus infections is described.
We further analysed SIC and DRS seroprevalence among CKD and ESRD cohorts. The results revealed that sera from 19% of CKD patients (n=100) and 35.7% of ESRD patients (n=70) reacted with SIC antigen. Thus, relative to the healthy controls significantly high proportion of CKD and ESRD patients are SIC antibody-positive (chi-square p=0.03 and ,0.001 respectively) (Figure 1). Antibody positivity to SIC seems to predict increased predisposition for both CKD and ESRD, the OR being 3.05 (95% CI 1.08, 8.61; p=0.04) and 7.22 (95% CI 2.57, 20.28; p,0.001) respectively relative to the healthy group. After adjustment for age and sex the ORs showed a similar although somewhat reduced effect: 2.33 (95% CI 0.75, 7.22; p=0.14) and 3.95 (95% CI 2.16, 21.24; p,0.001) respectively. By contrast, seropositivity to DRS in CKD or ESRD was not significantly different to that in the healthy group whether adjusted for age and sex or not (p,0.3 in all cases).. There was no evidence in this study that SIC seropositivity ...
There is a growing awareness that complement plays an integral role in human physiology and disease, with an expanding list of pathologies that are linked to
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The SCOP classification for the Complement control module/SCR domain family. Additional information, provided for both this family and the superfamily it belongs to, includes SUPERFAMILY links to genome assignments, alignments, domain combinations, taxonomic visualisation and hidden Markov model information.
Membrane cofactor protein (MCP), a regulatory molecular of the complement system with cofactor activity for the factor I-mediated inactivation of C3b and C4b, is widely distributed, being present on leukocytes, platelets, endothelial cells, epithelial cells, and fibroblasts. MCP was purified from a human T cell line (HSB2) and the NH2-terminal 24-amino acid sequence obtained by Edman degradation. An oligonucleotide probe based on this sequence was used to identify a clone from a human monocytic (U937) cDNA library. Nucleotide sequencing showed a 43-bp 5-untranslated region, an open reading frame of 1,152 bp, and a 335-bp 3-untranslated region followed by a 16-bp poly(A) track. The deduced full-length MCP protein consists of a 34-amino acid signal peptide and a 350-amino acid mature protein. The protein has, beginning at the NH2 terminus, four approximately 60-amino acid repeat units that match the consensus sequence found in a multigene family of complement regulatory proteins (C3b-receptor or ...
The complement inhibitor C4b-binding protein (C4BP) prevents necrotic cells from spilling their pro-inflammatory guts, according to a study on page 1937. Trouw and colleagues now show that C4BP and its binding partner, anticoagulant protein S (PS), cooperate to grab onto necrotic cells and to inhibit the release of cellular DNA.. C4BP short-circuits the complement cascade by binding to the activated complement components C3b and C4b and presenting them to the proteolytic complement inhibitor Factor I for degradation. This inhibitory capacity of C4BP can be coopted by bacterial pathogens, which coat themselves with this protein to avoid complement-mediated destruction by phagocytic cells.. This group recently identified a role for the C4BP-PS complex: it binds to apoptotic cells through the phosphatidylserine-binding domain of PS. This association could prevent the deposition and activation of complement on the surface of the apoptotic cells, allowing the dying cells to be removed without ...
article{b6c22ab7-8314-43e4-a60f-8c80bb2fb02a, author = {Blom, Anna and Kask, Lena and Ramesh, Bala and Hillarp, Andreas}, issn = {0003-9861}, language = {eng}, number = {2}, pages = {108--118}, publisher = {Academic Press}, series = {Archives of Biochemistry and Biophysics}, title = {Effects of zinc on factor I cofactor activity of C4b-binding protein and factor H.}, url = {http://dx.doi.org/10.1016/j.abb.2003.08.018}, volume = {418}, year = {2003 ...
Mark, L, Spiller, OB, Okroj, M, Chanas, S, Aitken, JA, Wong, SW, Damania, B, Blom, AM and Blackbourn, DJ (2007) Molecular characterization of the rhesus rhadinovirus (RRV) ORF4 gene and the RRV complement control protein it encodes ...
Protein S is a vitamin K dependent cofactor for the anticoagulant activity of activated protein C (APC). Two forms of protein S are present in plasma : free protein S (40%) and protein S linked to the C4b-binding protein (60%). Only the free form has functional cofactor activity. Protein S deficiency may be hereditary or acquired - as in normal pregnancy. It has been associated with a high risk of developing venous thromboembolism especially in young people. As only the free form of Protein S has the cofactor activity it is only this form that is measured. Measurement of Protein S in pregnancy is rarely useful.. ...
Amines, aminooxy (also known as oxylamine), hydrazide, azide, alkyne, BCN, and tyramide reactive dyes, as well as dye free acids, are generally stable in aqueous solution when stored at -20°C for 6-12 months or longer, as long as no compounds are present that may react with the dyes functional group. See the product information sheets for specific reactive dyes more information.. Coelenterazines and D-luciferin. Coelenterazines are stable in solid form when stored as recommended; they are not stable in aqueous solution. Concentrated coelenterazine stock solutions (typically 1-100 mg/mL) should be prepared in ethanol or methanol; do not use DMSO or DMF to dissolve coelenterazines, because these solvents will oxidize the compounds. Ethanol or methanol stocks of coelenterazine can be stored at -20°C or below for six months or longer; alcohol stocks may evaporate during storage, so use tightly sealing screw cap vials and wrap the vials with Parafilm for long term storage. Propylene glycol also ...
Amines, aminooxy (also known as oxylamine), hydrazide, azide, alkyne, BCN, and tyramide reactive dyes, as well as dye free acids, are generally stable in aqueous solution when stored at -20°C for 6-12 months or longer, as long as no compounds are present that may react with the dyes functional group. See the product information sheets for specific reactive dyes more information.. Coelenterazines and D-luciferin. Coelenterazines are stable in solid form when stored as recommended; they are not stable in aqueous solution. Concentrated coelenterazine stock solutions (typically 1-100 mg/mL) should be prepared in ethanol or methanol; do not use DMSO or DMF to dissolve coelenterazines, because these solvents will oxidize the compounds. Ethanol or methanol stocks of coelenterazine can be stored at -20°C or below for six months or longer; alcohol stocks may evaporate during storage, so use tightly sealing screw cap vials and wrap the vials with Parafilm for long term storage. Propylene glycol also ...
This report focuses on the global Cell Free Protein Expression status, future forecast, growth opportunity, key market and key players. The study objectives are to present the Cell Free Protein Expression development in United States, Europe and China.
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Homo sapiens membrane cofactor protein (CD46, trophoblast-lymphocyte cross-reactive antigen) (MCP), transcript variant h, mRNA. (H00004179-R27) - Products - Abnova
Homo sapiens membrane cofactor protein (CD46, trophoblast-lymphocyte cross-reactive antigen) (MCP), transcript variant n, mRNA. (H00004179-R17) - Products - Abnova
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The kidney is particularly susceptible to complement-mediated injury in a number of clinical settings, and congenital deficiency or defects in the complement-regulatory proteins MCP and factor H are strongly associated with the development of renal disease. In the current study, we demonstrated that Crry (the murine homolog of MCP in the kidney) is the only membrane-bound regulator of complement expressed by murine TECs. Crry is expressed on the cell membrane, and its expression is concentrated in the basolateral portion of the cell. Polarized TECs regulate complement more efficiently on the basolateral surface of the cells than on the apical surface, in part because of Crry expression at this site. As with renal ischemia/reperfusion (I/R) (21), chemical hypoxia of the TECs causes a reduction in surface Crry levels, and the distribution within the cell is also altered.. Spontaneous complement activation on the surface of TECs is also controlled by endogenous factor H. When rH 19-20 was added to ...
61840DNAVaccinia virus 1tttttattat ttgtacgatg tccaggataa catttttacg gataaataaa tatgaaggtg 60gagagcgtga cgttcctgac attgttggga ataggatgcg ttctatcatg ctgtactatt 120ccgtcacgac ccattaatat gaaatttaag aatagtgtgg agactgatgc taatgctaat 180tacaacatag gagacactat agaatatcta tgtctacctg gatacagaaa gcaaaaaatg 240ggacctatat atgctaaatg tacaggtact ggatggacac tctttaatca atgtattaaa 300cggagatgcc catcgcctcg agatatcgat aatggccaac ttgatattgg tggagtagac 360tttggctcta gtataacgta ctcttgtaat agcggatatc atttgatcgg tgaatctaaa 420tcgtattgtg aattaggatc tactggatct atggtatgga atcccgaggc acctatttgt 480gaatctgtta aatgccaatc ccctccatct atatccaacg gaagacataa cggatacgag 540gatttttata ccgatgggag cgttgtaact tatagttgca atagtggata ttcgttgatt 600ggtaactctg gtgtcctgtg ttcaggagga gaatggtccg atccacccac gtgtcagatt 660gttaaatgtc cacatcctac aatatcaaac ggatacttgt ctagcgggtt taaaagatca 720tactcataca acgacaatgt agactttaag tgcaagtacg gatataaact atctggttcc 780tcatcatcta cttgctctcc aggaaataca tggaagccgg aacttccaaa atgtgtacgc 8402244PRTVaccinia virus ...
In 1977, three years after the discovery of the γ-carboxy glutamic acid,1 Richard DiScipio reported on the identification of a new vitamin K-dependent protein which was named protein S.2 Three years later, Frederick Walker reported that bovine protein S functioned as a cofactor to activated protein C (APC) in the degradation of factor Va,3 and it was later shown that APC-dependent degradation of factor VIIIa in the tenase complex requires the synergistic contribution of protein S and factor V.4 In the early 1980s, Björn Dahlbäck and Johan Stenflo described the presence of two circulating forms of protein S, a free form and a complex of protein S with C4b-binding protein (C4b-BP), a regulatory protein of the complement cascade,5 with only the free protein S form functioning as a cofactor to APC.6 Association of familial protein S deficiency with recurrent thrombosis was reported in 19847 and it was soon shown that even a reduction of the free protein S form in plasma, in spite of total protein ...
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BACKGROUND:. Free protein S (that portion of plasma protein S which is not in complex with C4b binding protein) is a cofactor for the anticoagulant effect of activated protein C. Patients presenting with acute myocardial infarction have significantly reduced levels of free protein S. If the major hypothesis proved correct, patients at high risk of myocardial infarction could be identified and could be targeted for future studies to examine specific intervention therapy.. DESIGN NARRATIVE:. The blinded and prospective study began in 1992, although the grant was first awarded in 1983. The goal was to determine if low levels of free protein S were associated with an increased incidence of myocardial infarction. Plasma samples were obtained yearly from 2,224 men aged 50-59 years who were participants in the Second Northwick Park Heart Study sponsored by the British Medical Research Council Epidemiology and Medical Care Unit. Clinical endpoints for the study were documented fatal and non-fatal ...
CD59 / Complement Regulatory Protein / Protectin Antibody - Without BSA and Azide, Mouse Monoclonal Antibody [Clone SPM616 ] validated in IHC, IF, FC (AH12772-100), Abgent
Suramin is a competitive inhibitor of heparin binding to many proteins, including viral envelope proteins, protein tyrosine phosphatases, and fibroblast growth factors (FGFs). It has been clinically evaluated as a potential therapeutic in treatment of cancers caused by unregulated angiogenesis, triggered by FGFs. Although it has shown clinical promise in treatment of several cancers, suramin has many undesirable side effects. There is currently no experimental structure that reveals the molecular interactions responsible for suramin inhibition of heparin binding, which could be of potential use in structure-assisted design of improved analogues of suramin. We report the structure of suramin, in complex with the heparin-binding site of vaccinia virus complement control protein (VCP), which interacts with heparin in a geometrically similar manner to many FGFs. The larger than anticipated flexibility of suramin manifested in this structure, and other details of VCP-suramin interactions, might ...
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1- 4 I4 --- XID X-ray name, ,[MBC2005] NNNN, in Simbad 6- 12 F7.2 aW/m2 FX Flux in (0.5-10)keV band (10-15erg/cm2/s) 14- 18 F5.2 --- HR Hardness ratio 20- 24 F5.2 [10-7W] logLX ?=- X-ray luminosity in (0.5-10)keV band 26- 35 F10.6 deg RAdeg ?=- Optical right ascension (J2000) 37- 45 F9.6 deg DEdeg ?=- Optical declination (J2000) 47 I1 --- s [1/2]? Source of position (1) 49 A1 --- l_log(X/Rc) Limit flag on log(FX/FRc) 50- 54 F5.2 --- log(X/Rc) ?=- Log of X-ray to Rc optical flux ratio 56 A1 --- l_log(X/K) Limit flag on log(FX/FK) 57- 61 F5.2 --- log(X/K) ?=- Log of X-ray to K optical flux ratio 63 A1 --- l_Rc-K Limit flag on Rc-K 64- 68 F5.2 mag Rc-K ?=- Johnson-Cousins R-K colour index (2) 70 A1 --- l_[3.6/4.5] Limit flag on [3.6]-[4.5] 71- 75 F5.2 mag [3.6/4.5] ?=- IRAC [3.6]-[4.5] colour index (2) 77 A1 --- l_[5.8/8.0] Limit flag on [5.8]-[8.0] 78- 82 F5.2 mag [5.8/8.0] ?=- IRAC [5.8]-[8.0] colour index (2) 84 A1 --- l_log(24/Rc) Limit flag on log(F24/FRc) 85- 89 F5.2 --- log(24/Rc) ?=- Log of ...
By a series of chromatographic procedures involving precipitation by salt, gel filtration, anionic exchange, and hydroxyapatite elution, a protein--termed the lipopolysaccharide inactivator (LPS-I)--has been isolated from normal human serum. As a res
Daf Cf65 Daf Cf75 And Daf Cf85 Series Repair Service Manual Pdf Service Manual: 20 assigned downloads, like DAF CF65, DAF CF75 and DAF CF85 Series Repair Service Manual from autohouse
Genws o weiriau (Poaceae) a dyfir fel grawnfwyd neu fel bwyd i anifeiliaid yw sorghwm neu sorgwm. Ceir rhywogaethau yn tyfun naturiol ar hyd a lled y trofannau, ond credir bod y rhan fwyaf or mathau syn cael eu tyfu yn dod o Affrica yn wreiddiol. Lledaenwyd yr arfer o dyfu Sorghwm gan y Mwslimiaid yn y Canol Oesoedd. Ceir cofnodion fod llawer ohono yn cael ei dyfu yn Irac yn y 10g, ac roedd yn cael ei dyfu yn yr Aifft ac yn ddiweddarach yn y rhan Islamig o Sbaen. Oddi yno, lledaenodd ir rhan Gristionogol o Sbaen, ac erbyn y 12g i Ffrainc. ...
This study was initiated to explore the effect of recombinant rat Crry linked to the Fc portion of rat IgG2a (Crry-Ig) on the induction of experimental autoimmune anterior uveitis (EAAU) and on established disease. EAAU was induced in Lewis rats by immunization with bovine melanin-associated antigen (MAA). MAA sensitized animals received Crry-Ig, rat IgG2a (isotype control) or PBS separately before the onset of EAAU or after the onset of clinical disease. Administration of Crry-Ig suppressed the induction of EAAU while all animals injected with IgG2a or PBS developed the normal course of EAAU. Treatment with Crry-Ig resulted in the suppression of ocular complement activation as well as the functional activity of complement in the peripheral blood. At the peak of EAAU, levels of IFN-γ, IP-10, ICAM-1 and LECAM-1 were significantly reduced within the eyes of Crry-Ig treated Lewis rats. Importantly, administration of Crry-Ig even after the onset of EAAU resulted in a sharp decline in the disease ...
Results Brain pathological injury was the most serious at 24 h after reperfusion, The complement regulatory protein CD46 expression decreased gradually after local cerebral ischaemia-reperfusion injury, the lowest at 24 h after reperfusion, and returned to normal at 96 h after reperfusion.complement regulatory protein CD46 expression was negative correlated with brain pathological injury.. ...
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陣發性夜間血紅素尿症(paroxysmal nocturnal haemoglobinuria, PNH)是一種罕見的造血幹細胞疾病,因後天基因突變而造成[1]。一般來說,正常紅血球的細胞膜上有幾種保護性蛋白質,例如:蛋白衰變加速因子(decay accelerating factor, CD55)以及溶解細胞膜抑制物(membrane inhibitor of reactive lysis, CD59),使紅血球不會因補體(免疫系統的一部分)的攻擊而破裂[1]。然而,PNH患者因為在X染色體上的phosphatidylinositol glycan A (PIG-A)基因發生突變,造成某些醣脂質,例如glycosylphosphatidylinositols (GPI)無法形成,而使紅血球上的保護性蛋白質無法藉著GPI結合在紅血球的細胞膜上[1]。紅血球沒有這些蛋白質的保護就容易因人體內補體系統的攻擊而破裂,引起持續、慢性的血管內溶血性疾病,這也是造成疾病症狀及後續嚴重併發症的原因[2-4 ...
Goat Polyclonal Anti-Complement Component C1r Antibody [Unconjugated]. Validated: WB, IP. Tested Reactivity: Human. 100% Guaranteed.
Simpson, R. J., Florida-James, G., Whyte, G. P., Middleton, N., Shave, R., George, K. & Guy, K. (2007). The effects of marathon running on expression of the complement regulatory proteins CD55 (DAF) and CD59 (MACIF) on red blood cells. European journal of applied physiology. 99, 201-204. doi:10.1007/s00421-006-0326-2. ISSN 1439-6327. ...
Simpson, R. J., Florida-James, G., Whyte, G. P., Middleton, N., Shave, R., George, K. & Guy, K. (2007). The effects of marathon running on expression of the complement regulatory proteins CD55 (DAF) and CD59 (MACIF) on red blood cells. European journal of applied physiology. 99, 201-204. doi:10.1007/s00421-006-0326-2. ISSN 1439-6327. ...
Mouse Monoclonal Anti-Complement C4d Antibody (C4D204) [DyLight 550]. Acute Humoral Rejection Marker. Validated: ICC/IF, IHC-Fr, IHC-P. Tested Reactivity: Human. 100% Guaranteed.
Fremeaux-Bacchi, V.; Kemp, E. J.; Goodship, J. A.; Dragon-Durey, M. A.; Strain, L.; Loirat, C.; Deng, H. W.; Goodship, T. H. J. The development of atypical haemolytic-uraemic syndrome is influenced by susceptibility factors in factor H and membrane cofactor protein: evidence from two independent cohorts. Journal of medical genetics. 2005, NOV. 42(11):852-856 ...
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TIGAR Human Recombinant produced in E.Coli is a single, non-glycosylated polypeptide chain containing 270 amino acids and having a molecular mass of 30.1kDa.
this suit was fun to wear and i got a lot of complements on the fringe beads. the beads didnt get annoying in the water either! throw on some shorts and it becomes a cute top ...
Increasingly, the challenge of management is to create and supply knowledge in order to sustain organizational performance. However, few books on management strategy have been written using this concept as a foundation. This unique volume adopts a knowledge-based approach that will complement and perhaps supplant other perspectives.
Ischemia and reperfusion of organs is an unavoidable consequence of transplantation. Inflammatory events associated with reperfusion injury are in part attributed to excessive complement activation. Systemic administration of complement inhibitors reduces reperfusion injury but leaves patients vulnerable to infection. Here, we report a novel therapeutic strategy that decorates cells with an anti-complement peptide. An analog of the C3 convertase inhibitor Compstatin (C) was synthesized with a hexahistidine (His6) tag to create C-His6. To decorate cell membranes with C-His6, fusogenic lipid vesicles (FLVs) were used to incorporate lipids with nickel (Ni2+) tethers into cell membranes, and these could then couple with C-His6. Ni2+ tether levels to display C-His6 were modulated by changing FLV formulation, FLV incubation time and FLV levels. SKOV-3 cells decorated with C-His6 effectively reduced complement deposition in a classical complement activation assay. We conclude that our therapeutic ...
We describe a highly efficient two-step single-cell reverse transcriptase-polymerase chain reaction technique for analyzing gene expression at the single-cell level. Good reproducibility and a linear dose response indicated that the technique has high specificity and sensitivity for detection and quantification of rare RNA. Actin could be used as an internal standard. The expression of message for Rubisco small subunit (RbcS), chlorophyll a/b-binding protein (Cab), sucrose (Suc):fructan-6-fructosyl transferase (6-SFT), and Actin were measured in individual photosynthetic cells of the barley (Hordeum vulgare) leaf. Only Actin was found in the non-photosynthetic epidermal cells. Cab, RbcS, and 6-SFT genes were expressed at a low level in mesophyll and parenchymatous bundle sheath (BS) cells when sampled from plants held in dark for 40 h. Expression increased considerably after illumination. The amount of 6-SFT, Cab, and RbcS transcript increased more in mesophyll cells than in the parenchymatous ...
Definition of Cobra venom factor with photos and pictures, translations, sample usage, and additional links for more information.
Graduate School of Biotechnology and Ginseng Bank, College of Life Science, Kyung Hee University, Yongin 446-701, Korea, dcyang [at] khu [dot] ac [dot] kr ...
Decay-accelerating factor (CD55), a regulator of the alternative and classical pathways of complement activation, is expressed on all serum-exposed cells. It is used by pathogens, including many enteroviruses and uropathogenic Escherichia coli, as a receptor prior to infection. We describe the x-ray structure of a pathogen-binding fragment of human CD55 at 1.7 A resolution containing two of the three domains required for regulation of human complement. We have used mutagenesis to map biological functions onto the molecule; decay-accelerating activity maps to a single face of the molecule, whereas bacterial and viral pathogens recognize a variety of different sites on CD55.
CRI 213. Research Interests. Complement is a group of about 50 soluble and cell surface proteins that represent a crucial component of both the innate and adaptive immune systems. Research in the laboratory is focused on the biology of the complement system, and how it modulates an inflammatory response and shapes adaptive immunity. Within the context of complement-modulated immunity, areas of study relate to ischemic injury and disease (such as stroke, spinal cord injury and post-transplant ischemia reperfusion injury), alloimmunity (transplant rejection) and cancer immunity. A further area of study is the dual role of complement in liver injury and regeneration, important in the context of liver resection or small-for-size transplant. Integrated within these studies is the development and characterization of various site-targeted strategies for complement inhibition. These strategies (some of which are in clinical development) are being investigated in various mouse models of injury and ...
1G40: Crystal structure of a complement control protein that regulates both pathways of complement activation and binds heparan sulfate proteoglycans.
Click here to launch the GLIMPSE/MIPSGAL Image Viewer. GLIMPSE (Galactic Legacy Infrared Midplane Extraordinaire) is a survey of the inner part of the Milky Way Galaxy in which we reside. The images come from the IRAC instrument on board the Spitzer Space Telescope, one of NASAs four "Great Observatories". The telescope was pointed to 111,000 different positions in the sky and snapshots were taken in four different infrared wavelengths, creating a total of 444,000 images. The MIPSGAL survey followed up using the MIPS instrument with another 400,000 images at three longer infrared wavelengths. These surveys have 100 times the sensitivity and over 10 times the resolution of previous surveys, allowing us to see stars and dusty objects throughout most of the Galaxy for the first time.. From all this data two images have been created that you can explore on this site: the IRAC image, and the IRAC/MIPS image. If printed, each would be about 180 feet long.. ...
Quantity100 testsVolume0.4ImmunogenHuman Acute Lymphocytic Leukemia (ALL) T cellsBackground InformationCD46 (MCP; membrane cofactor protein) is a m...
Zhao F, Afonso S, Lindner S, Hartmann A, Löschmann I, Nilsson B, Ekdahl KN, Weber LT, Habbig S, Schalk G, Kirschfink M, Zipfel PF, Skerka C (2019) C3-glomerulopathy autoantibodies mediate distinct effects on complement C3- and C5-convertases. Front Immunol 10, 1030. Details PubMed Open Access PDF Zipfel PF, Wiech T, Rudnick R, Afonso S, Person F, Skerka C (2019) Complement inhibitors in clinical trials for glomerular diseases. Front Immunol 10, 2166. Details PubMed Open Access PDF ...
So, here in Arkansas we have already got way too many little bugs flying around at night. So, one day i was reading an article that suggested I give my...
Complete information for CACNA2D4 gene (Protein Coding), Calcium Voltage-Gated Channel Auxiliary Subunit Alpha2delta 4, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare disease of hematopoietic stem cells due to a mutation in the PIG-A gene leading to a deficiency of GPI-anchored proteins. Lack of two specific GPI-anchored proteins, CD55 and CD59, leads to uncontrolled complement activation that result in both intravascular and extravascular hemolysis. Free hemoglobin leads to nitric oxide depletion that mediates the pathophysiology of some of the common clinical signs of PNH. Clinical symptoms of PNH include evidence of hemolytic anemia, bone marrow failure, smooth muscle dystonias and thromboses.
Purpose: Plasmapheresis in combination with immunoglobulin and rituximab is often used to induce accommodation in ABO-incompatible (ABOi) living-donor transplantation; however, this regimen cannot be applied to cases of ABOi deceased-donor transplantation. Here, we investigated whether an anti-complement component 5 (C5) antibody-based regimen can induce accommodation in ABOi heart transplantation.. *Methods: Sensitization using human blood type A antigen, induced both IgM and IgG anti-A antibodies in wild-type mice. Heterotrophic ABOi heart transplantation was performed from human blood type A-transgenic C57BL/6J mice to sensitized syngeneic wild-type C57BL/6J or allogeneic DBA/2 mice.. *Results: Both anti-C5 antibody and triple immunosuppressants (corticosteroid, tacrolimus, mycophenolate mofetil) suppressed antibody-mediated rejection, immune cell infiltration, and deposition of IgG and C4d in ABOi heart syngrafts. Allogeneic ABOi heart transplantation induced ABMR to greater degree than ...
During sublytic complement attack on human neutrophils, plasma-membrane vesicles are shed from the cell surface as a cell-protection mechanism. By using surface-iodinated neutrophils it was found that less than 2% of surface label was recovered in shed vesicles under conditions where 40% of complement component C9 was shed. SDS/PAGE of 125I-labelled shed vesicles and plasma membranes showed differences in iodination pattern, demonstrating the sorting of membrane proteins into the shed vesicles. Analysis of 32P-labelled phospholipids after labeling of neutrophils with [32P]Pi before sublytic complement attack showed the presence of phosphatidic acid, phosphatidylcholine, phosphatidyl-ethanolamine, phosphatidylinositol and polyphosphoinositides in shed vesicles. Quantitative analysis using [3H]acetic anhydride-labelling method showed that the molar proportions of phosphatidylethanolamine, phosphatidylinositol, phosphatidylserine and sphingomyelin were the same in shed vesicles as in plasma ...
RHEUMATOID ARTHRITIS. Rheumatoid arthritis (RA) is a chronic inflammatory disease that affects mainly diarthrodial joints and periarticular structures, and can acquire a systemic character. Rheumatoid arthritis affects approximately 1% of the world population, being two to three times more common in women.1. The etiology of RA has not been completely clarified. However, environmental and genetic factors have contributed to the development of the disease. In the early stages of RA, proliferation and edema of the synovial layer cells occur, with infiltration of B and T cells, macrophages, and granulocytes. The synovium thickens, and the joint becomes swollen and painful. With progression, synovial proliferation leads to the formation of pannus, a tissue that invades the articular cartilage and bone. Joint destruction is irreversible. Osteoclasts reabsorb bone, and there is release of proteolytic enzymes, such as metal-loproteinases, aggrecanases, and cathepsins, responsible for the destruction of ...
CRP seems to be not only a biomarker for atherosclerosis but also a mediator of plaque formation.3 By binding to enzymatically degraded low-density lipoprotein, CRP is able to activate the classical pathway of complement,13 serving as a potential link between complement activation and atherosclerosis.9,10 To protect against complement-mediated cell lysis, nucleated cells express complement inhibitor proteins on their surface. By upregulating the expression of these proteins in endothelial cells, CRP may serve to protect ECs from complement-mediated injury.. The ability of CRP to bind to nucleated cells and cause complement activation without cytolysis14 has been largely attributed to its ability to recruit the inhibitory plasma protein factor H.15 However, our results indicate that CRP may play a more active, protective role by stimulating the expression of DAF, CD46, and CD59 in endothelial cells. The kinetics of DAF expression were analyzed in greater detail because DAF seems to be the most ...
miR 146a was analyzed by miRNA qRT PCR using the TaqMan MicroRNA Reverse Transcription Kit, TaqMan Fast Advance PCR Master Mix, and TaqMan MicroRNA primers. All reactions were analyzed check this using StepOne Real Time PCR System. After Inhibitors,Modulators,Libraries the collection of leukocytes with the LeukoLOCK fil ters, the leukocyte free blood was transferred to 10 ml Vacutainer SST plus blood collection tubes. Blood was centrifuged at 1,000 g for 20 minutes. The plasma was transferred to a 15 ml conical tube and stored at ?20 C. Anti dsDNA ELISA was per formed as previously described. In brief, anti human IgG secondary antibody was used and samples were con sidered positive when the absorbance was greater than the mean plus three SD from the healthy controls. Complement levels C3 and C4 complement Inhibitors,Modulators,Libraries levels were obtained from clin ical data.. C3 levels lower than 90 mg dl and C4 levels less than 15 mg dl were considered as low complement levels in the ...
The complement system is a key component of the innate immune system that is involved in eliminating unwanted self and nonself material via cellular and humoral mechanisms
The Complement System is one of the subject in which we provide homework and assignment help. Our feature includes 24x7 live online statistics tutors available to help you. You can get speedy and cost Immunology help at assignmenthelp.net
Product Name: PrEST Antigen SUSD4Synonym: FLJ10052Product Type: ChemicalCAS NO: 52-51-7Wee1 inhibitorsAssay: |80% (SDS-PAGE)Concentration:
An immune-based approach to allow antibodies in the plasma of HIV-1-infected individuals to regain their activity of antibody-dependent complement-mediated lysis (2010 ...
PGK1 an apparent multifunctional protein. A glycolytic enzyme and a polymerase alpha cofactor protein (primer recognition protein). Note: This description may include information from UniProtKB ...
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C4b-binding protein inhibits the haemolytic function of cell-bound C4b. C4b-binding protein and C3b inactivator control the C3 ... C3 convertase (EC 3.4.21.43, C42 , C4bC2b, C3bBb, complement C.hivin.4.hivin2, complement C3 convertase) belongs to family of ... "Modulation of the Classical Pathway C3 Convertase by Plasma Proteins C4 Binding Protein and C3b Inactivator". Proc Natl Acad ... complement receptor 1 (CR1), C4b-binding protein and Factor H. Convertase assembly is suppressed by the proteolytic cleavage of ...
... , also known as C3b/C4b inactivator, is a protein that in humans is encoded by the CFI gene. Complement ... is a protein of the complement system, first isolated in 1966 in guinea pig serum, that regulates complement activation by ... Maga TK, Nishimura CJ, Weaver AE, Frees KL, Smith RJ (Jun 2010). "Mutations in alternative pathway complement proteins in ... this precursor protein is then cleaved by furin to yield the mature fI protein, which is a disulfide-linked dimer of heavy ...
... cells from complement-mediated damage. CFHR5 (Complement Factor H-Related protein 5) is able to bind to act as a cofactor for ... Pangburn MK, Schreiber RD, Müller-Eberhard HJ (July 1977). "Human complement C3b inactivator: isolation, characterization, and ... there are several different kinds of regulatory proteins that disrupt the complement activation process: Complement Receptor 1 ... Factor I requires a C3b-binding protein cofactor such as complement factor H, CR1, or Membrane Cofactor of Proteolysis (MCP or ...
Complement Inactivator Proteins at the US National Library of Medicine Medical Subject Headings (MeSH). ... "regulators of complement activation (RCA)" or "complement control proteins (CCP)". Complement control proteins work in concert ... Complement control proteins also play a role in malignancy. Complement proteins protect against malignant cells- both by direct ... Most of the complement control proteins act on the convertases, C3b.Bb and C4b.2a, which are bimolecular complexes formed early ...
"Characterization of the streptococcal C5a peptidase using a C5a-green fluorescent protein fusion protein substrate". J. ... Wexler, D.E.; Chenoweth, D.E.; Cleary, P.P. (1985). "Mechanism of action of the group A streptococcal C5a inactivator". Proc. ... Bohnsack, J.F.; Mollison, K.W.; Buko, A.M.; Ashworth, J.C.; Hill, H.R. (1991). "Group B streptococci inactivate complement ...
... complement c1 inactivator proteins MeSH D12.776.124.486.274.920.250.500 -- complement c1 inhibitor protein MeSH D12.776.124.486 ... complement c3b inactivator proteins MeSH D12.776.124.486.274.920.325.200 -- complement factor h MeSH D12.776.124.486.274.920. ... complement factor b MeSH D12.776.124.486.274.920 -- complement inactivator proteins MeSH D12.776.124.486.274.920.124 -- ... 325.210 -- complement factor i MeSH D12.776.124.486.274.920.662 -- complement c4b-binding protein MeSH D12.776.124.486.274.930 ...
M protein also inhibits opsonization by the alternative complement pathway by binding to host complement regulators. The M ... Wexler DE, Chenoweth DE, Cleary PP (1985). "Mechanism of action of the group A streptococcal C5a inactivator". Proc Natl Acad ... In addition, the capsule and several factors embedded in the cell wall, including M protein, lipoteichoic acid, and protein F ( ... as antibodies produced by the immune system against M protein target the bacteria for engulfment by phagocytes. M proteins are ...
Dai L, Song J, Lu X, Deng YQ, et al «Structures of the Zika Virus Envelope Protein and Its Complex with a Flavivirus Broadly ... Yu Y, Deng YQ, Zou P, Wang Q, et al «A peptide-based viral inactivator inhibits Zika virus infection in pregnant mice and ... fet que podria desencadenar una resposta defensiva del cos contra el virus i també contra el seu propi sistema del complement, ... Liang, Q; Luo, Z; Zeng, J; Chen, W; et al «Zika Virus NS4A and NS4B Proteins Deregulate Akt-mTOR Signaling in Human Fetal ...
Protein Coding), Complement Factor I, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards ... Cloning and characterization of the promoter for the human complement factor I (C3b/C4b inactivator) gene. (PMID: 9479036) ... Protein Symbol:. P05156-CFAI_HUMAN. Recommended name:. Complement factor I Protein Accession:. P05156. Secondary Accessions: * ... CFI (Complement Factor I) is a Protein Coding gene. Diseases associated with CFI include Complement Factor I Deficiency and ...
Complement C1 Inactivator Proteins/analysis. *Complement C1 Inactivator Proteins/genetics*. *DNA/blood ... Identical single-base changes in the C1 inhibitor gene that may result in dysfunctional inhibitor proteins are described in two ...
Complement Factor I Antibody (Internal), Rabbit Anti Human Polyclonal Antibody validated in WB, IHC-P (ALS17749), Abgent ... CFI, AHUS3, C3BINA, C3b-inactivator, C3B/C4B inactivator, Complement component I, Complement component factor i, Factor I, FI, ... The Autophagy Receptor Motif Plotter predicts and scores autophagy receptor binding sites in your protein. Identifying proteins ... KAF, I factor, I factor (complement), C3b-INA, Complement factor I, Light chain of factor I. ...
... protein, the main function of which is the inhibition of the complement system to prevent spontaneous activation. fact lexicon ... Complement c1 inactivator proteins (C1-inhibitor) -- a serine protease inhibitor (serpin) ... Complement c1 inactivator proteins (C1-inhibitor) C1-inhibitor. also called Complement c1 inactivator proteins and has 6 more ... a serine protease inhibitor (serpin) protein, the main function of which is the inhibition of the complement system to prevent ...
Complement C1s. Complement C1 Inhibitor Protein. Complement C1 Inactivator Proteins. Immunologic Factors. Physiological Effects ... Complement C4 Serum Levels [ Time Frame: Pre-infusion to 1 hour post-infusion ]. Change in complement C4 serum levels from pre- ... Drug Information available for: SERPING1 protein, human Genetic and Rare Diseases Information Center resources: Hereditary ...
Complement C1s. Complement C1 Inhibitor Protein. Complement C1 Inactivator Proteins. Immunologic Factors. Physiological Effects ... Drug Information available for: SERPING1 protein, human Genetic and Rare Diseases Information Center resources: Hereditary ... and C1-Inhibitor antigen in normal or elevated concentration of dysfunctional protein). ...
... was recognized in whole normal human serum and separated from C3b inactivator by its distinct physicochemical and functional ... Control of the amplification convertase of complement by the plasma protein beta1H. J M Weiler, M R Daha, K F Austen, and D T ... Control of the amplification convertase of complement by the plasma protein beta1H ... Control of the amplification convertase of complement by the plasma protein beta1H ...
Complement C3b inactivator immunological test system.. II. 866.5270. C-reactive protein immunological test system.. II. ... Complement components immunological test system.. II. 866.5250. Complement C[bdi2] inhibitor (inactivator) immunological test ... Bence-Jones proteins immunological test system.. II. 866.5240. ...
0/Complement C1 Inactivator Proteins; 0/Complement C1 Inhibitor Protein; 0/Estrogen Antagonists; 0/SERPING1 protein, human; ... Complement C1 Inactivator Proteins / adverse effects, therapeutic use. Complement C1 Inhibitor Protein / metabolism. Danazol / ...
Complement C1 Inactivator Proteins/chemistry. Complement C1 Inactivator Proteins/genetics. Complement C1 Inhibitor Protein/ ... 0 (Antifibrinolytic Agents); 0 (Complement C1 Inactivator Proteins); 0 (Complement C1 Inhibitor Protein); 0 (Complement ... Complement C1 Inactivator Proteins); 0 (Complement C1 Inhibitor Protein); 0 (Kinins); 0 (SERPING1 protein, human); 9001-30-3 ( ... Complement C1 Inactivator Proteins); 0 (Complement C1 Inhibitor Protein); 0 (Peptides); 0 (Recombinant Proteins); 0 (SERPING1 ...
Complement C1 Inactivator Proteins / analysis, immunology*. Enzyme-Linked Immunosorbent Assay. Female. Follow-Up Studies. ... 0/Antibodies, Anti-Idiotypic; 0/Complement C1 Inactivator Proteins; 0/Immunoglobulin A; 0/Immunoglobulin G; 0/Immunoglobulin M ... We studied the clinical features, complement profiles, and associated diseases in 19 new patients with diagnosed acquired ... angioedema type 2. SUBJECTS AND METHODS: Plasma concentrations and functional activity of complement components were measured ...
Compstatin, a 13-residue peptide, is an effective inhibitor of the activation of complement component C3 and thus blocks a ... Undesired complement activation is a major cause of tissue injury in various pathological conditions and contributes to several ... Complement Inactivator Proteins / pharmacology* Actions. * Search in PubMed * Search in MeSH * Add to Search ... The Emerging Role of Complement Proteins as a Target for Therapy of IgA Nephropathy. Rizk DV, Maillard N, Julian BA, Knoppova B ...
Complement System Proteins [D12.776.124.486.274]. *Complement Inactivator Proteins [D12.776.124.486.274.920] ... COMPLEMENT FACTOR H; COMPLEMENT FACTOR I). This abnormally stabilized enzyme induces a continuous COMPLEMENT ACTIVATION and ... "Complement C3 Nephritic Factor" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH ( ... This graph shows the total number of publications written about "Complement C3 Nephritic Factor" by people in Harvard Catalyst ...
Complement C1 Inactivator Proteins [D12.776.124.486.274.920.250]. *Complement C1 Inhibitor Protein [D12.776.124.486.274.920. ... "Complement C1 Inhibitor Protein" by people in Harvard Catalyst Profiles by year, and whether "Complement C1 Inhibitor Protein" ... "Complement C1 Inhibitor Protein" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH ( ... including the COMPLEMENT C1R and the COMPLEMENT C1S proteases of the CLASSICAL COMPLEMENT PATHWAY, and the MANNOSE-BINDING ...
Complement Inactivator Proteins at the US National Library of Medicine Medical Subject Headings (MeSH). ... "regulators of complement activation (RCA)" or "complement control proteins (CCP)". Complement control proteins work in concert ... Complement control proteins also play a role in malignancy. Complement proteins protect against malignant cells- both by direct ... Most of the complement control proteins act on the convertases, C3b.Bb and C4b.2a, which are bimolecular complexes formed early ...
Complement C1 Inactivator Proteins/genetics/metabolism*. Minor. *Animals. *Case-Control Studies. *Female ... Molecular weights of the marker proteins are depicted in kDa to the right. Proteins were visualized using silver staining. ... Molecular weights of the marker proteins are depicted in kDa to the right. Proteins were visualized using silver staining. ... Proteins were visualized using silver staining. B): SDS PAGE analysis of BS3 conjugated pC1-inh (lane 1), pC1-inh (lane 2), ...
If the C3b inactivator protein is impaired, the complement system gets completed and causes RBC destruction4. In PCH, the cold ... which lack proteolytically cleaved complement on their surface and inhibit complement-mediated lysis9. Steroid is beneficial in ... This binding time is sufficient to activate the complement cascade to stage C3b. Many C3b RBCs escape the macrophages in ... PCH - paroxysmal cold hemoglobinuria, DAT- direct antiglobulin test, C3 - complement third component, RBC -Red blood cell) ...
Carboxypeptidase R is an inactivator of complement-derived inflammatory peptides and an inhibitor of fibrinolysis. Immunol. Rev ... Activated protein C suppresses tissue factor expression on U937 cells in the endothelial protein C receptor-dependent manner. ... The endothelial cell protein C receptor augments protein C activation by the thrombin-thrombomodulin complex. Proc. Natl. Acad ... Activation mechanism of anticoagulant protein C in large blood vessels involving the endothelial cell protein C receptor. J. ...
Rabbit recombinant monoclonal C4 binding protein/C4BPB antibody [EPR17101]. Validated in WB, IP, IHC, ICC/IF and tested in Rat ... It binds as a cofactor to C3b/C4b inactivator (C3bINA), which then hydrolyzes the complement fragment C4b. It also accelerates ... Anti-C4 binding protein/C4BPB antibody [EPR17101]. See all C4 binding protein/C4BPB primary antibodies. ... It also interacts with anticoagulant protein S and with serum amyloid P component. The beta chain binds protein S. ...
Protein Coding), Complement Component 4 Binding Protein Alpha, including: function, proteins, disorders, pathways, orthologs, ... It binds as a cofactor to C3b/C4b inactivator (C3bINA), which then hydrolyzes the complement fragment C4b. It also accelerates ... Protein Symbol:. P04003-C4BPA_HUMAN. Recommended name:. C4b-binding protein alpha chain. Protein Accession:. P04003. Secondary ... Proline-rich protein (C4BPA_HUMAN). *cDNA, FLJ93660, Homo sapiens complement component 4 binding protein, alpha (C4BPA),mRNA ( ...
Human papillomavirus 16 E7 inactivator of retinoblastoma family proteins complements human cytomegalovirus lacking UL97 protein ... Lamin A/C proteins tether the pRB and p107 proteins to perinucleolar foci that are required for their function (20, 33). ... Protein array identification of substrates of the Epstein-Barr virus protein kinase BGLF4. J. Virol. 83:5219-5231. ... EBV-PK is the only protein kinase encoded by the EBV genome (6) and is expressed as an early lytic viral protein during viral ...
Complement factor I, also known as C3b/C4b inactivator, is a protein that in humans is encoded by the CFI gene. Complement ... is a protein of the complement system, first isolated in 1966 in guinea pig serum, that regulates complement activation by ... Maga TK, Nishimura CJ, Weaver AE, Frees KL, Smith RJ (Jun 2010). "Mutations in alternative pathway complement proteins in ... this precursor protein is then cleaved by furin to yield the mature fI protein, which is a disulfide-linked dimer of heavy ...
Complement Factor I Monoclonal Antibody (Clone OX-21)-NP_000195.2 (MBS245037) product datasheet at MyBioSource, Primary ... NCBI Protein Information complement factor I; C3b-inactivator; C3B/C4B inactivator; complement component I; light chain of ... C3b-inactivator; C3B/C4B inactivator; Complement component I; Complement component factor i; Factor I; FI; KAF; I factor; I ... UniProt Protein Name Complement factor I UniProt Synonym Protein Names C3B/C4B inactivatorCleaved into the following 2 chains: ...
These findings indicate a strong restriction of distinct borrelial proteins towards binding of polymorphic FH of various ... Association with and adaption to various hosts most likely correlates with the spirochetes ability to acquire complement ... These findings indicate a strong restriction of distinct borrelial proteins towards binding of polymorphic FH of various ... Association with and adaption to various hosts most likely correlates with the spirochetes ability to acquire complement ...
OR ffp.mp.) AND (exp Complement C1 Inactivator Proteins/ OR exp Complement C1 Inhibitor Protein/ OR exp Complement C1/ OR c1 ...
  • Identical single-base changes in the C1 inhibitor gene that may result in dysfunctional inhibitor proteins are described in two different families with type II hereditary angioneurotic edema. (nih.gov)
  • The inhibitory activity was found to reside in a protein that was purified to homogeneity and elicited a monospecific antibody in a rabbit. (pnas.org)
  • Complement control proteins work in concert to regulate the system and keep it from damaging host tissue while simultaneously directing it towards foreign particles such as viruses and bacteria, and unwanted material such as cell debris and antibody-antigen complexes. (wikipedia.org)
  • Complement proteins protect against malignant cells- both by direct complement attack and through initiation of Complement-dependent cytotoxicity, which synergises with specific monoclonal antibody therapies. (wikipedia.org)
  • The mouse monoclonal antibody recognizes human Complement component 4 c (C4c), a component in the complement cascade and a degradation product of C4b which is cleaved by C4b/C3b inactivator to yield C4d and C4c. (cellsciences.com)
  • The C3b cleavage product iC3b binds to tumor cells and through the interaction with complement receptor 3 (CD11b/CD18) on mononuclear phagocytes and natural killer (NK) cells enhances antibody-dependent cellular cytotoxicity (ADCC). (nih.gov)
  • Immunization with both protein and DNA vaccines resulted in a Th1-type T-cell response, comparable antibody titers, and similar immunoglobulin G isotype profiles. (asm.org)
  • Immune Blotting Western Blot Test Flow Cytometry and Fluorescence Western blotting technique is used for iden- The fluorescent antibody techniques are ex- tification of a specific protein in a complex tremely valuable qualitative tools, but they mixture of proteins. (gurmeeteater.ee)
  • An inhibitory activity for an erythrocyte in termediate bearing the properdin (P)-stabilized amplification C3 convertase, PC3bBb, was recognized in whole normal human serum and separated from C3b inactivator by its distinct physicochemical and functional characteristics. (pnas.org)
  • This protein was identified as beta1H and found to have a serum concentration of 516 +/- 89 mug/ml (mean +/- 1 SD). (pnas.org)
  • It also interacts with anticoagulant protein S and with serum amyloid P component. (abcam.com)
  • Resistance to complement mediated killing, or serum resistance, is a common trait of pathogenic bacteria. (semanticscholar.org)
  • The complex is believed to be unstable until it binds properdin, a serum protein. (wikipedia.org)
  • Group A streptococci possess a wide variety of virulence factors, including M protein, hyaluronic acid capsule, serum opacity factor, C5a peptidase, and extracellular enzymes and toxins ( 8 ). (asm.org)
  • Borrelia burgdorferi has developed efficient mechanisms for evading the innate immune response during mammalian infection and has been shown to be resistant to the complement-mediated bactericidal activity of human serum. (asm.org)
  • The combined data lead us to conclude that the CspA-mediated binding of human FH confers serum resistance by directly inhibiting complement deposition on the surface of B. burgdorferi . (asm.org)
  • In fact, with regard to the major borrelial genospecies that cause Lyme disease, B. burgdorferi and Borrelia afzelii are resistant to the complement-mediated bactericidal activity of serum, while most strains of Borrelia garinii are killed by human serum ( 4 , 7 , 10 , 48 ). (asm.org)
  • Many human pathogens, including serum-resistant B. burgdorferi , evade complement destruction by binding complement factor H (FH) and FH-like protein 1 (FHL-1) ( 4 , 29 , 32 , 40 , 55 ). (asm.org)
  • Consistent with this notion, the terminal complement components (C5b, C6, C7, C8, and C9) are deposited more efficiently and abundantly on the surface of serum-sensitive strains of Borrelia spp. (asm.org)
  • A unique monoclonal Ig λ light chain dimer (protein LOI) was isolated from the serum and urine of a patient with hypocomplementemic membranoproliferative glomerulonephritis. (jimmunol.org)
  • According to Figure 1-D, the epithelium of the anterior midgut was slightly marked by MAC proteins after the forced feeding with 50 µL of normal human serum. (nih.gov)
  • Kirjavainen V, Jarva H, Biedzka Sarek M, Blom A, Skurnik M, Meri S. Yersinia enterocolitica serum resistance proteins YadA and ail bind the complement regulator C4b-binding protein. (labome.org)
  • Two types exist: type I, in which reduced serum levels of functionally active C1 inactivator occur, and type II, in which normal or even elevated levels of functionally inactive C1 inactivator are present. (viracor-eurofins.com)
  • However, an acute phase response may obscure complement consumption since the rate of breakdown may be matched by the increase rate of synthesis with resultant normal levels in the serum. (tripod.com)
  • Serum levels of complement components tend to increase during infections as part of an acute phase response. (tripod.com)
  • FH6,7/Fc bound strongly to each of seven NTHi clinical isolates tested and efficiently promoted complement-mediated killing by normal human serum. (frontiersin.org)
  • Complement System 7 The complement system includes serum and activate or inhibit reactions in the cascade. (gurmeeteater.ee)
  • The importance of complement regulation for good health is highlighted by recent work that seems to imply that individuals carrying point mutations or single nucleotide polymorphisms in their genes for factor H may be more susceptible to diseases including atypical hemolytic uremic syndrome, dense deposit diseases (or membranoproliferative glomrulonephritis type 2) and - most notably because of its prevalence in the elderly - age-related macular degeneration. (wikipedia.org)
  • The C4 protein derives from the C4A-C4B genes. (cellsciences.com)
  • Deletion of complement factor H-related genes CFHR1 and CFHR3 is associated with atypical hemolytic uremic syndrome. (cdc.gov)
  • Differential gene expression in the RPE cells of complement factor genes was identified using gene arrays, and selected gene transcripts were validated by q-RT-PCR. (forskningsdatabasen.dk)
  • One role of UL97 is to inactivate the retinoblastoma tumor suppressor protein (pRb), which is a key regulator of cellular genes. (lsuhscmicrobiology.com)
  • Large, international, genome-wide association studies have shown that deletion of complement factor H-related genes 1 and 3 ( CFHR3,1Δ ) is associated with a reduced risk of developing IgAN, although the prognostic value of these deletions in IgAN remains unknown. (cdc.gov)
  • Our recent genome-wide association study of IgAN identified susceptibility loci on 1q32 containing the complement regulatory protein-encoding genes CFH and CFHR1-5, with rs6677604 in CFH as the top single-nucleotide polymorphism and CFHR3-1 deletion (CFHR3-1∆) as the top signal for copy number variation. (cdc.gov)
  • The terminal complement complex (TCC) is thought to contribute to complement-dependent cytotoxicity (CDC), which is one of the mechanisms for eliminating tumor cells by therapeutic antibodies. (nih.gov)
  • Check out links to articles that cite our custom service antibodies, peptides, and proteins in major peer-reviewed journals, organized by research category. (abgent.com)
  • Monitoring patients with the C1q assay, which detects antibodies that fix complement, offers a minimally invasive means of identifying patients at risk for transplant glomerulopathy and graft loss. (labome.org)
  • Only mice immunized with the crp DNA plasmid produced antibodies capable of lysing the parasites in the presence of complement and were protected against a lethal challenge with T. cruzi trypomastigotes. (asm.org)
  • Antibodies that block the complement regulatory activity of the CRP promote complement-mediated lysis of the parasites and have been detected in sera from chagasic patients ( 15 ). (asm.org)
  • In renal transplant, the allograft is responsible for triggering many innate and adaptive immune mechanisms, either mediated by cells, such as macrophages and lymphocytes, or by soluble components, such as antibodies and the complement system, which can ultimately lead to graft rejection [ 1 ]. (hindawi.com)
  • However, the M protein is also the weakest point in this pathogen's defense, as antibodies produced by the immune system against M protein target the bacteria for engulfment by phagocytes. (wikipedia.org)
  • C-reactive protein (CRP) is the major acute phase protein in humans. (semanticscholar.org)
  • Respiratory droplets(M12) Hand contact with nasal discharge and skin contact with impetigo lesions The pathogen can also be found in its carrier state (anus, vagina, skin, pharynx) Can also be spread from cattle to humans through raw milk and contaminated foods (salads, milk, eggs) In 1928, Rebecca Lancefield published a method for serotyping S. pyogenes based on its M protein, a virulence factor displayed on its surface. (wikipedia.org)
  • The M protein binding site was initially localized to SCRs 6 to 15 as demonstrated by ligand dot blotting, chemical cross-linking, and enzyme-linked immunosorbent assay. (asm.org)
  • Poxviruses, unlike some other large DNA viruses, do not undergo a latent stage but rely on the expression of viral proteins to evade host immune responses. (nih.gov)
  • Characterization of complement factor H-related (CFHR) proteins in plasma reveals novel genetic variations of CFHR1 associated with atypical hemolytic uremic syndrome. (cdc.gov)
  • Several polymorphisms in the complement components factor H and CFHR1 are associated with higher risk to develop atypical Haemolytic Uraemic Syndrome (aHUS) in Caucasians. (cdc.gov)
  • CFHR1 and CFHR3, on 1q31.3, may be involved in the regulation of complement during synapse elimination, and were found to be deleted in a Z-RTT but duplicated in two classic patients. (cdc.gov)
  • The stabilization of C3bBb by activated properdin minimizes intrinsic decay and protects C3b in the bimolecular complex from C3b inactivator. (pnas.org)
  • Complement C3 Nephritic Factor" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (harvard.edu)
  • This is a sub-part (blood proteins only) of List of MeSH codes (D12.776), itself a part of the list of the "D" codes for MeSH. (wikipedia.org)
  • TM is a complex membrane protein with a lectin-like domain from the amino terminus, six epidermal growth factor (EGF)-like repeats, a region with O-linked sugar addition sites that also contains the sites for the addition of chondroitin sulfates, a transmembrane domain, and a short cytoplasmic tail. (rupress.org)
  • Outer-membrane protein P5 has been implicated in FH binding by NTHi, and FH6,7/Fc binding was greatly diminished in five of seven P5 deficient isogenic mutant strains tested, implicating an alternative FH binding protein in some strains. (frontiersin.org)
  • It was also established that naturally occurring steroids, e.g. hydrocortisone and cortisone, did not inhibit human complement activity under similar conditions. (nih.gov)