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 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 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.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 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 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 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 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).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 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 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.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.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 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 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.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 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).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 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.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 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 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 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.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.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 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 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.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 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 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.Complement C2a: The COOH-terminal fragment of COMPLEMENT 2, released by the action of activated COMPLEMENT C1S. It is a SERINE PROTEASE. C2a combines with COMPLEMENT C4B to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE).Receptor, Anaphylatoxin C5a: A G-protein-coupled receptor that signals an increase in intracellular calcium in response to the potent ANAPHYLATOXIN peptide COMPLEMENT C5A.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 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 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 C1 Inactivator Proteins: Serum proteins that inhibit, antagonize, or inactivate COMPLEMENT C1 or its subunits.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.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 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 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.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 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.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.Complement C3-C5 Convertases, Classical Pathway: Important enzymes in the CLASSICAL COMPLEMENT ACTIVATION PATHWAY. They cleave COMPLEMENT C3 and COMPLEMENT C5.Complement C2b: The N-terminal fragment of COMPLEMENT 2, released by the action of activated COMPLEMENT C1S.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)Cobra Venoms: Venoms from snakes of the genus Naja (family Elapidae). They contain many specific proteins that have cytotoxic, hemolytic, neurotoxic, and other properties. Like other elapid venoms, they are rich in enzymes. They include cobramines and cobralysins.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.Steroid 21-Hydroxylase: An adrenal microsomal cytochrome P450 enzyme that catalyzes the 21-hydroxylation of steroids in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP21 gene, converts progesterones to precursors of adrenal steroid hormones (CORTICOSTERONE; HYDROCORTISONE). Defects in CYP21 cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL).Complement C3-C5 Convertases, Alternative Pathway: Important enzymes in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY. They cleave COMPLEMENT C3 and COMPLEMENT C5.Complement C1 Inhibitor Protein: An endogenous 105-kDa plasma glycoprotein produced primarily by the LIVER and MONOCYTES. It inhibits a broad spectrum of proteases, including the COMPLEMENT C1R and the COMPLEMENT C1S proteases of the CLASSICAL COMPLEMENT PATHWAY, and the MANNOSE-BINDING PROTEIN-ASSOCIATED SERINE PROTEASES. C1-INH-deficient individuals suffer from HEREDITARY ANGIOEDEMA TYPES I AND II.Immunoglobulin G: The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.Hemolysis: The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.Complement C3 Convertase, Alternative Pathway: A serine protease that is the complex of COMPLEMENT C3B and COMPLEMENT FACTOR BB. It cleaves multiple COMPLEMENT C3 into COMPLEMENT C3A (anaphylatoxin) and COMPLEMENT C3B in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY.Complement C5 Convertase, Classical Pathway: A serine protease that cleaves multiple COMPLEMENT 5 into COMPLEMENT 5A (anaphylatoxin) and COMPLEMENT 5B in the CLASSICAL COMPLEMENT ACTIVATION PATHWAY. It is a complex of CLASSICAL PATHWAY C3 CONVERTASE (C4b2a) with an additional COMPLEMENT C3B, or C4b2a3b.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Complement C3 Convertase, Classical Pathway: A serine protease that cleaves multiple COMPLEMENT 3 into COMPLEMENT 3A (anaphylatoxin) and COMPLEMENT 3B in the CLASSICAL COMPLEMENT ACTIVATION PATHWAY. It is a complex of COMPLEMENT 4B and COMPLEMENT 2A (C4b2a).Antigens, CD46: A ubiquitously expressed complement receptor that binds COMPLEMENT C3B and COMPLEMENT C4B and serves as a cofactor for their inactivation. CD46 also interacts with a wide variety of pathogens and mediates immune response.Opsonin Proteins: Proteins that bind to particles and cells to increase susceptibility to PHAGOCYTOSIS, especially ANTIBODIES bound to EPITOPES that attach to FC RECEPTORS. COMPLEMENT C3B may also participate.Blood Proteins: Proteins that are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.Lupus Erythematosus, Systemic: A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.Complement C5 Convertase, Alternative Pathway: A serine protease that cleaves multiple COMPLEMENT C5 into COMPLEMENT C5A (anaphylatoxin) and COMPLEMENT C5B in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY. It is the complex of ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb) with an additional COMPLEMENT C3B, or C3bBb3b.Phagocytosis: The engulfing and degradation of microorganisms; other cells that are dead, dying, or pathogenic; and foreign particles by phagocytic cells (PHAGOCYTES).Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.Complement Pathway, Mannose-Binding Lectin: Complement activation triggered by the interaction of microbial POLYSACCHARIDES with serum MANNOSE-BINDING LECTIN resulting in the activation of MANNOSE-BINDING PROTEIN-ASSOCIATED SERINE PROTEASES. As in the classical pathway, MASPs cleave COMPLEMENT C4 and COMPLEMENT C2 to form C3 CONVERTASE (C4B2A) and the subsequent C5 CONVERTASE (C4B2A3B) leading to cleavage of COMPLEMENT C5 and assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.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 C5a, des-Arginine: A derivative of complement C5a, generated when the carboxy-terminal ARGININE is removed by CARBOXYPEPTIDASE B present in normal human serum. C5a des-Arg shows complete loss of spasmogenic activity though it retains some chemotactic ability (CHEMOATTRACTANTS).Mice, Inbred C57BLMacrophage-1 Antigen: An adhesion-promoting leukocyte surface membrane heterodimer. The alpha subunit consists of the CD11b ANTIGEN and the beta subunit the CD18 ANTIGEN. The antigen, which is an integrin, functions both as a receptor for complement 3 and in cell-cell and cell-substrate adhesive interactions.Protein Binding: The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.Neutrophils: Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Kidney Glomerulus: A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.Serum: The clear portion of BLOOD that is left after BLOOD COAGULATION to remove BLOOD CELLS and clotting proteins.Glomerulonephritis, Membranoproliferative: Chronic glomerulonephritis characterized histologically by proliferation of MESANGIAL CELLS, increase in the MESANGIAL EXTRACELLULAR MATRIX, and a thickening of the glomerular capillary walls. This may appear as a primary disorder or secondary to other diseases including infections and autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Various subtypes are classified by their abnormal ultrastructures and immune deposits. Hypocomplementemia is a characteristic feature of all types of MPGN.Immunoglobulin M: A class of immunoglobulin bearing mu chains (IMMUNOGLOBULIN MU-CHAINS). IgM can fix COMPLEMENT. The name comes from its high molecular weight and originally being called a macroglobulin.Schistosoma: A genus of trematode flukes belonging to the family Schistosomatidae. There are over a dozen species. These parasites are found in man and other mammals. Snails are the intermediate hosts.Genetic Complementation Test: A test used to determine whether or not complementation (compensation in the form of dominance) will occur in a cell with a given mutant phenotype when another mutant genome, encoding the same mutant phenotype, is introduced into that cell.Enzyme-Linked Immunosorbent Assay: An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.Mice, Knockout: Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.Glomerulonephritis: Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.Arteriolosclerosis: Thickening of the walls of small ARTERIES or ARTERIOLES due to cell proliferation or HYALINE deposition.Antibodies, Monoclonal: Antibodies produced by a single clone of cells.Major Histocompatibility Complex: The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) TRANSPLANTATION ANTIGENS, genes which control the structure of the IMMUNE RESPONSE-ASSOCIATED ANTIGENS, HUMAN; the IMMUNE RESPONSE GENES which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement.Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.Autoantibodies: Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.RNA, Messenger: RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.Macrophages: The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)Cell Line: Established cell cultures that have the potential to propagate indefinitely.Immunity, Innate: The capacity of a normal organism to remain unaffected by microorganisms and their toxins. It results from the presence of naturally occurring ANTI-INFECTIVE AGENTS, constitutional factors such as BODY TEMPERATURE and immediate acting immune cells such as NATURAL KILLER CELLS.Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.Mutation: Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.Rabbits: The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.Disease Models, Animal: Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.Cloning, Molecular: The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.Mice, Inbred BALB CBinding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Blood Bactericidal Activity: The natural bactericidal property of BLOOD due to normally occurring antibacterial substances such as beta lysin, leukin, etc. This activity needs to be distinguished from the bactericidal activity contained in a patient's serum as a result of antimicrobial therapy, which is measured by a SERUM BACTERICIDAL TEST.Antigens, CD: Differentiation antigens residing on mammalian leukocytes. CD stands for cluster of differentiation, which refers to groups of monoclonal antibodies that show similar reactivity with certain subpopulations of antigens of a particular lineage or differentiation stage. The subpopulations of antigens are also known by the same CD designation.Electrophoresis, Polyacrylamide Gel: Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.Mannose-Binding Lectin: A specific mannose-binding member of the collectin family of lectins. It binds to carbohydrate groups on invading pathogens and plays a key role in the MANNOSE-BINDING LECTIN COMPLEMENT PATHWAY.Alleles: Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).Recombinant Proteins: Proteins prepared by recombinant DNA technology.Complement C3 Nephritic Factor: An IgG autoantibody against the ALTERNATIVE PATHWAY C3 CONVERTASE, found in serum of patients with MESANGIOCAPILLARY GLOMERULONEPHRITIS. The binding of this autoantibody to C3bBb stabilizes the enzyme thus reduces the actions of C3b inactivators (COMPLEMENT FACTOR H; COMPLEMENT FACTOR I). This abnormally stabilized enzyme induces a continuous COMPLEMENT ACTIVATION and generation of C3b thereby promoting the assembly of MEMBRANE ATTACK COMPLEX and cytolysis.Glycoproteins: Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.Immunoglobulins: Multi-subunit proteins which function in IMMUNITY. They are produced by B LYMPHOCYTES from the IMMUNOGLOBULIN GENES. They are comprised of two heavy (IMMUNOGLOBULIN HEAVY CHAINS) and two light chains (IMMUNOGLOBULIN LIGHT CHAINS) with additional ancillary polypeptide chains depending on their isoforms. The variety of isoforms include monomeric or polymeric forms, and transmembrane forms (B-CELL ANTIGEN RECEPTORS) or secreted forms (ANTIBODIES). They are divided by the amino acid sequence of their heavy chains into five classes (IMMUNOGLOBULIN A; IMMUNOGLOBULIN D; IMMUNOGLOBULIN E; IMMUNOGLOBULIN G; IMMUNOGLOBULIN M) and various subclasses.Haptoglobins: Plasma glycoproteins that form a stable complex with hemoglobin to aid the recycling of heme iron. They are encoded in man by a gene on the short arm of chromosome 16.DNA: A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).Surface Plasmon Resonance: A biosensing technique in which biomolecules capable of binding to specific analytes or ligands are first immobilized on one side of a metallic film. Light is then focused on the opposite side of the film to excite the surface plasmons, that is, the oscillations of free electrons propagating along the film's surface. The refractive index of light reflecting off this surface is measured. When the immobilized biomolecules are bound by their ligands, an alteration in surface plasmons on the opposite side of the film is created which is directly proportional to the change in bound, or adsorbed, mass. Binding is measured by changes in the refractive index. The technique is used to study biomolecular interactions, such as antigen-antibody binding.Peptides, Cyclic: Peptides whose amino and carboxy ends are linked together with a peptide bond forming a circular chain. Some of them are ANTI-INFECTIVE AGENTS. Some of them are biosynthesized non-ribosomally (PEPTIDE BIOSYNTHESIS, NON-RIBOSOMAL).Lupus Nephritis: Glomerulonephritis associated with autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Lupus nephritis is histologically classified into 6 classes: class I - normal glomeruli, class II - pure mesangial alterations, class III - focal segmental glomerulonephritis, class IV - diffuse glomerulonephritis, class V - diffuse membranous glomerulonephritis, and class VI - advanced sclerosing glomerulonephritis (The World Health Organization classification 1982).Antibodies, Antinuclear: Autoantibodies directed against various nuclear antigens including DNA, RNA, histones, acidic nuclear proteins, or complexes of these molecular elements. Antinuclear antibodies are found in systemic autoimmune diseases including systemic lupus erythematosus, Sjogren's syndrome, scleroderma, polymyositis, and mixed connective tissue disease.Sequence Homology, Amino Acid: The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.Blotting, Western: Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.Cosmids: Plasmids containing at least one cos (cohesive-end site) of PHAGE LAMBDA. They are used as cloning vehicles.Polymerase Chain Reaction: In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.Bacterial Proteins: Proteins found in any species of bacterium.Gene Expression Regulation: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.Biological Markers: Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.Mannose-Binding Protein-Associated Serine Proteases: Serum serine proteases which participate in COMPLEMENT ACTIVATION. They are activated when complexed with the MANNOSE-BINDING LECTIN, therefore also known as Mannose-binding protein-Associated Serine Proteases (MASPs). They cleave COMPLEMENT C4 and COMPLEMENT C2 to form C4b2a, the CLASSICAL PATHWAY C3 CONVERTASE.Adrenal Hyperplasia, Congenital: A group of inherited disorders of the ADRENAL GLANDS, caused by enzyme defects in the synthesis of cortisol (HYDROCORTISONE) and/or ALDOSTERONE leading to accumulation of precursors for ANDROGENS. Depending on the hormone imbalance, congenital adrenal hyperplasia can be classified as salt-wasting, hypertensive, virilizing, or feminizing. Defects in STEROID 21-HYDROXYLASE; STEROID 11-BETA-HYDROXYLASE; STEROID 17-ALPHA-HYDROXYLASE; 3-beta-hydroxysteroid dehydrogenase (3-HYDROXYSTEROID DEHYDROGENASES); TESTOSTERONE 5-ALPHA-REDUCTASE; or steroidogenic acute regulatory protein; among others, underlie these disorders.Species Specificity: The restriction of a characteristic behavior, anatomical structure or physical system, such as immune response; metabolic response, or gene or gene variant to the members of one species. It refers to that property which differentiates one species from another but it is also used for phylogenetic levels higher or lower than the species.Homozygote: An individual in which both alleles at a given locus are identical.Kidney: Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.Immunologic Factors: Biologically active substances whose activities affect or play a role in the functioning of the immune system.ZymosanTime Factors: Elements of limited time intervals, contributing to particular results or situations.Protein Structure, Tertiary: The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Gene Dosage: The number of copies of a given gene present in the cell of an organism. An increase in gene dosage (by GENE DUPLICATION for example) can result in higher levels of gene product formation. GENE DOSAGE COMPENSATION mechanisms result in adjustments to the level GENE EXPRESSION when there are changes or differences in gene dosage.Haplotypes: The genetic constitution of individuals with respect to one member of a pair of allelic genes, or sets of genes that are closely linked and tend to be inherited together such as those of the MAJOR HISTOCOMPATIBILITY COMPLEX.Membrane Proteins: Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.HLA Antigens: Antigens determined by leukocyte loci found on chromosome 6, the major histocompatibility loci in humans. They are polypeptides or glycoproteins found on most nucleated cells and platelets, determine tissue types for transplantation, and are associated with certain diseases.Membrane Glycoproteins: Glycoproteins found on the membrane or surface of cells.Sequence Homology, Nucleic Acid: The sequential correspondence of nucleotides in one nucleic acid molecule with those of another nucleic acid molecule. Sequence homology is an indication of the genetic relatedness of different organisms and gene function.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.Monocytes: Large, phagocytic mononuclear leukocytes produced in the vertebrate BONE MARROW and released into the BLOOD; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles.Molecular Weight: The sum of the weight of all the atoms in a molecule.Kinetics: The rate dynamics in chemical or physical systems.Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products.Exons: The parts of a transcript of a split GENE remaining after the INTRONS are removed. They are spliced together to become a MESSENGER RNA or other functional RNA.B-Lymphocytes: Lymphoid cells concerned with humoral immunity. They are short-lived cells resembling bursa-derived lymphocytes of birds in their production of immunoglobulin upon appropriate stimulation.Proteinuria: The presence of proteins in the urine, an indicator of KIDNEY DISEASES.Flow Cytometry: Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.Antibody Formation: The production of ANTIBODIES by proliferating and differentiated B-LYMPHOCYTES under stimulation by ANTIGENS.Serine Endopeptidases: Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.Streptococcus pneumoniae: A gram-positive organism found in the upper respiratory tract, inflammatory exudates, and various body fluids of normal and/or diseased humans and, rarely, domestic animals.Collectins: A class of C-type lectins that target the carbohydrate structures found on invading pathogens. Binding of collectins to microorganisms results in their agglutination and enhanced clearance. Collectins form trimers that may assemble into larger oligomers. Each collectin polypeptide chain consists of four regions: a relatively short N-terminal region, a collagen-like region, an alpha-helical coiled-coil region, and carbohydrate-binding region.Restriction Mapping: Use of restriction endonucleases to analyze and generate a physical map of genomes, genes, or other segments of DNA.Genes: A category of nucleic acid sequences that function as units of heredity and which code for the basic instructions for the development, reproduction, and maintenance of organisms.DNA Primers: Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.C-Reactive Protein: A plasma protein that circulates in increased amounts during inflammation and after tissue damage.Genotype: The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.Up-Regulation: A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.Lipopolysaccharides: Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed)Protein PrecursorsSteroid Hydroxylases: Cytochrome P-450 monooxygenases (MIXED FUNCTION OXYGENASES) that are important in steroid biosynthesis and metabolism.Blotting, Northern: Detection of RNA that has been electrophoretically separated and immobilized by blotting on nitrocellulose or other type of paper or nylon membrane followed by hybridization with labeled NUCLEIC ACID PROBES.T-Lymphocytes: Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.DNA, Complementary: Single-stranded complementary DNA synthesized from an RNA template by the action of RNA-dependent DNA polymerase. cDNA (i.e., complementary DNA, not circular DNA, not C-DNA) is used in a variety of molecular cloning experiments as well as serving as a specific hybridization probe.Blotting, Southern: A method (first developed by E.M. Southern) for detection of DNA that has been electrophoretically separated and immobilized by blotting on nitrocellulose or other type of paper or nylon membrane followed by hybridization with labeled NUCLEIC ACID PROBES.Cytokines: Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.Macular Degeneration: Degenerative changes in the RETINA usually of older adults which results in a loss of vision in the center of the visual field (the MACULA LUTEA) because of damage to the retina. It occurs in dry and wet forms.Disease Susceptibility: A constitution or condition of the body which makes the tissues react in special ways to certain extrinsic stimuli and thus tends to make the individual more than usually susceptible to certain diseases.Models, Molecular: Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization: A mass spectrometric technique that is used for the analysis of large biomolecules. Analyte molecules are embedded in an excess matrix of small organic molecules that show a high resonant absorption at the laser wavelength used. The matrix absorbs the laser energy, thus inducing a soft disintegration of the sample-matrix mixture into free (gas phase) matrix and analyte molecules and molecular ions. In general, only molecular ions of the analyte molecules are produced, and almost no fragmentation occurs. This makes the method well suited for molecular weight determinations and mixture analysis.Reverse Transcriptase Polymerase Chain Reaction: A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.Cell Membrane: The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.Pedigree: The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition.Case-Control Studies: Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.Polymorphism, Restriction Fragment Length: Variation occurring within a species in the presence or length of DNA fragment generated by a specific endonuclease at a specific site in the genome. Such variations are generated by mutations that create or abolish recognition sites for these enzymes or change the length of the fragment.Gene Frequency: The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.Guinea Pigs: A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.Immune Adherence Reaction: A method for the detection of very small quantities of antibody in which the antigen-antibody-complement complex adheres to indicator cells, usually primate erythrocytes or nonprimate blood platelets. The reaction is dependent on the number of bound C3 molecules on the C3b receptor sites of the indicator cell.Mice, Inbred DBAEscherichia coli: A species of gram-negative, facultatively anaerobic, rod-shaped bacteria (GRAM-NEGATIVE FACULTATIVELY ANAEROBIC RODS) commonly found in the lower part of the intestine of warm-blooded animals. It is usually nonpathogenic, but some strains are known to produce DIARRHEA and pyogenic infections. Pathogenic strains (virotypes) are classified by their specific pathogenic mechanisms such as toxins (ENTEROTOXIGENIC ESCHERICHIA COLI), etc.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.Staphylococcus aureus: Potentially pathogenic bacteria found in nasal membranes, skin, hair follicles, and perineum of warm-blooded animals. They may cause a wide range of infections and intoxications.Transfection: The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Lung: Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.Arthritis, Rheumatoid: A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.Antibodies, Bacterial: Immunoglobulins produced in a response to BACTERIAL ANTIGENS.Proteomics: The systematic study of the complete complement of proteins (PROTEOME) of organisms.Fluorescent Antibody Technique: Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.Interleukin-6: A cytokine that stimulates the growth and differentiation of B-LYMPHOCYTES and is also a growth factor for HYBRIDOMAS and plasmacytomas. It is produced by many different cells including T-LYMPHOCYTES; MONOCYTES; and FIBROBLASTS.Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).Epithelial Cells: Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.Structure-Activity Relationship: The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.Gene Library: A large collection of DNA fragments cloned (CLONING, MOLECULAR) from a given organism, tissue, organ, or cell type. It may contain complete genomic sequences (GENOMIC LIBRARY) or complementary DNA sequences, the latter being formed from messenger RNA and lacking intron sequences.Signal Transduction: The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.Genetic Predisposition to Disease: A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.Hemoglobinuria, Paroxysmal: A condition characterized by the recurrence of HEMOGLOBINURIA caused by intravascular HEMOLYSIS. In cases occurring upon cold exposure (paroxysmal cold hemoglobinuria), usually after infections, there is a circulating antibody which is also a cold hemolysin. In cases occurring during or after sleep (paroxysmal nocturnal hemoglobinuria), the clonal hematopoietic stem cells exhibit a global deficiency of cell membrane proteins.Polymorphism, Single Nucleotide: A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.

Interaction between terminal complement proteins C5b-7 and anionic phospholipids. (1/604)

We have recently shown that C5b-6 binds to the erythrocyte membrane via an ionic interaction with sialic acid before the addition of C7 and subsequent membrane insertion. In this study we assessed the role of anionic lipids in the binding of the terminal complement proteins to the membrane and the efficiency of subsequent hemolysis. Human erythrocytes were modified by insertion of dipalmitoyl phosphatidylcholine (DPPC), dipalmitoyl phosphatidylserine (DPPS), dipalmitoyl phosphatidylethanolamine (DPPE), or dipalmitoyl phosphatidic acid (DPPA). Lipid incorporation and the hemolytic assays were done in the presence of 100 micromol/L sodium orthovanadate to prevent enzymatic redistribution of lipid. We found that the neutral lipids, DPPC and DPPE, did not affect C5b-7 uptake or hemolysis by C5b-9. In contrast, the two acidic phospholipids, DPPS and DPPA, caused a dose-dependent increase in both lysis and C5b-7 uptake. We conclude that the presence of anionic lipids on the exterior face of the membrane increases C5b-7 uptake and subsequent hemolysis. It is known that sickle cell erythrocytes have increased exposure of phosphatidylserine on their external face and are abnormally sensitive to lysis by C5b-9. The data presented here provide a plausible mechanism for this increased sensitivity.  (+info)

Reaction of an activated complex of guinea-pig complement components, C56, with unsensitized erythrocytes and with erythrocytes carrying C3b molecule. (2/604)

During the interaction of guinea-pig complement intermediate cells, EAC423, with guinea-pig C5 and C6, an activated complex of C5 and C6, C56, was demonstrated in the fluid phase of the reaction mixture. C56 also was eluted from EAC42356 which had been generated by the interaction of EAC423 with C5 and C6. Both preparations of C56 showed quite similar characteristics and were not distinguished from one another. Both were capable of reacting with unsensitized erythrocytes (E) in the presence of C7 to form EC567. Further, they were able to react with EAC43 in the absence of C7 to form EAC43568 but did react with EAC43 pretreated with C3b inactivator, dithiothreitol or N-bromosuccinimide. These results indicate that guinea-pig C56 generated on EAC423 has a tendency to dissociate into the fluid phase. Nevertheless, the dissociated C56 can bind again to intact C3b molecule on the cells. The ability of cell-bound C3b to combine with C56 may lead to localization of C56 to the cell membrane carrying C3b, resulting in acceleration of attachment of C567 to the membrane. This assumption could be supported by the finding that the replacement of E by EAC43 increased the susceptibility of the cells to lytic action of complement induced by cobra venom factor. Thus, a new function of cell-bound C3b as localizing C56 to the membrane of sensitized cells was indicated.  (+info)

rC5a directs the in vitro migration of human memory and naive tonsillar B lymphocytes: implications for B cell trafficking in secondary lymphoid tissues. (3/604)

Human C5a is a potent chemoattractant for granulocytes, monocytes, and dendritic cells. In mice C5a has been shown to be chemotactic for germinal center (GC) B cells. To date, no information is available on the effects of C5a on human B cell locomotion. Here we demonstrate that rC5a increases polarization and migration of human tonsillar B cells. The locomotory response was due to both chemokinetic and chemotactic activities of rC5a. Moreover, memory and, at a lesser extent, naive B cell fractions from purified tonsillar populations displayed rC5a-enhanced migratory properties, whereas GC cells did not. Flow cytometry revealed C5aR (CD88) on approximately 40% memory and 10% naive cells, respectively, whereas GC cells were negative. Immunohistochemistry showed that a few CD88+ cells were of the B cell lineage and localized in tonsillar subepithelial areas, where the majority of memory B cells settle. Pretreatment of memory B cells with the CD88 mAb abolished their migratory responsiveness to rC5a. Finally, the C5 gene was found to be expressed in naive, GC, and memory B lymphocytes at both the mRNA and the protein level. This study delineates a novel role for C5a as a regulator of the trafficking of human memory and naive B lymphocytes and supports the hypothesis that the B cells themselves may serve as source of C5 in secondary lymphoid tissues.  (+info)

Active sites in complement components C5 and C3 identified by proximity to indels in the C3/4/5 protein family. (4/604)

We recently suggested that sites of length polymorphisms in protein families (indels) might serve as useful guides for locating protein:protein interaction sites. This report describes additional site-specific mutagenesis and synthetic peptide inhibition studies aimed at testing this idea for the paralogous complement C3, C4, and C5 proteins. A series of C5 mutants was constructed by altering the C5 sequence at each of the 27 indels in this protein family. Mutants were expressed in COS cells and were assayed for hemolytic activity and protease sensitivity. Mutants at five indels showed relatively normal expression but substantially reduced sp. act., indicating that the mutations damaged sites important for C5 function. Twenty-three synthetic peptides with C5 sequences and 10 with C3 sequences were also tested for the ability to inhibit C hemolytic activity. Three of the C5 peptides and one of the C3 peptides showed 50% inhibition of both C hemolytic and bactericidal activities at a concentration of 100 microM. In several cases both the mutational and peptide methods implicated the same indel site. Overall, the results suggest that regions important for function of both C3 and C5 lie proximal to residues 150-200 and 1600-1620 in the precursor sequences. Additional sites potentially important for C5 function are near residue 500 in the beta-chain and at two or three sites between the N-terminus of the alpha'-chain and the C5d fragment. One of the latter sites, near residue 865, appears to be important for proteolytic activation of C5.  (+info)

In vitro and in vivo responses of murine granulocytes to human complement-derived, haemolytically inactive C5b67 (iC5b67). (5/604)

Haemolytically inactive C5b67 (iC5b67), which was made from purified human components and decayed to a haemolytically inactive form, was evaluated as an agonist for murine leucocytes both in vitro and in vivo. In an in vitro assay, iC5b67 stimulated chemotaxis for both neutrophils purified from mouse bone marrow and splenic eosinophils of IL-5 transgenic mice. The stimulation was dose-dependent, with high dose inhibition. As with human neutrophils, iC5b67 also failed to up-regulate CR3 (CD11b/CD18) expression and to stimulate superoxide generation in murine bone marrow neutrophils, in vitro. In vivo, iC5b67 elicited an inflammatory response in a mouse model of pleuritis. A marked infiltration of neutrophils, which peaked at 4 h, was followed by an infiltration of eosinophils and mononuclear leucocytes. This inflammatory response was dose- and time-dependent. However, the protein concentration in the pleural wash fluid did not increase, indicating that iC5b67 did not induce a capillary leak. Although the infiltration of neutrophils could not be reproduced by pure C7 or human serum albumin (HSA), C5b6 did induce an influx of neutrophils. We were able to document the existence of C7, both antigenically and functionally, in pleural washes of normal mice, making it likely that the activity of C5b6 resulted from the in situ formation of C5b67 and iC5b67. The mouse model of pleuritis promises to be a useful in vivo system in which to evaluate the pro- and anti-inflammatory effects of iC5b67 that have been noted in vitro.  (+info)

Triggering a second T cell receptor on diabetogenic T cells can prevent induction of diabetes. (6/604)

In this paper, we test the hypothesis that triggering of a second T cell receptor (TCR) expressed on diabetogenic T cells might initiate the onset of diabetes. A cross between two TCR-transgenic strains, the BDC2.5 strain that carries diabetogenic TCRs and the A18 strain that carries receptors specific for C5, was set up to monitor development of diabetes after activation through the C5 TCR. F1 BDC2. 5 x A18 mice developed diabetes spontaneously beyond 3-4 mo of age. Although their T cells express both TCRs constitutively, the A18 receptor is expressed at extremely low levels. In vitro activation of dual TCR T cells followed by adoptive transfer into neonatal or adult F1 mice resulted in diabetes onset and death within 10 d after transfer. In contrast, in vivo immunization of F1 mice with different forms of C5 antigen not only failed to induce diabetes but protected mice from the spontaneous onset of diabetes. We propose that antigenic stimulation of cells with low levels of TCR produces signals inadequate for full activation, resulting instead in anergy.  (+info)

Pneumococcal surface protein A inhibits complement activation by Streptococcus pneumoniae. (7/604)

Pneumococcal surface protein A (PspA) is a surface-exposed protein virulence factor for Streptococcus pneumoniae. In this study, no significant depletion of serum complement was observed for the serum of mice infected with pneumococci that express PspA. In contrast, in mice infected with an isogenic strain of pneumococci lacking PspA, significant activation of serum complement was detected within 30 min after infection. Also, the PspA-deficient strain but not the PspA-expressing strain was cleared from the blood within 6 h. The contribution of PspA to pneumococcal virulence was further investigated by using mice deficient for C5, C3, or factor B. In mice deficient for C3 or factor B, PspA-negative pneumococci became fully virulent. In contrast, in C5-deficient mice as in wild-type mice, PspA-deficient pneumococci were avirulent. These in vivo data suggest that, in nonimmune mice infected with pneumococci, PspA interferes with complement-dependent host defense mechanisms mediated by factor B. Immunoblots of pneumococci opsonized in vitro suggested that more C3b was deposited on PspA-negative than on PspA-positive pneumococci. This was observed with and without anticapsular antibody. Furthermore, processing of the alpha chain of C3b was reduced in the presence of PspA. We propose that PspA exerts its virulence function by interfering with deposition of C3b onto pneumococci and/or by inhibiting formation of a fully functional alternative pathway C3 convertase. By blocking recruitment of the alternative pathway, PspA reduces the amount of C3b deposited onto pneumococci, thereby reducing the effectiveness of complement receptor-mediated pathways of clearance.  (+info)

Enhancement of lectin pathway haemolysis by immunoglobulins. (8/604)

We recently reported that indicator sheep erythrocytes (E) coated with mannan and sensitized with mannan-binding lectin (MBL) (E-M-MBL) are lysed by human serum in the absence of calcium via the lectin pathway of complement activation by a process which requires alternative pathway amplification and is associated with increased binding of and control by complement regulatory proteins C4 bp and factor H. In the present study, we investigated the effect of immunoglobulin (Ig) on this haemolysis. Co-sensitization of indicator E with anti-E haemolysin led to threefold enhancement of lectin pathway haemolysis in the absence of calcium, associated with increased binding of C3 and C5. Lysis was enhanced approximately twofold when E-M-MBL were chemically or immunologically coated with IgM or IgA, and fourfold when coated with IgG, prior to lysis in human serum-Mg-ethyleneglycol tetraacetic acid. The presence of haemolysin did not reduce the binding or inhibitory activity of C4 bp, and the enhancing activity of haemolysin was retained in serum depleted of C4 bp. By contrast, binding of factor H was greatly reduced in the presence of haemolysin, which had no enhancing effect in serum depleted of factor H. These experiments demonstrate the ability of IgG, IgM and IgA to enhance lectin pathway cytolysis, and that this enhancement occurs by neutralization of the inhibitory activity of factor H. Immunoglobulin enhancement of lectin pathway cytolysis represents another interaction between the innate and adaptive systems of immunity.  (+info)

*Alternative-complement-pathway C3/C5 convertase

C5 convertase, (C3b)n,Bb, complement C 3(C 5) convertase (amplification), alternative complement pathway C3(C5) convertase, C5 ... Alternative-complement-pathway C3/C5 convertase (EC 3.4.21.47, complement component C3/C5 convertase (alternative), proenzyme ... bond in complement component C5 alpha-chain to yield C5a and C5b This enzyme is a bimolecular complex of complement fragment Bb ... Alternative-complement-pathway C3/C5 convertase at the US National Library of Medicine Medical Subject Headings (MeSH) ...

*Complement component 5

... is a protein that in humans is encoded by the C5 gene. Complement component 5 is involved in the ... 1995). "Inherited human complement C5 deficiency. Nonsense mutations in exons 1 (Gln1 to Stop) and 36 (Arg1458 to Stop) and ... 1991). "Complete cDNA sequence of human complement pro-C5. Evidence of truncated transcripts derived from a single copy gene". ... 1988). "Molecular analysis of human complement component C5: localization of the structural gene to chromosome 9". Biochemistry ...

*Factor H

"The development of atypical hemolytic uremic syndrome depends on complement C5". Journal of the American Society of Nephrology ... Moreover, the complement inhibitory activities of factor H, and other complement regulators, are often used by pathogens to ... Factor H is a member of the regulators of complement activation family and is a complement control protein. It is a large (155 ... Deletion of two adjacent genes with a high degree of homology to complement factor H, named complement factor H-related 3 and ...

*Cord factor

... complement C5 and interleukin-6 in the initiation and development of the mycobacterial cord factor trehalose 6,6'-dimycolate ...

*Eculizumab

... specifically binds to the terminal complement component 5, or C5, which acts at a late stage in the complement ... Eculizumab is a recombinant humanized monoclonal antibody against the complement protein C5. It is an immunoglobulin G-kappa ( ... By inhibiting the complement cascade at this point, the normal, disease-preventing functions of proximal complement system are ... Eculizumab inhibits the cleavage of C5 by the C5 convertase into C5a a potent anaphylatoxin with prothrombotic and ...

*M. Amin Arnaout

... a finding that suggested the potential of B cell or complement C5 depletion as adjunct therapies in certain forms of kidney ... He was the first to show that C3 nephritic factor is an autoantibody that activates the alternative complement pathway, ...

*Leiner's disease

It is caused by a deficit of the complement protein, C5; however, case reports have described it in relation to deficits in ...

*Complement component 5a

C5a is a protein fragment released from cleavage of complement component C5 by protease C5-convertase into C5a and C5b ... C5a, the other cleavage product of C5, acts as a highly inflammatory peptide, encouraging complement activation, formation of ... The origin of C5 is in the hepatocyte, but its synthesis can also be found in macrophages, where it may cause local increase of ... Complement peptide C5a, C4a, and C3a receptors". Pharmacol. Rev. 65 (1): 500-43. doi:10.1124/pr.111.005223. PMID 23383423. ...

*Protein S

... also binds to the nascent complement complex C5,6,7 and prevents this complex from inserting into a membrane. This ... In the circulation, Protein S exists in two forms: a free form and a complex form bound to complement protein C4b-binding ... function prevents the inappropriate activation of the complement system, which would cause uncontrolled systemic inflammation. ...

*Complement factor B

Rawal N, Pangburn MK (March 2001). "Structure/function of C5 convertases of complement". International Immunopharmacology. 1 (3 ... Complement factor B is a protein that in humans is encoded by the CFB gene. This gene encodes complement factor B, a component ... CFB complement factor B". Ambrus JL, Peters MG, Fauci AS, Brown EJ (March 1990). "The Ba fragment of complement factor B ... Christie DL, Gagnon J (January 1983). "Amino acid sequence of the Bb fragment from complement Factor B. Sequence of the major ...

*Complement membrane attack complex

... two regulators of complement. The membrane attack complex is initiated when the complement protein C5 convertase cleaves C5 ... Another complement protein, C6, binds to C5b. The C5bC6 complex is bound by C7. This junction alters the configuration of the ... Deficiencies of C5 to C9 components does not lead to generic infections, but only to increased susceptibility to Neisseria spp ... MAC is composed of a complex of four complement proteins (C5b, C6, C7, and C8) that bind to the outer surface of the plasma ...

*C3b

In such cases treatment with the complement-inhibitory anti-C5 monoclonal antibody, eculizumab, is found to be highly effective ... Binding of a C3b molecule to the C4bC2b complex (C4b2b3b) results in the formation of a C5 convertase, which cleaves C5 into ... The C1 complement complex binds to these antibodies resulting in its activation via cross proteolysis. This activated C1 ... C3b is the larger of two elements formed by the cleavage of complement component 3, and is considered an important part of the ...

*Eosinophilia

... complement complex (C5-C6-C7), interleukin 5, and histamine (though this has a narrow range of concentration). Harm resulting ...

*Porphyromonas gingivalis

Other studies have found that P. gingivalis can subvert the complement pathway through C5αR and C3αR, which modulates the ... Low-Abundance Biofilm Species Orchestrats Inflammatory Periodontal Disease through the Commensal Microbiota and the Complement ...

*Anaphylatoxin

... that are produced as part of the activation of the complement system. Complement components C3, C4 and C5 are large ... This term is reserved only for fragments of the complement system. C3, C4A, C4B, C4B-1, C5, FBLN1, FBLN2 Allergy Anaphylatoxin ... Ogata, R. T.; Rosa, P. A.; Zepf, N. E. (1989). "Sequence of the gene for murine complement component C4". The Journal of ... C3a works with C5a to activate mast cells, recruit antibody, complement and phagocytic cells and increase fluid in the tissue, ...

*Terminal complement pathway deficiency

Initial complement tests often include C3 and C4, but not C5 through C9. Instead, the CH50 result may play a role in diagnosis ... Terminal complement pathway deficiency is a genetic condition affecting the complement membrane attack complex (MAC). It ... Suspect terminal complement pathway deficiency with patients who have more than one episode of Neisseria infection. ... Lint TF, Zeitz HJ, Gewurz H (November 1980). "Inherited deficiency of the ninth component of complement in man". J. Immunol. ...

*List of EC numbers (EC 3)

... complement component C5 convertase. Now EC 3.4.21.43, classical-complement-pathway C3/C5 convertase EC 3.4.21.45: complement ... complement subcomponent C1r EC 3.4.21.42: complement subcomponent C1s EC 3.4.21.43: classical-complement-pathway C3/C5 ... factor I EC 3.4.21.46: complement factor D EC 3.4.21.47: alternative-complement-pathway C3/C5 convertase EC 3.4.21.48: ...

*Polysaccharide encapsulated bacteria

There are several types of complement deficiency, two of note are C3 and C5,6,7,8,9. A C3 deficiency allows for infection by ... A C5,6,7,8,9 (the membrane attack complex) deficiency lead to unopposed Neisseria infections. Vaccination is essential in such ... Patients with complement deficiency are at risk of infections with encapsulated organisms. ...

*Meningococcal disease

Persons with component deficiencies in the final common complement pathway (C3,C5-C9) are more susceptible to N. meningitidis ... In addition, complement component-deficient populations frequently experience frequent meningococcal disease since their immune ... CS1 maint: Multiple names: authors list (link) Ross SC, Densen P; Densen (September 1984). "Complement deficiency states and ... "Deficiency of the sixth component of complement and susceptibility to Neisseria meningitidis infections: studies in 10 families ...

*NmVac4-A/C/Y/W-135

People with component deficiencies in the final common complement pathway (C3,C5-C9) are more susceptible to N. meningitidis ... Orren A, Potter PC, Cooper RC, du Toit E (October 1987). "Deficiency of the sixth component of complement and susceptibility to ... In addition, complement component-deficient population frequently experience frequent meningococcal disease, since their immune ... In encapsulated gram negative bacteria, protection results primarily from a direct complement-mediated bactericidal effect. ...

*Genome-wide association study

... a novel C3d-targeted C3/C5 convertase inhibitor for treatment of human complement alternative pathway-mediated diseases". Blood ... These SNPs were located in the gene encoding complement factor H, which was an unexpected finding in the research of ARMD. The ... "Complement factor H variant increases the risk of age-related macular degeneration". Science. 308 (5720): 419-21. doi:10.1126/ ... "Complement factor H polymorphism in age-related macular degeneration". Science. 308 (5720): 385-9. doi:10.1126/science.1109557 ...

*Collectin

... has a cleavage activity and it is essential for forming lectin C3 and C5 convertases and for activation of the complement. For ... Collectin MBL is involved in activation of the lectin complement pathway. There are three serine proteases, MASP-1, 2 and 3 ( ... Check date values in: ,date= (help) Fujita, Teizo (2002-05). "Evolution of the lectin-complement pathway and its role in innate ... MBL can bind to microorganisms and this interaction can lead to opsonization through complement activation, or it can opsonize ...

*C5-convertase

The complement component C5 can be also activated by fluid phase C5 convertase. C5 is activated by CVFBb in the presence of ... Target of function The target of C5 convertase is complement protein C5. C5 is a two-chain (α, β) plasma glycoprotein (Mr = ... In these respects, the mode of action of C5 is completely analogous to that of the other components of complement. The C5 step ... CVFBb does not require C3 for cleavage of C5, whereas C4b2boxy need native C3 for cleavage of C5 protein. The modified C5 ...

*Alternative complement pathway

The C5-convertase of the alternative pathway consists of (C3b)2BbP (sometimes referred to as C3b2Bb). After the creation of C5 ... Inhibition of the alternative complement pathway by antisense oligonucleotides targeting complement factor B improves lupus ... C5-convertase cleaves C5 into C5a and C5b. C5b binds sequentially to C6, C7, C8 and then to multiple molecules of C9 to form ... cells from complement-mediated damage. CFHR5 (Complement Factor H-Related protein 5) is able to bind to act as a cofactor for ...

*Complement system

The complex of C3b(2)Bb is a protease which cleaves C5 into C5b and C5a. C5 convertase is also formed by the Classical Pathway ... Polymorphisms of complement component 3, complement factor B, and complement factor I, as well as deletion of complement factor ... Three biochemical pathways activate the complement system: the classical complement pathway, the alternative complement pathway ... The complement system is regulated by complement control proteins, which are present at a higher concentration in the blood ...

*Vandenberg Air Force Base

When designed and manufactured, the Titan I provided an additional nuclear deterrent to complement the U.S. Air Force's SM-65 ... The OLF could be disassembled, loaded onto two C-5 aircraft, shipped to the overseas Orbiter landing site, and reassembled to ...
In this study, we have shown that C5 is an essential component in liver regeneration following toxic injury. Mice deficient in this complement protein were unable to mount a normal regenerative response after toxic exposure to CCl4. This was demonstrated by the delayed entry of C5−/− hepatocytes into the cell cycle, the severely compromised mitotic activity detected in C5−/− livers, as well as the extensive parenchymal necrosis and fat deposition in the deficient mice that persisted until 96 h after the injury (data not shown). Reconstitution of the C5−/− mice with murine C5 resulted in a significant recovery of their regenerative phenotype, as shown by the restored hepatocyte DNA synthetic response and mitotic activity at 48 h after the toxic challenge. It should be noted that the C5−/− mice showed signs of acute necrosis and persisting degeneration until 4 days after the exposure to CCl4, a time at which the wild-type animals had completely recovered from injury. Both wild-type ...
C5a / C5a des Arg antibody [2942] (complement component 5) for IA, WB. Anti-C5a / C5a des Arg mAb (GTX11877) is tested in Human samples. 100% Ab-Assurance.
We have made use of T cell receptor (TCR)-transgenic mice with CD4+ T cells expressing a receptor specific for the self-antigen C5 (fifth component of complement) to study the role of different antigen-presenting cells in the determination of CD4+ T cell effector type. Contact of T cells from C5 TCR-transgenic mice with C5 protein or C5 peptide in vivo or in vitro induces biased T helper cell (Th) 1 type responses resulting in exclusive production of high levels of interferon gamma and interleukin (IL) 2. Transgenic mice, in contrast to nontransgenic littermates, do not generate an antibody response to C5. We show in this paper that B cell presentation in vitro induces a switch to the Th2 subset indicated by production of IL-4, and targetting C5 to B cells in vivo results in the generation of C5-specific antibodies. ...
The fourth and fifth components are important to set the conditions for a more representative redistricting after the 2020 census. The first three are important for other reasons. Maintaining the Democratic majority in the House is a necessary, but not sufficient requirement to return the US back to a solid political and economic footing. Retaking both the presidency and the Senate are both necessary and sufficient requirements to actually being able to do so. If the Democrats retake the presidency, but dont retake the Senate, the next president will be a lame duck before her or his hand ever comes off the bible at the inauguration. No one they nominate, for political or judicial or diplomatic appointments, will ever get a vote. Nor will any legislation that passes a Democratic majority House, other than, perhaps, continuing resolutions to keep the government running at a previous years top line budget number. Right now the only way to reverse the damage that has been done, and to ensure that ...
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Belkaid (2003) has shown that IL-10 plays an essential role in L. major persistence in genetically resistant C57BL/6 mice after spontaneous healing of their lesions. They have demonstrated that a sterile cure was achieved in IL-10−/− mice but not in IL-10-sufficient mice. This requirement for IL-10 in establishing latency was determined in mice infected either by intradermal injection of L. major metacyclic promastigotes or by exposure of the skin to infected sandflies that mimic natural infection. Most importantly, IL-10-sufficient C57BL/6 mice treated transiently during the chronic phase with anti-IL-10 receptor antibodies achieved a sterile cure, suggesting that IL-10 was actively involved in preventing complete parasite elimination even in the presence of a Th1 response.. A role for Treg in the pathogenesis of Leishmania infection is not restricted to resistant strains. In susceptible BALB/c mice, cells that suppress L. major protective immunity have been shown to belong to an IL-4- and ...
The primary endpoint of death or MI at 30 days occurred in 15.2% of the pexelizumab group and 16.3% of the placebo group (relative risk reduction [RRR] 6.7%, p=0.201). Among the components of the composite, MI occurred in 12.6% of the pexelizumab group and 13.3% of the placebo group, (p=0.311) and death in 3.8% and 4.6%, respectively (RRR 17%, p=0.177). Results of the primary endpoint were similar in the different risk factor subgroups. Serious adverse events did not differ by treatment group (31.2% for pexelizumab and 32.5% for placebo). Sepsis occurred less often in the pexelizumab group (2.1% for 3.1%).. ...
A casein kinase released from activated human platelets has been shown to phosphorylate a number of plasma proteins. When platelets are activated they release substantial amounts of ATP and divalent cations which are necessary for phosphorylation of proteins. The aim of this study was to elucidate the optimal conditions for phosphorylation of the human complement component C4, identify phosphorylation site in the molecule and to investigate possible impact on the functions of phosphorylated C4. For this purpose, C4 must be prepared from human plasma, which was done using a modification of a previously published method. The results showed a pure and 100 % active protein. C4 was incubated with [g-32P]ATP and cations. After SDS-PAGE and autoradiography it was shown that C4 was phosphorylated in the a-chain. Maximal phosphorylation was achieved when C4 was phosphorylated in the presence of 20 mM Ca2+. Incubation of phosphorylated and unphosphorylated C4 with trypsin showed that phosphorylated C4 was ...
The men protects the face, neck, and shoulders. It consists of a facemask with several horizontal metal bars running the entire width of the face, from the chin to the top of the head. To this is attached a long rectangular thick cloth padding that curves over the top of the head and extends to cover the shoulders. A throat protector is attached to the bottom of the facemask. The men is held in place with a pair of woven cords that wrap around the head and are tied at the back. The back of the men is left open for ventilation and the back of the head is unprotected. The target areas of the men are the centre top, and upper left and right sides for cutting strikes and the centre of the throat protector for a thrust.[5] ...
Cleavage of C5 requires complement fragment C3b which binds C5 and renders it susceptible to cleavage by the C4b,2a complex. Includes former EC 3.4.21.44. Complement component C2a is in peptidase family S1 (trypsin family). Links to other databases: BRENDA, EXPASY, KEGG, MEROPS, Metacyc, PDB, CAS registry number: 56626-15-4. References 1. Kerr, M.A. The second component of human complement. Methods Enzymol. 80 (1980) 54-64. [PMID: 7043188]. 2. Müller-Eberhard, H.J. Molecular organization and function of the complement system. Annu. Rev. Biochem. 57 (1988) 321-347. [PMID: 3052276]. ...
All patients received open-label eculizumab administered intravenously on the following dose schedule: Induction dose - 900 mg per week for four weeks and a dose of 1200 mg one week later; Maintenance dose - 1200 mg every two weeks. Patients who received plasma exchange or infusion during the eculizumab treatment period received a supplemental dose of 600 mg within one hour before plasma infusion or within one hour after the completion of each plasma exchange ...
Hello,. I recently received a question about infusing eculizumab during dialysis to save chair time for the patient. I am aware that eculizumab is theoretically too large to be dialyzed out, but I am wondering if anyone else has experience doing this at their institution and whether there were any issues experienced?. Thanks in advance ...
Cleavage of Arg-,-Ser bond in complement component C3 alpha-chain to yield C3a and C3b, and Arg-,-Xaa bond in complement component C5 alpha-chain to yield C5a and ...
By blocking the complement cascade with eculizumab, clinically evident intravascular hemolysis in PNH is abolished. 8 In this study, we tested for the presence of C3 fragments on the surface of PNH red cells as a possible mechanism for the residual hemolysis occurring in some eculizumab-treated patients. We observed increased levels of C3 fragments on the surface of PNH red cells in many patients who were receiving eculizumab, as also recently reported by Risitano et al.19 The deposition of C3 fragments on PNH red blood cells in this setting could represent the revelation of a pathway of red cell clearance in PNH which is usually obscured by the rapidity of intravascular hemolysis in the absence of eculizumab therapy. Indeed, a small proportion of red cells from a patient with PNH not treated with eculizumab was shown by flow cytometric analysis to have C3 deposition that was undetectable by DAT. This is likely due to the lack of sensitivity of the DAT assay and demonstrates that low levels of ...
Fibrin formation and turnover are intimately associated with inflammation and wound healing. To explore whether fibrin(ogen)-derived peptides exert direct effects upon cells involved in inflammation and tissue repair we examined the capacity of human fibrinopeptide B (hFpB), a thrombin-derived proteolytic cleavage product of the fibrinogen B beta-chain, to stimulate neutrophils (PMN), monocytes, and fibroblasts. hFpB caused directed cell migration of PMN and fibroblasts that was optimal at approximately 10(-8) M. This chemotactic activity was blocked by preincubating hFpB with antiserum to hFpB. hFpB was not chemotactic for monocytes. The chemotactic potency of hFpB for PMN was equivalent to that of anaphylatoxin from the fifth component of human complement (C5a), leukotriene B4 (LTB4), and formyl-methionyl-leucyl-phenylalanine (fMLP), and for fibroblasts its chemotactic activity was comparable to that of platelet-derived growth factor. hFpB did not interact with PMN receptors for C5a, LTB4, or ...
Fibrin formation and turnover are intimately associated with inflammation and wound healing. To explore whether fibrin(ogen)-derived peptides exert direct effects upon cells involved in inflammation and tissue repair we examined the capacity of human fibrinopeptide B (hFpB), a thrombin-derived proteolytic cleavage product of the fibrinogen B beta-chain, to stimulate neutrophils (PMN), monocytes, and fibroblasts. hFpB caused directed cell migration of PMN and fibroblasts that was optimal at approximately 10(-8) M. This chemotactic activity was blocked by preincubating hFpB with antiserum to hFpB. hFpB was not chemotactic for monocytes. The chemotactic potency of hFpB for PMN was equivalent to that of anaphylatoxin from the fifth component of human complement (C5a), leukotriene B4 (LTB4), and formyl-methionyl-leucyl-phenylalanine (fMLP), and for fibroblasts its chemotactic activity was comparable to that of platelet-derived growth factor. hFpB did not interact with PMN receptors for C5a, LTB4, or ...
Goat Polyclonal Anti-Complement Component C1r Antibody [Unconjugated]. Validated: WB, IP. Tested Reactivity: Human. 100% Guaranteed.
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.
All participants will receive open-label eculizumab by intravenous infusion during the Primary Treatment Period, starting on Day 1 and for a total of 52/53 weeks. The dosing regimen will be based on the participants body weight. As body weight changes during the study, the participants weight cohort and dose may change accordingly.. After completing the 52/53-week Primary Treatment Period, participants may continue receiving eculizumab in the Extension Treatment Period for 104 weeks. ...
Vitamin D (VitD) has a role in the regulation of calcium and phosphate metabolism and in addition impacts the activity of the immune system. VitD deficiency might be linked to increased susceptibility to respiratory tract infection. The aim of the present study was to characterize the impact of VitD deficiency on the susceptibility to bacterial infection in murine models. C57BL/6N mice were fed a diet with or without VitD for 10 weeks. The VitD-deficient or -sufficient mice were infected with Pseudomonas aeruginosa or Streptococcus pneumoniae The colonization and inflammatory response in the lung were analyzed at defined time points. The serum 25-hydroxy-VitD concentration was significantly lower in mice on the VitD-deficient diet. In infection experiments with Pseudomonas aeruginosa or Streptococcus pneumoniae, no differences could be observed in the numbers of viable bacteria or in differential cell counts in the bronchoalveolar lavage fluids. Measurements of inflammatory cytokines (KC and ...
Results At baseline, vWF, sVCAM-1, the EMP count, and F1+2 and D-dimer levels were significantly elevated in the patients, including those with no history of clinical thrombosis. Treatment with eculizumab was associated with significant decreases in plasma markers of coagulation activation (F1+2, p=0.012, and D-dimers, p=0.01), and reactional fibrinolysis (P-AP, p=0.0002). Eculizumab treatment also significantly reduced plasma markers of endothelial cell activation (t-PA, p=0.0005, sVCAM-1, p,0.0001, and vWF, p=0.0047) and total (p=0.0008) and free (p=0.0013) TFPI plasma levels. ...
... The activated complement system recognizes and eliminates invading microorganisms and thus is beneficial for the host.
The PRIMO-CABG II trial did not meet its prespecified primary endpoint of death or MI at 30 days, the secondary endpoints of death at 30 days, or the development of new or worsening congestive heart failure (relative risk, 0.91, 0.82, and 1.01, respectively; p > 0.05). However, in a combined analysis of both pivotal trials, PRIMO-CABG I and II (n = 7,353), death at 30 days was significantly reduced for the greatest risk subset (n = 2,156, pexelizumab 5.7% vs. placebo 8.1%, p = 0.024). Furthermore, this mortality reduction persisted throughout the 180-day follow-up period (pexelizumab 11.1% vs. placebo 14.4%; p = 0.036).. ...
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Complement is the term used to describe a group of serum proteins that are critically important in our defense against infection. There are deficiencies of each of the individual components of complement. Patients with complement deficiencies encounter clinical problems that depend on the role of the specific complement protein in normal function.
Quick Tips content is self-published by the Dell Support Professionals who resolve issues daily. In order to achieve a speedy publication, Quick Tips may represent only partial solutions or work-arounds that are still in development or pending further proof of successfully resolving an issue. As such Quick Tips have not been reviewed, validated or approved by Dell and should be used with appropriate caution. Dell shall not be liable for any loss, including but not limited to loss of data, loss of profit or loss of revenue, which customers may incur by following any procedure or advice set out in the Quick Tips ...
chr04:complement(join(34150379..34150670,34150237..34150289,34150030..34150153,34149819..34149940,34148628..34148735,34148427..34148528 ...
chr08:complement(join(8594165..8594329,8592744..8592818,8592340..8592396,8592099..8592259,8591848..8591988,8591180..8591282,8590996..8591095,8590688..8590899 ...
What is Complement Component Gene? Definition of Complement Component Gene. Complement Component Gene FAQ. Learn more about Complement Component Gene. Complement Component Gene facts.
In this study, we showed that blocking complement activation accelerates the early healing rate in a mouse model of cutaneous wound healing. We also found that the components of the complement system responsible for this effect include C3, C5, and signaling through C5aR1, but not C5aR2 or C3aR. Furthermore, reconstitution of C3-deficient animals with purified human C3 or serum from C3+/+ mice abrogated the effect, confirming the involvement of complement in the process. The absence of these molecules resulted in a reduction in the intensity of inflammation involved in the initial events of healing. We postulate that the reduced inflammation allowed the process to advance faster to the subsequent events of healing (proliferation, maturation), thus accelerating the whole process. Moreover, we observed an increase of vascularization accompanied by a significantly higher presence of mast cells in complement-deficient mice.. A major role of complement effectors is to attract, activate, and control ...
Complement component C9 binds to the C5b-8 complex as the final protein of the membrane attack complex. After binding, it undergoes a conformational change and inserts itself into the cell membrane, forming transmembrane channels.
The first indication is paroxysmal nocturnal hemoglobinuria (PNH), a rare disease of the bone marrow. Apellis drug candidate APL-2, an inhibitor of complement component C3, is designed to provide PNH patients with an alternative to the current standard-of-care. In its second program, Apellis is testing whether APL-1, another inhibitor of complement component C3, can affect the underlying disease mechanism in COPD and slow down disease progression. Finally, Apellis third program aims to reduce the growth of retinal lesions through the intravitreal injection of APL-2 in patients suffering from geographic atrophy, the advanced form of dry age-related macular degeneration (AMD), for which no treatments exist. All three complement immunotherapy programs focus on the potential of complement inhibition to correct pathogenic Th17 immune responses.. Cedric Francois, MD, PhD and CEO of Apellis commented "We are excited to test the immense potential of complement immunotherapy. Our clinical programs are ...
... is produced by our E.coli expression system and the target gene encoding Asn679-Arg755 is expressed.
A new cluster of complement component genes, including C4BP, C3bR, and FH, is described. Family segregation data indicate that FH is linked to the genes for C4-bp and C4bR, previously reported to be linked and to maintain linkage disequilibrium. This cluster is not linked to the major histocompatibility complex, which contains the genes for the complement components, C4, C2, and factor B, or to the C3 locus. These data further suggest that the organization of genes for functionally related proteins in clusters may be a rule for the complement system. ...
Shiga-toxin producing E. coli Haemolytic Uraemic Syndrome (STEC HUS) follows a gut infection with Shiga-toxin producing E. coli (STEC), which causes severe (often bloody) diarrhoea. Around 1000 UK children are infected with STEC each year and approximately 100 of these develop STEC HUS when a toxin from STEC causes damage to small blood vessels, especially in the kidneys. About 50-60% of children with STEC HUS need artificial kidney support (dialysis), which may last several weeks. About 2-3% of children with STEC HUS die, and about 20-25% get HUS in their brain, causing fits or a stroke. Many make a full recovery, but about 25-30% will have permanent kidney damage or more rarely brain damage. Previous studies have investigated a number of different treatments for STEC HUS, but have failed to show significant benefit. Eculizumab is a medicine that blocks part of the immune system called complement. Evidence suggests complement plays a role in STEC HUS. Eculizumab is very effective in a related ...
Constituent of the membrane attack complex (MAC) that plays a key role in the innate and adaptive immune response by forming pores in the plasma membrane of target cells.
Application Index: Complement Proteins offered by Sigma-alderich online.The complement system is a complex cascade involving proteolytic cleavage of serum glycoproteins often activated by cell receptors. This cascade ultimately results in induction of the inflammatory response, phagocyte chemotaxis and opsonization, and cell lysis.
Dr. Sylvester Ogbata (SO), from the University of Tennessee Health Science Center in Memphis, Tennessee, discusses his abstract for the National Kidney Foundations 2016 Spring Clinical Meetings (SCM16), Gemcitabine Induced Atypical Hemolytic Syndrome Treated With Eculizumab: 2 Cases, with Dr. Kenar Jhaveri, AJKD Blog Editor. AJKDblog: Why dont you tell us a little about your…
The complement system is an important part of the humoral response in innate immunity, consisting of three different pathways. The third complement…
aHUS is commonly treated with a drug called eculizumab. For now, it is the only medicine approved in the United States to treat aHUS. Eculizumab can improve platelet and red blood cell counts. It may also reverse acute kidney injury and prevent kidney failure if it is taken soon enough. Eculizumab is given by injection at a doctors office ...
For performing VDRL of serum , we heat serum to inactivate complement proteins which may otherwise interfere , but why dont we do same for CSF even though it too has complement proteins in it?. Is it because of lesser stability of WBCs in CSF( which is hypotonic) and on heating may rupture to release cardiolipin? But I cant comprehend how its worse than having complement proteins?. ...
C3 antibody (complement component 3) for FACS, IE, ICC/IF, WB. Anti-C3 pAb (GTX72994) is tested in Human, Mouse, Pig, Rat, Baboon, Guinea pig, Hamster, Horse, Rabbit samples. 100% Ab-Assurance.
Abstract: : Purpose: Terminal complement components (C5,C5b-9)and several complement inhibitors are ubiquitous drusen components. This implies that complement activation may be a key element in drusen formation; but the specific complement activator(s) and activation pathway are unknown. The classical pathway is triggered by the binding of immune complexes to C1q. Alternative and lectin pathways that are antibody-independent also exist. Other molecules that interact with, or substitute for, C1q can also activate complement directly. Methods: The RPE/choroid was excised from human donor eyes with and without drusen. Vibratome sections were examined using differential interference contrast (DIC) and confocal microscopy (CM). Some sections were re-embedded and examined by electron microscopy (TEM). For CM, sections were probed with: a.) monoclonal antibodies (Ab) raised against activation-specific fragments of complement C3, HLA-DR antigen, and IgG; b.) Abs to mitochondrial, Golgi, and lysosomal ...
The structure of the human C5aR antagonist, C5a-A8, reveals a three-helix bundle conformation similar to that observed for human C5a-desArg, whereas murine C5a and C5a-desArg both form the canonical four-helix bundle. These conformational differences are discussed in light of the differential C5aR activation properties observed for the human and murine complement anaphylatoxins across species. Complement is an ancient part of the innate immune system that plays a pivotal role in protection against invading pathogens and helps to clear apoptotic and necrotic cells. Upon complement activation, a cascade of proteolytic events generates the complement effectors, including the anaphylatoxins C3a and C5a. Signalling through their cognate G-protein coupled receptors, C3aR and C5aR, leads to a wide range of biological events promoting inflammation at the site of complement activation. The function of anaphylatoxins is regulated by circulating carboxypeptidases that remove their C-terminal arginine ...
Rationale: Antiphospholipid syndrome (APS) in pregnancy may trigger the life-threatening catastrophic antiphospholipid syndrome (CAPS). Complement activation is implicated in the pathogenesis, and inhibition of complement factor C5 is suggested as an additional treatment option. Patient concerns, diagnosis and interventions: We present a pregnant patient treated with the C5-inhibitor eculizumab due to high risk of developing devastating APS-related complications. The complement inhibitory effects of the treatment were examined both in the patient and the premature infant. Outcomes: Complement activity in the mother recovered considerably faster than anticipated; however, no new thrombosis or CAPS developed during the last week of pregnancy or postpartum. Blood sampling from the umbilical vein and artery, and from the infant after delivery showed low complement activity; however, only 0.3% of the eculizumab concentration detected in the mother, consistent with low placental passage of eculizumab. ...
Test results may vary depending on your age, gender, health history, the method used for the test, and other things. Your test results may not mean you have a problem. Ask your healthcare provider what your test results mean for you. The normal range for a complement C4 blood test is 16 to 48 milligrams per deciliter (mg/dL), or 0.16 to 0.48 grams per liter (g/L). Your complement levels will often shoot up dramatically just after an infection or injury. When your complement system is activated in response to ongoing disease such as lupus, levels usually go down. You can inherit a deficiency in your complement C4, but it is much more common to acquire a deficiency. If only your C4 complement level is low, and all other complement components are normal, it is usually because of an inherited component deficiency. More often, you will have lowered levels of several complement components at once. This is the result of an acquired disease. If your C3 and C4 levels are reduced, this may be a sign that ...
Define macrophage chemotactic factor (MCF). macrophage chemotactic factor (MCF) synonyms, macrophage chemotactic factor (MCF) pronunciation, macrophage chemotactic factor (MCF) translation, English dictionary definition of macrophage chemotactic factor (MCF). n. Any of various large, phagocytic white blood cells that develop from monocytes, are found in the spleen, liver, and other tissues, and have a variety of...
Constituent of the membrane attack complex (MAC) that plays a key role in the innate and adaptive immune response by forming pores in the plasma membrane of target cells (PubMed:9634479, PubMed:9212048, PubMed:26841934). C9 is the pore-forming subunit of the MAC (PubMed:4055801, PubMed:26841934, PubMed:30111885).
Terminal complement (which eculizumab prevents from forming) is required to prevent Neisseria Meningitidis which is a bacteria which can cause meningitis and other forms of meningococcal disease. Therefore patients being treated with eculizumab are predisposed to developing infections caused by the Neisseria group of bacteria. To reduce this risk, all PNH patients starting treatment with eculizumab are vaccinated with a vaccine against the meningococcal strains A, C, W and Y. The vaccine against serotype B (the most common serotype in the UK) is licensed and is used in patients treated with eculizumab. Patients are also advised to take 500mg of either penicillin or erythromycin twice daily as a prophylactic antibiotic ...
wistar complement wistar rat complement serum | order wistar complement wistar rat complement serum | How to use: wistar complement wistar rat complement serum | su
wistar complement wistar rat complement serum | order wistar complement wistar rat complement serum | How to use: wistar complement wistar rat complement serum | su
Definition : Immunoassay reagents intended to perform qualitative and/or quantitative analyses on a body fluid sample (typically serum) to detect and/or measure levels of one or more of the proteins C5 to C9 found in the final complement pathway. Deficiency of complement components C5 to C9 are associated with several diseases, especially recurrent neisserial infections.. Entry Terms : "C5-9 (Complement Component) Determination Reagents" , "Reagents, Immunoassay, Protein, Complement Component, C5-C9". UMDC code : 19804 ...
Learn more about Alexions product Soliris® (eculizumab) for the treatment of patients with PNH, aHUS, and gMG and its approved uses and risks including BOXED WARNING
Data from an open-label extension study of eculizumab was on display at the American Association of Neuromuscular & Electrodiagnostic Medicine Meeting.
Learn how uncontrolled or excessive complement activation may play a role in several autoimmune and inflammatory diseases, and why APL-2 (pegcetacoplan) targeting of complement proteins at the level of C3 is being investigated as a treatment.
Granulocytic infiltrate occurs in the absence of demyelination, terminal complement complex formation, and overt tissue destruction in NMO white matter. a H&
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
Im doing a project for my cell class (sorry if this is in the wrong forum--I couldnt find a homework forum) about the eosinophil chemotactic factor. I was wondering if someone could point me in the right direction for a few answers. My professor seemed to think everything could be found online and I dont doubt him, Im just getting conflicting answers. Heres what I have so far ...
Compliance Statement D: For laboratory tests using a manufactured RUO kit. This test was developed and its performance characteristics determined by ARUP Laboratories. The U. S. Food and Drug Administration has not approved or cleared this test; however, FDA clearance or approval is not currently required for clinical use. The results are not intended to be used as the sole means for clinical diagnosis or patient management decisions ...
Introduction to the Complement System The innate and adaptive immune systems are no longer considered as distinct separate entities but are now recognized
マウス・モノクローナル抗体 ab17931 交差種: Hu 適用: WB,ELISA,IHC-P,Flow Cyt…C9抗体一覧…画像、プロトコール、文献などWeb上の情報が満載のアブカムの Antibody 製品。国内在庫と品質保証制度も充実。
This is going to be a sponsored log complements of LG. Big thanks to Inarius for setting this up for me! I will post up the general product
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.
C5a is a protein fragment released from cleavage of complement component C5 by protease C5-convertase into C5a and C5b fragments. C5b is important in late events of the complement cascade, an orderly series of reactions which coordinates several basic defense mechanisms, including formation of the Membrane Attack Complex (MAC), one of the most basic weapons of the innate immune system, formed as an automatic response to intrusions from foreign particles and microbial invaders. It essentially pokes microscopic pinholes in these foreign objects, causing loss of water and sometimes death. C5a, the other cleavage product of C5, acts as a highly inflammatory peptide, encouraging complement activation, formation of the MAC, attraction of innate immune cells, and histamine release involved in allergic responses. The origin of C5 is in the hepatocyte, but its synthesis can also be found in macrophages, where it may cause local increase of C5a. C5a is a chemotactic agent and an anaphylatoxin; it is ...
Porcine complement regulators protect aortic smooth muscle cells poorly against human complement-induced lysis and proliferation: consequences for xenotransplantation. Xenotransplantation 12 (3) , pp. 217-226. 10.1111/j.1399-3089.2005.00217.x ...
Looking for Complement system? Find out information about Complement system. The sequential activation of complement proteins resulting in lysis of a target cell Explanation of Complement system
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.
Activation of complement C5 generates the potent anaphylatoxin C5a and leads to pathogen lysis, inflammation and cell damage. The therapeutic potential of C5 inhibition has been demonstrated by eculizumab, one of the worlds most expensive drugs. However, the mechanism of C5 activation by C5 convertases remains elusive, thus limiting development of therapeutics. Here we identify and characterize a new protein family of tick-derived C5 inhibitors. Structures of C5 in complex with the new inhibitors, the phase I and phase II inhibitor OmCI, or an eculizumab Fab reveal three distinct binding sites on C5 that all prevent activation of C5. The positions of the inhibitor-binding sites and the ability of all three C5-inhibitor complexes to competitively inhibit the C5 convertase conflict with earlier steric-inhibition models, thus suggesting that a priming event is needed for activation.
- Data presented at 12th Congress of European Hematology -...CHESHIRE Conn. June 11 2007 /PRNewswire-FirstCall/ -- AlexionPharm... The Terminal Complement Inhibitor Eculizumab Reduces Thrombosisin Pa... Safety and Efficacy of the Terminal Complement InhibitorEculizumab i... The Clinical Benefit of Eculizumab Is Demonstrable in allSubpopulati...,Studies,Show,Efficacy,and,Safety,of,Alexions,Soliris,in,Broad,Population,of,PNH,Patients,medicine,advanced medical technology,medical laboratory technology,medical device technology,latest medical technology,Health
Complement C6, 50 µg. C6 is a component of complement cascade. It is part of the membrane attack complex which can insert into the cell membrane and cause cell to lyse.
Combining with the C1q component of the classical complement cascade and transmitting the signal from one side of the membrane to the other to initiate a change in cell activity.
Looking for online definition of complement in the Medical Dictionary? complement explanation free. What is complement? Meaning of complement medical term. What does complement mean?
In a significant development the FDA in the USA approved Soliris (Eculizumab) for use in atypical Hemolytic Uremic Syndrome. To those saying,
Looking for complement number system? Find out information about complement number system. System of number handling in which the complement of the actual number is operated upon; used in some computers to facilitate arithmetic operations Explanation of complement number system
An intracellular complement system (ICS) has recently been described in immune and nonimmune human cells. This system can be activated in a convertase-independent manner from intracellular stores of the complement component C3. The source of these stores has not been rigorously investigated. In the present study, Western blotting identified a band corresponding to C3 in freshly isolated human peripheral blood cells that was absent in corresponding cell lines. One difference between native cells and cell lines was the time absent from a fluid-phase complement source; therefore, we hypothesized that loading C3 from plasma was a route of establishing intracellular C3 stores. We found that many types of human cells specifically internalized C3(H2O), the hydrolytic product of C3, and not native C3, from the extracellular milieu. Uptake was rapid, saturable, and sensitive to competition with unlabeled C3(H2O), indicating a specific mechanism of loading. Under steady-state conditions, approximately 80% ...
|strong|Mouse anti Human C3d antibody, clone 053A-514.3.1.4|/strong| recognizes human complement component 3d (C3d) neoantigen, a ~33 kDa polypeptide fragment generated over the course of complem…
In the late 19th century, blood serum was found to contain a "factor" or "principle" which was capable of killing bacteria. In 1896, Jules Bordet, a young Belgian scientist in Paris at the Pasteur Institute, demonstrated that this principle could be analyzed into two components: a heat-stable and a heat-labile component. (Heat-labile meaning that it lost its effectiveness if the serum was heated.) The heat-stable component was found to confer immunity against specific microorganisms, while the heat-labile component was found to be responsible for the non-specific antimicrobial activity conferred by all normal serum. This heat-labile component is what we now call "complement". The term "complement" was introduced by Paul Ehrlich in the late 1890s, as part of his larger theory of the immune system. According to this theory, the immune system consists of cells which have specific receptors on their surface to recognize antigens. Upon immunization with an antigen, more of these receptors are formed, ...
These studies suggested that cell lysates and supernatant collected from cultured PMNs that were exposed to cytokines or C. albicans hyphae opsonized with normal human serum had elevated levels of C6 and C7 proteins [18,19]; however, it was not conclusive that these proteins were produced by PMNs in culture because (1) the rise in C6 or C7 in culture could have been released by C. albicans hyphae or derived from normal human serum, (2) the inhibition of protein biosynthesis by cycloheximide did not affect the rise in C6 or C7 in PMN cultures [18], and (3) conclusive evidence showing that PMNs are actively expressing these terminal complement mRNAs or proteins has been lacking in the literature ...
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Date: 1906. : the process of binding serum complement to the product formed by the union of an antibody and the antigen for which it is specific that occurs when complement is.
Hi there: I want to establish a complement assay with porcine islet cells after incubation with certain antibodies to produce cell lysis! Does anyone have any protocols or hints? E.g. does it matter what species the complement is from, what concentration do I use etc.. Thanks in advance John ...
Study Flashcards On Immuno Five: Complement at Cram.com. Quickly memorize the terms, phrases and much more. Cram.com makes it easy to get the grade you want!
View Notes - biol1201 mar4 notes from BIOL 1201 at LSU. 3/4/08 The purpose of mitosis is to insure that the daughter cells have the identical genetic complement of the mother cell. True DNA is
The RIQAS Specific Protein EQA programme is designed to monitor the performance of up to 26 serum proteins including CRP, ASO, RF, Complement Proteins and Immunoglobulins. Three flexible size options are available to help reduce waste and costs.. Available Applications. http://inserts.randox.com/out.php. Parameters ...
TY - JOUR. T1 - Immunoglobulin G monoclonal antibodies to Cryptococcus neoformans protect mice deficient in complement component C3. AU - Shapiro, Scott. AU - Beenhouwer, David O.. AU - Feldmesser, Marta. AU - Taborda, Carlos. AU - Carroll, Michael C.. AU - Casadevall, Arturo. AU - Scharff, Matthew D.. PY - 2002. Y1 - 2002. N2 - Passive administration of monoclonal antibodies (MAbs) to the capsular polysaccharide of Cryptococcus neoformans can alter the course of infection in mice. In a murine model of cryptococcal infection, immunoglobulin G1 (IgG1), IgG2a, and IgG2b switch variants of the anti-capsular 3E5 MAb prolong the survival of lethally infected mice, whereas the 3E5 IgG3 MAb does not protect and in some cases enhances infection, shortening the life spans of infected mice. We examined the role of complement component C3 in Ab-mediated protection by determining the efficacy of the four mouse IgG subclasses against C. neoformans in mice genetically deficient in factor C3 as well as mice ...
OP28 The complement component C3 is expressed by the endometrial ectopic tissue and is involved in the endometriotic lesion formation C. Agostinis 1, G. Zito 1, D. De Santo1, R. Vidergar2, O. Radillo 1, F. Bossi 1, S. Zorzet2, G. Ricci 1, R. Bulla 2 1 Institute for Maternal and Child Health, IRCCS Burlo Garofolo, Trieste, Italy 2 Department of Life Sciences, University of Trieste, Trieste, Italy E-mail address: [email protected] (C. Agostinis). Background: The complement (C) system is one of the major components of humoral innate immunity, acting as the first lines of defence against microbes. The principal roles of C system are the opsonization and lysis of pathogens, but new roles in inflammatory and immunological processes are emerging. It is involved in numerous inflammatory diseases, such as SLE, PNH and endometriosis (EM). Several groups have been demonstrated that the glandular epithelial cells found in endometriotic implants produce and secrete the C component C3. The aim ...
Secretion of complement component C3 by U937 cells was studied. Preliminary evidence for a cell-associated proteolytic activity specific for C3 is given, as well as for a covalent-like binding of C3 fragments to the cell membranes. Secretion of C3, in the presence of 10 ng of phorbol 12-myristate 13-acetate/ml, is 120-140 ng/10(6) cells per 24 h on the third day after addition of the activator. As shown by SDS/polyacrylamide-gel electrophoresis, the intracellular pro-C3 (200 kDa) and the extracellular secreted C3 (alpha-chain 110 kDa and beta-chain 75 kDa) are identical with the forms of C3 previously characterized from human serum. Incubation of U937 cells in the presence of exogenous radiolabelled C3 shows that membrane-bound proteinase(s), not related to the classical-pathway or the alternative-pathway C3 convertases, is (are) able to cleave C3; this cleavage leads to the binding of the resulting C3 fragments to the cell membrane through reaction of membrane acceptors with the carbonyl group ...
When the complement system is activated, it triggers a variety of events leading to cleavage of one component known as C5. Once C5 is cleaved, a variety of events occur that propagate the formation of the membrane attack complex. This member attack complex generates pores, or holes, in cells ultimately leading to the cells demise. So when you have such a powerful system, regulators of the system are needed. These regulators sit on the outer membrane of cells, so the complement system recognizes that these cells are of the self. When those regulators are missing, as is the case in PNH, this leads to the destructions of the cells that are missing these protein shields.. Some of those shields, (2 proteins known as CD 55 and CD 59) are anchored the cell surface by a tail. We call this tail a GPI anchor - but in PNH this GPI anchor is missing because of a mutation in a gene called PIG-A. This defective gene leads to cause the cells inability to form this GPI anchor. So the complement regulator ...
Now, they may soon add a new risk factor to the list: activation of the complement system. The complement system is usually implicated in immune responses, but now theres a role for it in cardiovascular disease. In a new research report appearing in the January 2011 print issue of the FASEB Journal (http://www.fasebj.org), scientists from Europe and the United States show that anaphylatoxin C5a, a protein released when complement is activated, contributes to atherosclerotic disease. C5a causes plaques to break free from where they would be anchored to ultimately cause blockages elsewhere in the body. This new discovery not only shows that C5a is a new marker for identifying risk for heart attack and stroke, but it also establishes C5a as a new therapeutic target for preventing these problems.. "Given the huge impact of cardiovascular disease in general, and atherosclerosis in particular, on public health, we feel that unraveling mechanisms involved in the development and progression of the ...
Detailed description of complement system including classical pathway, alternate pathway and lectin pathway. Components of complement system includingC1, C2, C3, C4, C5, C6, C7, C8, C9, C1-INH, C3a-INA, Factors H and I, C3a-INA, C4-BP and Factor I, C3a-INA, Protein S (vitronectin).
Recombinant Complement Component 1, R Subcomponent A (C1RA) Protein (His tag). Species: Mouse (Murine). Source: Insect Cells. Order product ABIN3125986.
Complement, C3 Convertase, Regulation, Cells, Disease, Complement Factor H, Inhibition, Therapeutic, Transplant, Allograft, Donor, Donors, and Graft
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The C5b-9 complex (Terminal Complement Complex-TCC) is the final product of the terminal complement pathway. In this study, using the monoclonal antibody MCaE11 (specific for a C9 neoantigen) and an immunohistochemical technique, we examined the TCC deposits in synovial tissues from 4 patients affected by rheumatoid arthritis (RA) and 6 patients affected by osteoarthritis (OA). Synovial tissues from 8 patients affected by acute joint trauma were examined as controls. Furthermore, plasma TCC levels were measured in 44 RA patients and 51 controls, using the above mentioned antibody and a sandwich ELISA. Eight synovial fluids were also included in this study. Abundant TCC deposits were detected in the cytoplasm of the synovial lining cells and of large stromal mononuclear cells in all the RA and in 3 out of 6 OA synovial tissues characterized by histological signs of inflammation. No TCC deposits were found in non-inflamed synovial tissues from patients with joint trauma. In agreement with previous ...

Competitor Analysis: Complement C5 Inhibitors 2017 - Biosuperiors & BiosimilarsCompetitor Analysis: Complement C5 Inhibitors 2017 - Biosuperiors & Biosimilars

This Competitive Intelligence report about Complement C5 Inhibitors 2017 - Biosuperiors & Biosimilars provides a competitor ... 3. Novel Complement C5 Inhibitors. 4. Complement C5a Receptor Antagonist. 5. Corporate C5 Inhibitor R&D Pipelines ... The report includes a compilation of currently active projects in research and development of inhibitors of complement C5 or ... This Competitive Intelligence report about Complement C5 Inhibitors 2017 - Biosuperiors & Biosimilars provides a competitor ...
more infohttps://www.researchandmarkets.com/reports/4228592/competitor-analysis-complement-c5-inhibitors

Complement C5 Mediates Experimental Tubulointerstitial Fibrosis | American Society of NephrologyComplement C5 Mediates Experimental Tubulointerstitial Fibrosis | American Society of Nephrology

Complement C5 Mediates Experimental Tubulointerstitial Fibrosis. Peter Boor, Andrzej Konieczny, Luigi Villa, Anna-Lisa Schult, ... Complement C5 Mediates Experimental Tubulointerstitial Fibrosis. Peter Boor, Andrzej Konieczny, Luigi Villa, Anna-Lisa Schult, ... Complement C5 Mediates Experimental Tubulointerstitial Fibrosis. Peter Boor, Andrzej Konieczny, Luigi Villa, Anna-Lisa Schult, ... Complement C5 Mediates Experimental Tubulointerstitial Fibrosis Message Subject (Your Name) has sent you a message from ...
more infohttps://jasn.asnjournals.org/content/18/5/1508?ijkey=d71207c4a1a6317ad77d49a63d86df642a04bf8b&keytype2=tf_ipsecsha

Complement C5 Mouse anti-Human, Baboon, Alexa Fluor 750, Clone: C17/5,
 | Fisher ScientificComplement C5 Mouse anti-Human, Baboon, Alexa Fluor 750, Clone: C17/5, | Fisher Scientific

Novus Biologicals Complement C5 Antibody; Alexa Fluor 750; 0.1 mL ... Complement C5 Mouse anti-Human, Baboon, Alexa Fluor 750, Clone ... Complement C5 Monoclonal antibody specifically detects Complement C5 in Human,Baboon samples. It is validated for Western Blot, ... anaphylatoxin C5a analog, C3 and PZP-like alpha-2-macroglobulin domain-containing protein 4, C5, complement C5, complement ... Complement C5 Mouse anti-Human, Baboon, Alexa Fluor 750, Clone: C17/5, Novus Biologicals ...
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Effects of Complement C5 on Apoptosis in Experimental Autoimmune Encephalomyelitis | The Journal of ImmunologyEffects of Complement C5 on Apoptosis in Experimental Autoimmune Encephalomyelitis | The Journal of Immunology

C5-d, C5 deficient; C5-s, C5 sufficient; C5b-9, terminal complement complexes consisting of C5b, C6, C7, C8, and C9 proteins. ... C5-d and C5-sufficient (C5-s) mice had similar numbers of total apoptotic cells, whereas C5-s had significantly fewer than C5-d ... Quantitation of Fas expression in C5-d and C5-s mice with EAE. Spinal cords from C5-d (n = 3) and C5-s (n = 3) mice during ... Quantitation of FasL expression in C5-d and C5-s mice with EAE. Spinal cord cryostat sections from C5-d (n = 3) and C5-s (n = 3 ...
more infohttps://www.jimmunol.org/content/172/9/5702?ijkey=dabe8447f9b8f9d1c760aa66c121434fa7338fa1&keytype2=tf_ipsecsha

Complement C5-inhibitor rEV576 (coversin) ameliorates in-vivo effects of antiphospholipid antibodies. | Sigma-AldrichComplement C5-inhibitor rEV576 (coversin) ameliorates in-vivo effects of antiphospholipid antibodies. | Sigma-Aldrich

Complement C5-inhibitor rEV576 (coversin) ameliorates in-vivo effects of antiphospholipid antibodies.. [Z Romay-Penabad, A L ... Activation of the complement cascade is an important mechanism for antiphospholipid antibody-mediated thrombosis. We examined ... The data confirm involvement of complement activation in antiphospholipid antibody-mediated thrombogenesis and suggest that ... the effects of rEV576 (coversin), a recombinant protein inhibitor of complement factor 5 activation, on antiphospholipid ...
more infohttps://www.sigmaaldrich.com/catalog/papers/25228739

complement C5 | Ligand page | IUPHAR/BPS Guide to PHARMACOLOGYcomplement C5 | Ligand page | IUPHAR/BPS Guide to PHARMACOLOGY

complement C5 ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs. ... This peptide is cleaved into the complement C5 beta chain, complement C5 alpha chain and C5a anaphylatoxin (see the UniProt ... C5 inhibition is a clinically validated mechanism that is utilised for the control and suppression of complement-induced ... Investigational Phase 1/2 anti-C5 monoclonal RG6101 (SKY59 [3]; IMGT 783) was granted FDA orphan drug designation in September ...
more infohttp://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=8712

Complement C5-blocking Agent in Refractory Dermatomyositis | The Journal of RheumatologyComplement C5-blocking Agent in Refractory Dermatomyositis | The Journal of Rheumatology

Complement C5-blocking Agent in Refractory Dermatomyositis Message Subject (Your Name) has forwarded a page to you from The ... Complement C5-blocking Agent in Refractory Dermatomyositis. STANISLAS FAGUER, JULIE BELLIERE and DAVID RIBES ... Here, we report a case of acute refractory DM with concomitant thrombotic microangiopathy (TMA) that improved with the C5- ... Microvascular alterations and the role of complement in dermatomyositis. Brain 2016;139:1891-903. ...
more infohttp://www.jrheum.org/content/45/12/1710

Complement C5 Antibody (Biotin) for IHC, WB/Western LS-C684436Complement C5 Antibody (Biotin) for IHC, WB/Western LS-C684436

Complement C5 antibody LS-C684436 is a biotin-conjugated mouse monoclonal antibody to mouse Complement C5. Validated for IHC ... Complement C5 antibody LS-C684436 is a biotin-conjugated mouse monoclonal antibody to mouse Complement C5. Validated for IHC ... Complement C5 antibody LS-C684436 is a biotin-conjugated mouse monoclonal antibody to mouse Complement C5. Validated for IHC ... Complement C5 antibody was raised against recombinant C5a (Asn679~Arg755 (Accession # P06684)) expressed in E.coli ...
more infohttps://www.lsbio.com/antibodies/complement-c5-antibody-biotin-ihc-wb-western-ls-c684436/709864

Anti-Complement C5 Antibody | Mouse anti-Mouse Monoclonal Cy3 | LSBioAnti-Complement C5 Antibody | Mouse anti-Mouse Monoclonal Cy3 | LSBio

Complement C5 antibody LS-C698214 is a Cy3-conjugated mouse monoclonal antibody to mouse Complement C5. Validated for IHC and ... Complement C5 antibody LS-C698214 is a Cy3-conjugated mouse monoclonal antibody to mouse Complement C5. Validated for IHC and ... Complement C5 antibody LS-C698214 is a Cy3-conjugated mouse monoclonal antibody to mouse Complement C5. Validated for IHC and ... Complement C5 antibody was raised against recombinant C5a (Asn679~Arg755 (Accession # P06684)) expressed in E.coli ...
more infohttps://www.lsbio.com/antibodies/complement-c5-antibody-cy3-ihc-wb-western-ls-c698214/723642

SDevelopment of dextran sulfate sodium-induced colitis is aggravated in mice genetically deficient for complement C5SDevelopment of dextran sulfate sodium-induced colitis is aggravated in mice genetically deficient for complement C5

We used DBA2/J mice, which are genetically deficient in complement C5. DBA1/J mice have a normal complement system, and were ... SDevelopment of dextran sulfate sodium-induced colitis is aggravated in mice genetically deficient for complement C5. *Authors: ... The complement system is a potent effector of innate immunity. To elucidate the pathophysiological role of the complement ... SDevelopment of dextran sulfate sodium-induced colitis is aggravated in mice genetically deficient for complement C5. ...
more infohttps://www.spandidos-publications.com/ijmm/16/4/605

Complement C5 (C3 And PZP Like Alpha 2 Macroglobulin Domain Containing Protein 4 or C5) - Pipeline Review, H2 2017Complement C5 (C3 And PZP Like Alpha 2 Macroglobulin Domain Containing Protein 4 or C5) - Pipeline Review, H2 2017

C3 And PZP Like Alpha 2 Macroglobulin Domain Containing Protein 4 or C5) - Pipeline Review, H2 2017 Download the full report: ... Activation of C5 by a C5 convertase initiates the spontaneous assembly of the late complement components, C5-C9, into the ... 12, 2017 /PRNewswire/ -- Complement C5 (C3 And PZP Like Alpha 2 Macroglobulin Domain Containing Protein 4 or C5) - Pipeline ... Complement C5 (C3 And PZP Like Alpha 2 Macroglobulin Domain Containing Protein 4 or C5) - Pipeline Review, H2 2017. Friday, ...
more infohttp://www.medindia.net/health-press-release/Complement-C5-C3-And-PZP-Like-Alpha-2-Macroglobulin-Domain-Containing-Protein-4-or-C5-Pipeline-Review-H2-2017--344249-1.htm

Molecular insights into the surface-specific arrangement of complement C5 convertase enzymes | BMC Biology | Full TextMolecular insights into the surface-specific arrangement of complement C5 convertase enzymes | BMC Biology | Full Text

The C5 convertase is a multi-molecular protease complex that catalyses the cleavage of native C5 into its biologically ... Finally, we define two interfaces on C5 important for its recognition by surface-bound C5 convertases. We establish a highly ... Alternative pathway (AP) C5 convertases were generated on small streptavidin beads that were coated with purified C3b molecules ... In the presence of factor B and factor D, these C3b beads could effectively convert C5. Conversion rates of surface-bound C3b ...
more infohttps://bmcbiol.biomedcentral.com/articles/10.1186/s12915-015-0203-8

CAS No.219685-93-5,Immunoglobulin,anti-(human complement C5 a-chain) (human-mouse monoclonal 5G1.1-SC single chain) (9CI)...CAS No.219685-93-5,Immunoglobulin,anti-(human complement C5 a-chain) (human-mouse monoclonal 5G1.1-SC single chain) (9CI)...

where to buy 219685-93-5(Immunoglobulin,anti-(human complement C5 a-chain) (human-mouse monoclonal 5G1.1-SC single chain) (9CI ... human complement C5 a-chain) (human-mouse monoclonal 5G1.1-SC single chain) (9CI)) including MSDS sheet(poisoning, toxicity, ... human complement C5 a-chain) (human-mouse monoclonal 5G1.1-SC single chain) (9CI)) for price inquiry. ... Immunoglobulin,anti-(human complement C5 a-chain) (human-mouse monoclonal 5G1.1-SC single chain) (9CI) ...
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Complement Component C5/C5a Research Products: Novus BiologicalsComplement Component C5/C5a Research Products: Novus Biologicals

Browse our Complement Component C5/C5a product catalog backed by our Guarantee+. ... Complement Component C5/C5a products available through Novus Biologicals. ... PTMs for Complement Component C5/C5a. Learn more about PTMs related to Complement Component C5/C5a.. Cleavage. Methylation. ... Diseases related to Complement Component C5/C5a. Discover more about diseases related to Complement Component C5/C5a.. Spinal ...
more infohttps://www.novusbio.com/common-name/complement-component-c5-c5a

Content - Complement C5 (C3 And PZP Like Alpha 2 Macroglobulin Domain Containing Protein 4 or C5) - Pipeline Review, H2 2018 |...Content - Complement C5 (C3 And PZP Like Alpha 2 Macroglobulin Domain Containing Protein 4 or C5) - Pipeline Review, H2 2018 |...

C3 And PZP Like Alpha 2 Macroglobulin Domain Containing Protein 4 or C5) pipeline Target constitutes close to 33 molec ... Complement C5 (C3 And PZP Like Alpha 2 Macroglobulin Domain Containing Protein 4 or C5) - Overview. Complement C5 (C3 And PZP ... Complement C5 (C3 And PZP Like Alpha 2 Macroglobulin Domain Containing Protein 4 or C5) - Dormant Products. Complement C5 (C3 ... Complement C5 (C3 And PZP Like Alpha 2 Macroglobulin Domain Containing Protein 4 or C5) - Drug Profiles. AcPepA - Drug Profile ...
more infohttps://www.asdreports.com/market-research-content-469691/complement-c-c-pzp-like-alpha-macroglobulin-domain-containing-protein

Structural basis for therapeutic inhibition of complement C5. - Oxford NeuroscienceStructural basis for therapeutic inhibition of complement C5. - Oxford Neuroscience

Here we identify and characterize a new protein family of tick-derived C5 inhibitors. Structures of C5 in complex with the new ... However, the mechanism of C5 activation by C5 convertases remains elusive, thus limiting development of therapeutics. ... or an eculizumab Fab reveal three distinct binding sites on C5 that all prevent activation of C5. The positions of the ... The therapeutic potential of C5 inhibition has been demonstrated by eculizumab, one of the worlds most expensive drugs. ...
more infohttps://www.neuroscience.ox.ac.uk/publications/613121

Complement C3-C5 Convertases
      - C3 Convertase
     Summary Report | CureHunterComplement C3-C5 Convertases - C3 Convertase Summary Report | CureHunter

Serine proteases that cleave COMPLEMENT C3 into COMPLEMENT C3A and COMPLEMENT C3B, or cleave COMPLEMENT C5 into COMPLEMENT C5A ... These include the different forms of C3/C5 convertases in the classical and the alternative pathways of COMPLEMENT ACTIVATION. ... Complement C5 Convertases; Activator, C3; C3 Convertases, Complement; C3-C5 Convertases, Complement; C5 Convertases, Complement ... C3-C5; Convertase, Complement 3; Convertases, Complement C3; Convertases, Complement C3-C5; Convertases, Complement C5 ...
more infohttp://www.curehunter.com/public/keywordSummaryD050577-Complement-C3-C5-Convertases-C3-Convertase.do

C5 Complement, Antigen, Serum -
Mayo Clinic Laboratories RochesterC5 Complement, Antigen, Serum - Mayo Clinic Laboratories Rochester

Test ID C5AG C5 Complement, Antigen, Serum Useful For. Diagnosis of C5 deficiency ... The total complement assay (COM / Complement, Total, Serum) should be used as a screen for suspected complement deficiencies ... A deficiency of an individual component of the complement cascade will result in an undetectable total complement level. ...
more infohttps://testcatalog.org/show/C5AG

A Novel Role of Complement: Mice Deficient in the Fifth Component of Complement (C5) Exhibit Impaired Liver Regeneration | The...A Novel Role of Complement: Mice Deficient in the Fifth Component of Complement (C5) Exhibit Impaired Liver Regeneration | The...

BrdU-positive hepatocytes were counted in liver sections from C5+/+, C5−/−, C5−/− (+C5), and C5−/− (+C5a) mice at the indicated ... Low-power photomicrographs of BrdU-stained liver sections from C5+/+ (A-C), C5−/− (D-F), and C5−/− (+C5) mice (G and H) at ... A, BrdU incorporation profile of C5+/+ and C5−/− mice at various times after CCl4 treatment. C5+/+ and C5−/− mice were treated ... for C5−/− (+C5) sections. Round, dark nuclei indicate positively stained hepatocytes. Slides from C5+/+ and C5−/− mice were ...
more infohttps://www.jimmunol.org/content/166/4/2479?ijkey=60ad27f936c5782079f90048fb24e543268bf494&keytype2=tf_ipsecsha

Porcine C5c (Complement C5 Convertase) ELISA Kit Manufacturers in DelhiPorcine C5c (Complement C5 Convertase) ELISA Kit Manufacturers in Delhi

Complement C5 Convertase) ELISA Kit OSCAR DIAGNOSTIC SERVICES PVT. LTD.is an India based Company in Delhi. ... Porcine C5c (Complement C5 Convertase) ELISA Kit » Porcine C5c (Complement C5 Convertase) ELISA Kit. Porcine C5c (Complement C5 ... Porcine C5c (Complement C5 Convertase) ELISA Kit. Porcine C5c (Complement C5 Convertase) ELISA Kit. Porcine C5c (Complement C5 ... Porcine C5c (Complement C5 Convertase) ELISA Kit. Porcine C5c (Complement C5 Convertase) ELISA Kit. Porcine C5c (Complement C5 ...
more infohttps://www.odspl.com/sub-product/Porcine+C5c+%28Complement+C5+Convertase%29+ELISA+Kit.php

Complement C5 Gene Confers Risk for Acute Anterior Uveitis.  - PubMed - NCBIComplement C5 Gene Confers Risk for Acute Anterior Uveitis. - PubMed - NCBI

Complement C5 Gene Confers Risk for Acute Anterior Uveitis.. Xu D1, Hou S1, Jiang Y1, Zhang J1, Cao S1, Zhang D1, Luo L1, ... The C5 rs2269067 GG genotype confers risk for AAU in a Chinese population and is associated with an elevated C5 serum ... The frequency of the GG genotype of rs2269067 in C5 was increased in AAU patients with or without AS compared to controls (Pc ... However, the association of C3 and C5 SNPs with acute anterior uveitis (AAU) has not yet been investigated and was the purpose ...
more infohttps://phgkb.cdc.gov/PHGKB/phgHome.action?action=forward&dbsource=huge&id=115999

Effects of C5 Complement Inhibitor Pexelizumab on Outcome in High-Risk Coronary Artery Bypass Grafting: Combined Results From...Effects of C5 Complement Inhibitor Pexelizumab on Outcome in High-Risk Coronary Artery Bypass Grafting: Combined Results From...

YOU ARE HERE: Home , Latest in Cardiology , Effects of C5 Complement Inhibitor Pexelizumab on Outcome in High-Risk Coronary ... Effects of C5 Complement Inhibitor Pexelizumab on Outcome in High-Risk Coronary Artery Bypass Grafting: Combined Results From ... Complement C5, Europe, Percutaneous Coronary Intervention, Postoperative Period, Incidence, Heart Failure, Survival Analysis, ... What is the safety and efficacy of terminal complement inhibition in reducing perioperative myocardial infarction (MI) and ...
more infohttp://www.acc.org/latest-in-cardiology/journal-scans/2011/08/04/22/50/effects-of-c5-complement-inhibitor-pexelizumab-on-outcome

Human Complement C5 Level Assay | Molecular Otolaryngology and Renal Research LaboratoriesHuman Complement C5 Level Assay | Molecular Otolaryngology and Renal Research Laboratories

Complement C5 Level Assay Complement component 5 (C5) is a plasma glycoprotein (MW: 195 kDa) synthesized in the liver, ... C5α and C5β). Upon activation, C5 is cleaved into C5a (MW: 11 kDa) and C5b (MW: 185 kDa) by C5 convertase. C5a is a potent ... Consumption of AP complement components is dependent on the degree of dysregulation of the C3 and C5 convertases. Plasma C5 ... Defining the complement biomarker profile of C3 glomerulopathy, CJASN 2014).. Indications for screening Screening is ...
more infohttps://morl.lab.uiowa.edu/clinical-diagnostics/complement-assays/tests-included/human-complement-c5-level-assay

Complement component C5 and C6 mutation screening indicated in meningococcal disease in South AfricaComplement component C5 and C6 mutation screening indicated in meningococcal disease in South Africa

Terminal complement components comprise the final 5 components of the complement cascade (C5 to C9). All combine on antibody- ... C5 and C6 protein levels. C5 protein levels were detected with a specific C5 enzyme-linked immunosorbent assay (ELISA) ... C5 protein levels. C5 levels were tested in 2 of the 3 homozygous C5D-A252T patients (the third died of MD and only DNA was ... Inherited human complement C5 deficiency. Nonsense mutations in exons 1 (Gln1 to Stop) and 36 (Arg1458 to Stop) and compound ...
more infohttp://www.scielo.org.za/scielo.php?script=sci_arttext&pid=S0256-95742012000600068&lng=en&nrm=iso

Complement Component 5 (C5) AntikörperComplement Component 5 (C5) Antikörper

179 verschiedene C5 Antikörper vergleichen. Alle direkt auf antikörper-online bestellbar! ... complement C5 , prepro-C5 , anaphylatoxin , complement component C5 , complement C5a anaphylatoxin ... anti-Complement Component 5 (C5) Antikörper. Bezeichnung:. anti-Complement Component 5 Antikörper (C5). Auf www.antikoerper- ... Bezeichner auf Proteinebene für C5 complement component 5 , similar to complement component C5-1 , C3 and PZP-like alpha-2- ...
more infohttp://www.antikoerper-online.de/komplementsystem-pathway-11/c5-antibody-18445/
  • Here, we report a case of acute refractory DM with concomitant thrombotic microangiopathy (TMA) that improved with the C5-blocking agent eculizumab in the setting of other medications. (jrheum.org)
  • Structures of C5 in complex with the new inhibitors, the phase I and phase II inhibitor OmCI, or an eculizumab Fab reveal three distinct binding sites on C5 that all prevent activation of C5. (ox.ac.uk)
  • Data show the expression of a neoepitope which was exposed on complement C5 (C5) after binding to eculizumab in vivo. (antikoerper-online.de)
  • In silico docking confirmed the implication of a beta-hairpin located between residues 913 and 922, outside the known epitope, in the binding of eculizumab to C5. (innopsys.com)
  • Two residues in particular, Arg885 and Trp917, were defined as major participants in the interaction of C5 and eculizumab. (innopsys.com)
  • Their important role was confirmed by the recent publication of a crystal structure of eculizumab Fab bound to C5. (innopsys.com)
  • The drug eculizumab (trade name Soliris) prevents cleavage of C5 into C5a and C5b. (wikipedia.org)
  • A ) Complement FH levels in mouse plasma isolated from 19 C3KI mice (triangles), 34 C3KI/WT (squares), and 19 WT (circle) mice, P14-28, were established using an in-house sandwich ELISA described in Methods. (jci.org)
  • B ) C5 levels in mouse plasma isolated from 17 C3KI, 15 C3KI/WT, and 8 WT mice on P14-P28 were established using an in-house sandwich ELISA. (jci.org)
  • In experimental immune-complex glomerulonephritis, lack of the C5a receptor (C5aR) reduced infiltrating interstitial cells and tubulointerstitial damage but had no influence on glomerular injury, thereby pointing to a role of the anaphylatoxin C5a, a small peptide that is released from C5, in tubulointerstitial injury ( 12 ). (asnjournals.org)
  • Activation of complement C5 generates the potent anaphylatoxin C5a and leads to pathogen lysis, inflammation and cell damage. (ox.ac.uk)
  • The developed model and molecular insights are essential to understand the molecular basis of deregulated complement activity in human disease and will facilitate future design of therapeutic interventions against these critical enzymes in inflammation. (biomedcentral.com)
  • Molecular modelling of p.A252T has indicated an area of molecular stress in the C5 molecule which may provide a mechanism for the very low level in the circulation. (cdc.gov)
  • The report includes a compilation of currently active projects in research and development of inhibitors of complement C5 or antagonists of the C5a recepotr. (researchandmarkets.com)
  • In addition, the report lists company-specific R&D pipelines of C5 inhibitors. (researchandmarkets.com)
  • This enzyme catalyses the following chemical reaction Cleavage of Arg-Ser bond in complement component C3 alpha-chain to yield C3a and C3b, and Arg- bond in complement component C5 alpha-chain to yield C5a and C5b This enzyme is a bimolecular complex of complement fragment Bb with either C3b or cobra venom factor. (wikipedia.org)
  • Genotyping was performed for six SNPs in C3 and four SNPs in C5 in 395 AAU patients with ankylosing spondylitis (AS), 397 AAU patients without AS, and 597 healthy controls by PCR-restriction fragment length polymorphism (PCR-RFLP) or TaqMan SNP assay. (cdc.gov)
  • This study investigated the role of C5 in the development of renal tubulointerstitial fibrosis by ( 1 ) induction of renal fibrosis in wild-type and C5 −/− mice by unilateral ureteral ligation (UUO) and ( 2 ) investigation of the effects of a C5a receptor antagonist (C5aRA) in UUO. (asnjournals.org)
  • In C5 −/− mice, when compared with wild-type controls, markers of renal fibrosis (Sirius Red, type I collagen, fibronectin, α-smooth muscle actin, vimentin, and infiltrating macrophages) were significantly reduced on day 5 of UUO. (asnjournals.org)
  • Cortical mRNA of all PDGF isoforms and of TGF-β 1 ( i.e. , central mediators of renal disease) were significantly reduced in C5 −/− mice when compared with controls. (asnjournals.org)
  • In acute EAE, C5-d and C5-sufficient (C5-s) mice had similar numbers of total apoptotic cells, whereas C5-s had significantly fewer than C5-d during recovery. (jimmunol.org)
  • In addition, although both groups of mice displayed TUNEL + OLG, there were significantly fewer in C5-s than in C5-d during both acute EAE and recovery. (jimmunol.org)
  • DBA1/J mice have a normal complement system, and were used as controls. (spandidos-publications.com)
  • Reconstitution of C5-deficient mice with murine C5 or C5a significantly restored hepatocyte regeneration after toxic injury. (jimmunol.org)
  • Complement dysregulation in C3KI mice. (jci.org)
  • Furthermore, blockade of the C5a receptor (C5aR) abrogated the ability of hepatocytes to proliferate in response to liver injury, providing a mechanism by which C5 exerts its function, and establishing a critical role for C5aR signaling in the early events leading to hepatocyte proliferation. (jimmunol.org)
  • This potential involvement of complement in intricate morphogenetic and developmental processes, including tissue remodeling during limb regeneration and muscle cell differentiation in urodeles ( 14 ), provided the basis for an intriguing hypothesis that complement may also have been selected during evolution to participate in the regulation of the regenerative response in higher vertebrates. (jimmunol.org)
  • Most strikingly, complement factors appear to be involved in limb regeneration in certain urodele species. (jimmunol.org)
  • In this context, it has been recently proposed that complement factors may contribute to the regulation of amphibian limb regeneration, as indicated by the expression of the third component of complement (C3) in the regenerating limb blastema cells of certain urodele species ( 14 ). (jimmunol.org)
  • It is also known to be very species-specific for human C5, despite an important degree of conservation of the targeted macroglobulin domain, MG7, with that of other primates. (innopsys.com)
  • However, the association of C3 and C5 SNPs with acute anterior uveitis (AAU) has not yet been investigated and was the purpose of the study described. (cdc.gov)
  • Using a combined genetic and pharmacologic approach, C5, in particular C5a, is identified as a novel profibrotic factor in renal disease and as a potential new therapeutic target. (asnjournals.org)
  • The complement system, a phylogenetically ancient arm of the innate immune response ( 11 ), has recently been suggested to play novel roles in regulating noninflammatory processes, including cell proliferation and differentiation during development ( 12 , 13 ). (jimmunol.org)
  • Thus, our data provide in vivo modeling evidence that gain-of-function changes in complement C3 drive aHUS. (jci.org)