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.

2-Deoxyglucose selectively inhibits Fc and complement receptor-mediated phagocytosis in mouse peritoneal macrophages II. Dissociation of the inhibitory effects of 2-deoxyglucose on phagocytosis and ATP generation. (1/2484)

Macrophages incubated in 2-deoxy-D-glucose (2-dG)-containing medium showed a marked decrease in cellular ATP content, and were unable to ingest IgG- and complement-coated erythrocytes via the corresponding membrane receptors for these ligands. However, the inhibitory effects of 2-dG on Fc- and C3 receptor-mediated phagocytosis were not a consequence of lowered macrophage ATP levels since addition of glucose or mannose to the culture medium restored the capacity of the macrophages to ingest IgG- and C3-coated particles without increasing ATP levels. These results indicate that Fc- and C3 receptor-mediated phagocytosis (opsonin dependent) differs qualitatively from the ingestion of latex and zymosan particles (opsonin independent); they suggest that the same regulatory molecules govern the responses of phagocytic cells to signals initiated by both the Fc and C3 receptors. The possibility that these molecules are regulated by glycosylation is discussed.  (+info)

Activation of stimulus-specific serine esterases (proteases) in the initiation of platelet secretion. I. Demonstration with organophosphorus inhibitors. (2/2484)

The effect of organophosphorus inhibitors of serine esterases (proteases) on secretion from washed rabbit platelets was examined. Five noncytotoxic stimuli were employed: collagen, thrombin, heterologous anti-platelet antibody (in the absence of complement), rabbit C3 bound to zymosan, and platelet activating factor derived from antigen-stimulated, IgE-sensitized rabbit basophils. Diisoprophyl phosphofluoridate, three series of p-nitrophenyl ethyl phosphonates, and a series of cyclohexyl phenylalkylphosphonofluridates were all found to be inhibitory to the platelet secretion. These are irreversible inhibitors of serine proteases but in this system were only inhibitory if added to the platelets concurrently with the stimuli. Pretreatment of either the platelets or the stimuli with the inhibitors followed by washing, was without effect on the subsequent reaction. This suggested the involvement of stimulus-activatable serine proteases in the secretory process. The concept was supported by finding that nonphosphorylating phosphonates or hydrolyzed phosphonates or phosphonofluoridates were without inhibitory action. The effect of a series of phosphonates or phosphonoflouridates in inhibiting each stimulus exhibited a unique activity-structure profile. The demonstration of such unique profiles with four series of inhibitors for each of the five stimuli was interpreted as demonstrating that a specific activatable serine protease was involved in the platelet secretory response to each stimulus.  (+info)

Intestinal reperfusion injury is mediated by IgM and complement. (3/2484)

Intestinal ischemia-reperfusion injury is dependent on complement. This study examines the role of the alternative and classic pathways of complement and IgM in a murine model of intestinal ischemia-reperfusion. Wild-type animals, mice deficient in complement factor 4 (C4), C3, or Ig, or wild-type mice treated with soluble complement receptor 1 were subjected to 40 min of jejunal ischemia and 3 h of reperfusion. Compared with wild types, knockout and treated mice had significantly reduced intestinal injury, indicated by lowered permeability to radiolabeled albumin. When animals deficient in Ig were reconstituted with IgM, the degree of injury was restored to wild-type levels. Immunohistological staining of intestine for C3 and IgM showed colocalization in the mucosa of wild-type controls and minimal staining for both in the intestine of Ig-deficient and C4-deficient mice. We conclude that intestinal ischemia-reperfusion injury is dependent on the classic complement pathway and IgM.  (+info)

Rainbow trout leucocyte activity: influence on the ectoparasitic monogenean Gyrodactylus derjavini. (4/2484)

The ectoparasitic monogenean Gyrodactylus derjavini from rainbow trout Oncorhynchus mykiss was exposed in vitro to macrophages isolated as peritoneal exudate cells or as pronephros cells from the host. Cells colonized the parasite especially in the mannose-rich regions in the cephalic ducts where ciliated structures were abundant. Opsonization with fresh serum, in contrast to heat-inactivated serum, enhanced colonization also on other body parts. The adverse effect of the activated macrophages towards G. derjavini was associated with a heat-labile component released from these cells to the culture medium. Analysis of substances released from the cells showed reactivity for a number of enzymes, complement factor C3, interleukin (Il-1) and reactive oxygen metabolites. Chemotaxis assays with pronephric leucocytes showed chemoattractants in G. derjavini, and the respiratory burst level of macrophages was slightly elevated due to parasite exposure. It is suggested that skin leucocytes contribute to an increased level of complement factors in the trout skin during the host response, whereby a hostile microenvironment for the parasites is created. In addition, the IL-1 production could affect mucous cell secretion and hyperplasia and add to the antiparasitic action of the epithelium. Likewise, reactive oxygen metabolites and various enzymes are likely to be involved in the skin response.  (+info)

Distribution of complement C3 variants in individuals with cystic fibrosis. (5/2484)

The gene frequency for slow and fast electrophoretic variants of complement C3 in Caucasian individuals with cystic fibrosis was similar to the values expected for unaffected controls, thereby ruling out a suspected differential involvement of these phenotypes with the disease. In one family, cystic fibrosis and complement C3 phenotypes segregated independently.  (+info)

Third component of complement in cystic fibrosis. (6/2484)

In a study of C3 levels and phenotypes in 64 cystic fibrosis (CF) patients, 92 CF parents, 64 normal siblings, and 126 healthy controls, significant elevations of mean C3 levels were found in CF patients, their parents, and in one genetic sub-group of their siblins (SS females). C3 concentration in CF patients correlated with the degree of clinical impairment as measured by Shwachman-Kulczycki (S-K) score. No significant differences were found in the prevalences of C3 phenotypes or the S and F gene frequencies among the groups studied.  (+info)

Immune complexes and complement hypercatabolism in patients with leprosy. (7/2484)

The occurrence of immune complexes in the serum and the level of the C3 breakdown product C3d in the plasma from patients with leprosy were studied by quantitative methods and the results were compared in various forms of the disease. These studies were performed on sixty-two samples from twenty-six patients. The serum 125I-C1q binding activity was found to be increased by more than 2 s.d., as compared to the normal values, in most of the sera from patients with erythema nodosum leprosum (ENL) (80%) and uncomplicated lepromatous leprosy (82%), but also in the sera from patients with tuberculoid leprosy (58%). In vitro studies suggested that immune complexes involving mycobacterial antigens were present in leprosy sera. An increased C3d level (greater than 2s.d.) was also found in most of the plasma from patients with ENL (70%), but rarely in the plasma from patients with uncomplicated lepromatous leprosy (18%) and never in tuberculoid leprosy patients' plasma. The absence of a significant correlation between the 125I-C1q binding activity and the C3d level in leprosy patients may suggest that extravascular immune complexes are involved in the complement activation occurring in ENL. The quantitation of C3d in plasma may be of some practical interest in the early diagnosis of ENL complications of leprosy.  (+info)

Role of antibody and complement in opsonization of group B streptococci. (8/2484)

A requirement for the classic complement pathway in opsonization of group B streptococci was observed by using both a chemiluminescence and a radiolabeled bacterial uptake technique. The classic pathway increased levels of opsonization for types Ia and II stock and wild strains and for some type III wild strains. In contrast, other type III wild strains and the type III stock strain had accelerated kinetics of uptake in the presence of an intact classic pathway, but the level of opsonization was unchanged from that with antibody alone. We could not demonstrate a significant role for the alternative pathway in opsonizing stock or wild strains of group B streptococci. Futhermore, electrophoretic and complement consumption analysis by hemolytic titration failed to reveal alternative pathway activation by the majority of strains of this group. Therapy aimed at supplying opsonins for these organisms will require the presence of type-specific antibody.  (+info)

*Alternative-complement-pathway C3/C5 convertase

... (EC 3.4.21.47, complement component C3/C5 convertase (alternative), proenzyme ... C3 convertase, C3b,Bb,CVF,Bb,C5 convertase, (C3b)n,Bb, complement C 3(C 5) convertase (amplification), alternative complement ... Alternative-complement-pathway C3/C5 convertase at the US National Library of Medicine Medical Subject Headings (MeSH) ... This enzyme catalyses the following chemical reaction Cleavage of Arg-Ser bond in complement component C3 alpha-chain to yield ...

*C3a (complement)

"The role of complement factor C3 in lipid metabolism". Molecular Immunology. 15th European Meeting on Complement in Human ... The absence of C3 has also been shown to decrease IL-2 receptor expression on T cells. Levels of complement are regulated by ... C3 convertase activity is also regulated without C3b inactivation, through complement control proteins, including decay- ... C3a formation occurs through activation and cleavage of complement component 3 in a reaction catalyzed by C3-convertase. There ...

*Systemic lupus erythematosus

In the complement system low C3 levels are associated with systemic lupus erythematosus Apoptosis is increased in monocytes and ... "Complement C3 (Blood) - Health Encyclopedia - University of Rochester Medical Center". www.urmc.rochester.edu. Archived from ... "Antibodies to native DNA and serum complement (C3) levels. Application to diagnosis and classification of systemic lupus ... Serum components like complement factors, CRP, and some glycoproteins are, furthermore, decisively important for an efficiently ...

*Macular degeneration

Yates JR, Sepp T, Matharu BK, Khan JC, Thurlby DA, Shahid H (2007). "Complement C3 variant and the risk of age-related macular ... Despriet DD, Klaver CC, Witteman JC, Bergen AA, Kardys I, de Maat MP (2006). "Complement factor H polymorphism, complement ... "Complement C3 Variant and the Risk of Age-Related Macular Degeneration". N Engl J Med. 357 (6): 553-61. doi:10.1056/ ... The genes for the complement system proteins factor H (CFH), factor B (CFB) and factor 3 (C3) are strongly associated with a ...

*CFHR5

Like complement factor H, CFHR5 is able to bind to complement C3. A mutation in CHFR5 was found in patients with the disease ... The mutated form of the protein found in patients with this disease has impaired ability to bind to complement C3, suggesting ... Complement factor H-related protein 5 is a protein that in humans is encoded by the CFHR5 gene. CFHR5 is structurally related ... "Entrez Gene: CFHR5 complement factor H-related 5". McRae JL, Duthy TG, Griggs KM, et al. (2005). "Human factor H-related ...

*Thioester-containing protein 1

The discovery of C3 like molecules in a diverse range of species suggests that the complement pathway in particular the ... Similar to the complement protein C3 in function, TEP1 acts as a opsonin which facilitates extensive parasite killing. TEP1 ... Studies have shown that TEP1 is structurally and functionally homologous to the human complement protein C3. TEP1 is now known ... The structure of TEP1 and its vertebrate homologue - complement protein C3- is mostly conserved. However, there are some ...

*Pathophysiology of multiple sclerosis

It appears together with clusterin and complement C3, markers of complement-mediated inflammatory reactions. Also Fibroblast ... The Complement System". Retrieved 2006-05-10. Lucchinetti, Claudia; Wolfgang Brück, Joseph Parisi, Bernd Scheithauer, Moses ...

*Monoclonal gammopathy of undetermined significance

... interference with complement C3 and C4 measurement". Immunol. Invest. 28 (4): 269-276. doi:10.3109/08820139909060861. PMID ...

*Acute hemolytic transfusion reaction

Properdin then binds to complement C3 in the donor blood, facilitating the reaction through the alternate pathway cascade. The ... The release of red blood cell debris and the activation of complement system causes uncontrolled clotting (disseminated ... the donor's red blood cells are destroyed by recipient's preformed antibodies through the activation of complement system. Thus ...

*Anti-nuclear antibody

"Antibodies to native DNA and serum complement (C3) levels. Application to diagnosis and classification of systemic lupus ... Presence of high DNA-binding and low C3 levels have been shown to have extremely high predictive value (94%) for the diagnosis ... Unlike anti-dsDNA antibodies in SLE, these antibodies do not fix complement. Although they are most commonly found in drug ... Binding to these antigens within the kidney could cause inflammation and complement fixation, resulting in kidney damage. ...

*CFHR5 nephropathy

A kidney biopsy in patients with CFHR5 nephropathy classically shows deposition of complement C3 in the kidney, without any ... and occasional subepithelial basement membrane deposits which stain for complement C3. The diagnosis can be confirmed on a ... Complement factor H-related protein 5 (CFHR5) nephropathy (also known as Troodos nephropathy) is a form of inherited kidney ... This is evidence that the disease is caused by a problem with alternative complement pathway regulation, rather than activation ...

*C3-convertase

C3 convertase (EC 3.4.21.43, C42 , C4bC2b, C3bBb, complement C.hivin.4.hivin2, complement C3 convertase) belongs to family of ... Thus, the alternative C3 convertase (C3bBb) is formed and is able to cleave C3 via its dimeric Bb subunit. Since C3 convertases ... both C3 convertases will catalyze the proteolytic cleavage of C3 into C3a and C3b (hence the name "C3-convertase"). The smaller ... Cleavage of complement C3 by a free floating convertase, thrombin, plasmin or even a bacterial enzyme leads to formation of C3a ...

*Complement component 3

In the alternative complement pathway, C3 is cleaved by C3bBb, another form of C3-convertase composed of activated forms of C3 ... "Entrez Gene: C3 complement component 3". Sahu A, Lambris JD (Apr 2001). "Structure and biology of complement protein C3, a ... Complement component 3, often simply called C3, is a protein of the immune system. It plays a central role in the complement ... In humans it is encoded on chromosome 19 by a gene called C3. C3 plays a central role in the activation of complement system. ...

*Serum protein electrophoresis

Beta-2 comprises C3 (Complement protein 3). It is raised in the acute phase response. Depression of C3 occurs in autoimmune ... disorders as the complement system is activated and the C3 becomes bound to immune complexes and removed from serum. Fibrinogen ...

*C3b

C3a - the other fragment C3 is cleaved into along with C3b Liszewski, M. Kathryn; Atkinson, John P. (2015-06-10). "Complement ... Formation of a C3 convertase functions as a positive feedback loop, so as more C3b is cleaved, more C3 convertases are formed, ... For example, the uncontrolled cleavage of C3b is associated with the disease C3 glomerulopathy, in which deposits of C3 in the ... inactivate the complement component. Given the C3 is constantly being turned over in the alternative pathway and its ability to ...

*Adaptive immune system

Clustered Band 3 proteins with attached antibodies activate complement, and complement C3 fragments are opsonins recognized by ... These antibodies bind to antigens, making them easier targets for phagocytes, and trigger the complement cascade. About 10% of ... One set of innate immune mechanisms is humoral, such as complement activation. Another set comprises pattern recognition ... Arese P, Turrini F, Schwarzer E (2005). "Band 3/complement-mediated recognition and removal of normally senescent and ...

*Integrin alpha M

Arnaout MA, Todd RF, Dana N, Melamed J, Schlossman SF, Colten HR (July 1983). "Inhibition of phagocytosis of complement C3- or ... It is involved in the complement system due to its capacity to bind inactivated complement component 3b (iC3b). The ITGAM ( ... or complement receptor 3 (CR3). ITGAM is also known as CR3A, and cluster of differentiation molecule 11B (CD11B). The second ...

*Cicatricial pemphigoid

Diagnostic techniques: antibodies (IgG) precipitates complement (C3) in the lamina lucida of the basement membrane. Circulating ... IgG, C3 deposition at BM creating smooth line in immunofluorescent analysis. The management depends upon the severity of the ...

*Complement 3 deficiency

"Molecular analysis of hereditary deficiency of the third component of complement (C3) in two sisters". Intern. Med. 40 (12): ... Complement 3 deficiency is a genetic condition affecting complement component 3. It can cause systemic lupus erythematosus-like ...

*Pregnancy-associated plasma protein A

... specifically inhibits the third component of human complement (C3)". Placenta. 5 (1): 1-7. doi:10.1016/S0143-4004(84)80044-2. ... 1995). "Identification of angiotensinogen and complement C3dg as novel proteins binding the proform of eosinophil major basic ...

*Anaphylatoxin

... that are produced as part of the activation of the complement system. Complement components C3, C4 and C5 are large ... C3, C4A, C4B, C4B-1, C5, FBLN1, FBLN2 Allergy Anaphylatoxin receptors Anaphylaxis Complement system Inflammation Immune system ... "Primary structure of cobra complement component C3". Journal of Immunology. 149 (11): 3554-62. PMID 1431125. Ogata, R. T.; Rosa ... C3a works with C5a to activate mast cells, recruit antibody, complement and phagocytic cells and increase fluid in the tissue, ...

*Antibody-dependent enhancement

HIV-1 has also showed enhancement of infection in HT-29 cells when the viruses were pre-opsonized with complements C3 and C9 in ... Complement Component receptors CR2, CR3 and CR4 have been found to mediate this Complement -Mediated enhancement of infection. ... ADE in HIV can be complement mediated or Fc receptor mediated. Complements in presence of HIV-1 positive sera have been found ... The infection of HIV-1 leads to activation of complements fragments of these complements can assist viruses with infection by ...

*List of MeSH codes (D12.776)

... complement c3 nephritic factor MeSH D12.776.377.715.548.114.323.390 - immunoconglutinins MeSH D12.776.377.715.548.114.323.480 ... complement factor h MeSH D12.776.377.715.182.338 - hemopexin MeSH D12.776.377.715.182.580 - plasminogen MeSH D12.776.377.715. ...

*LRP1

Complement C3, CTGF, DLG4, Elastase, Factor IXa, Factor VIIa, Fibronectin, Gentamicin, GIPC1, Heat shock proteins gp96, hsp70, ... As a member of the LDLR family, LRP1 contains cysteine-rich complement-type repeats, EGF (gene) repeats, β-propeller domains, a ... and eleven cysteine-rich complement-type repeats, respectively. These repeats bind extracellular matrix proteins, growth ...

*Bernd Schröppel

Complement C3 allotypes and outcomes in liver transplantation. Liver Transplantation, 16:198-203, 2010. PMID 20104494 Schröppel ... PMID 20400193 Lin M, Yin N, Murphy B, Medof ME, Segerer S, Heeger PS, Schröppel B. Immune cell-derived c3 is required for ...

*Valle del Arroyo Cuña-Pirú Reserve

The reserve complements the Salto Encantado Provincial Park and the Cuñá Pirú Municipal Nature Park. It would be part of the ...
We have examined the relative roles of the macrophage (M phi) plasma membrane receptor for the cleaved third complement component (iC3b, CR3) and of the mannosyl/fucosyl receptor (MFR) in binding and ingestion of Leishmania donovani. In the absence of exogenous complement, the binding and ingestion of promastigotes, which are good activators of the alternative complement pathway, were inhibited by the anti-CR3 monoclonal antibody M1/70, by the Fab portion of an anti-C3 antibody, or by the nucleophile, sodium salicyl hydroxamate, an inhibitor of C3 fixation. This provides strong evidence that M phi-derived, cleaved C3 (iC3b) present on the promastigote surface mediates binding to CR3. Equivalent inhibition of promastigote binding and ingestion was also observed using the soluble inhibitors of MFR activity, mannan or ribonuclease B. No additive effect for blocking the two M phi receptors simultaneously was observed. For amastigotes, which are poor activators of the alternative pathway, a lesser ...
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.
CD11b (integrin alphaM subunit) is a 165-170 kDa type I transmembrane glycoprotein that non-covalently associates with integrin beta2 subunit (CD18); expression of the CD11b chain on the cell surface requires the presence of the CD18 antigen. CD11b/CD18 integrin (Mac-1, CR3) is highly expressed on NK cells, neutrophils, monocytes and less on macrophages. CD11b/CD18 integrin is implicated in various adhesive interactions of monocytes, macrophages and granulocytes, facilitating their diapedesis, as well as it mediates the uptake of complement coated particles, serving as a receptor for the iC3b fragment of the third complement component ...
CD11b (integrin alphaM subunit) is a 165-170 kDa type I transmembrane glycoprotein that non-covalently associates with integrin beta2 subunit (CD18); expression of the CD11b chain on the cell surface requires the presence of the CD18 antigen. CD11b/CD18 integrin (Mac-1, CR3) is highly expressed on NK cells, neutrophils, monocytes and less on macrophages. CD11b/CD18 integrin is implicated in various adhesive interactions of monocytes, macrophages and granulocytes, facilitating their diapedesis, as well as it mediates the uptake of complement coated particles, serving as a receptor for the iC3b fragment of the third complement component ...
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 ...
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 ...
The complement system is an important part of the humoral response in innate immunity, consisting of three different pathways. The third complement…
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 ...
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. ...
Although complement is considered a "master of sensing" that discriminates between foreign, altered, and healthy self surfaces, several triggers may lead to an ill-fated triage of potential danger (Fig. 2B). Dysfunctions, deficiencies, or polymorphisms of complement components are often factors that tip the balance (3), but tissue damage or confrontation with non-self surfaces (e.g., biomaterials, transplants) can also lead to excessive activation. Importantly, disruption of the complement balance with increased production of effector molecules may trickle down the immune system and contribute to autoimmune, inflammatory, degenerative, hematological, and ischemic disorders. Despite the variety of disease manifestations, the involvement of complement typically follows a common scheme that involves the recognition of potential (although not always "real") danger patterns, an insufficiently controlled amplification loop, and the stimulation of downstream inflammatory responses. The activated immune ...
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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 ...
1 reviews. Compare Complement C5a desArg ELISA Kits from leading suppliers on Biocompare. View specifications, prices, citations, reviews, and more.
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https://luminusdiagnostics.com/wp-content/uploads/2016/09/Luminus-Full-color-header-1.png 0 0 Daniel Battaglia https://luminusdiagnostics.com/wp-content/uploads/2016/09/Luminus-Full-color-header-1.png Daniel Battaglia2018-10-01 20:08:262018-12-11 20:21:53COMPLEMENT C3 ...
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 ...
This blood test measures component 4 (C4) of the complement system. Deficiency of C4 is closely linked to development of autoimmune diseases such as Lupus and Rheumatoid arthritis.
This blood test measures component 4 (C4) of the complement system. Deficiency of C4 is closely linked to development of autoimmune diseases such as Lupus and Rheumatoid arthritis.
The three distinct activation pathways of complement converge with the formation of a C5 convertase. The cleavage of C5 by this convertase initiates…
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A complement receptor is a receptor of the complement system, part of the innate immune system. Complement receptors bind proteins of the complement system, and can thus detect pathogens without mediation by antibodies. Complement activity is not antigen sensitive, but can be triggered by specific antigens. Many white blood cells express complement receptors on their surface, particularly monocytes and macrophages. All four complement receptors bind to fragments of complement component 3 or complement component 4 coated on pathogen surface, but the receptors have different functions. Complement receptor (CR) 1, 3, and 4 work as opsonins (stimulate phagocytosis), whereas CR2 is expressed only on B cells as a co-receptor. Red blood cells (RBCs) also express CR1. With these receptors, RBCs bring antigen-antibody complexes bound to complement fragments in the blood to the liver and spleen for degradation. Defects in these receptors can be associated with disease. Immune system Humoral immunity ...
highlighting the link between complement gene expression and IQ, in both schizophrenic patients and healthy controls. The study demonstrated a broad association between variations in complement gene expression and perturbed neurodevelopment. We were particularly interested to see that the final sentence of the paper stated that When complement gene-sets are taken as a whole, their relevance is to neurodevelopment, not illness . Their conclusion rightly touches on the emerging understanding of non-immune roles for complement in diverse biological processes (Hawksworth et al., 2018) .The complement group of proteins is ancient in evolutionary terms. Recognised complement components are found strewn throughout the animal kingdom including in rudimentary diploblastic species (Kimura et al., 2009) . In the human adult, complement functions as an essential pillar of the innate immune system. It is activated by various noxious stimuli and results in the production of the anaphylatoxins and membrane attack
Purpose.: Increasing evidence supports a role for complement in the pathogenesis of age-related macular degeneration (AMD). This study evaluated retinal microglia, T-lymphocytes, and complement deposition in a light-induced retinopathy model. The effect of a serotonin (5-hydroxytryptamine, 5-HT1A) agonist on these processes was investigated. Methods.: Rats were dark adapted for 24 hours before a 6-hour blue light exposure. Some animals were predosed subcutaneously with AL-8309A. Retinas were evaluated at different times after light exposure. Paraffin sections were stained with antibody for a microglial marker (Iba1), a T-lymphocyte marker (CD3), and complement components C1q, C3, factor B, factor H, and membrane attack complex (MAC). Results.: Light exposure resulted in substantial photoreceptor and RPE loss. Robust microglia activation and migration to the outer retina occurred rapidly. Substantial T-lymphocyte recruitment did not occur. Complement alternative pathway was strongly activated, ...
... is produced by our E.coli expression system and the target gene encoding Asn679-Arg755 is expressed.
Purpose The purpose of this study was to investigate complement activation and associated inflammatory mechanisms in normal, aged human retina. in the choriocapillaris, and in BM. Lectin binding of RCA-I was Rabbit polyclonal to CREB1 strong throughout the neuroretina. Conclusions Robust immunostaining for APP in older donor eyes suggested that amyloid beta peptides may be one of the triggers of complement activation during the normal aging process. Microglial markers CD11b and RCA-I also increase with age, suggesting a concomitant inflammatory response to C5b-9 deposits in the retinal pigment epithelium, BM, and CC. Immunoreactivity for CD36 was strong in both age groups; the lack of age dependence in this candidate receptor for amyloid beta suggested that complement activation may arise from interactions of amyloid beta with other candidate receptors in normal human retina. Latest research have got supplied book understanding TSA cell signaling in to the function from the supplement system and ...
The complement system is a major humoral component of vertebrate defenses for tagging and killing target microorganisms. Recent molecular analyses have uncovered a striking feature of bony fish complement, namely that several complement components are encoded by multiple genes. In this review, the structural diversity of C3, C4, C5, factor B, C2, C1r/s and MASP are discussed with special reference to their functional differentiation, mainly focusing on the common carp (Cyprinus carpio), a tetraploidized teleost. In carp, all the members (C3, C4, C5 and a non-complement protein alpha2-macroglobulin) of the thioester-containing protein family are present in multiple isotypes, differing in the primary structures of various functional sites. Three factor B/C2-like isotypes identified in carp showed distinct expression pattern (sites and inducibility), with one behaving as an acute-phase reactant. Two C1r/C1s/MASP2-like isotypes also contain an amino acid substitution that likely affects their substrate
... The activated complement system recognizes and eliminates invading microorganisms and thus is beneficial for the host.
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.
Complement C3 has been shown to mediate antigen uptake by professional APCs and presentation to CD4+ and CD8+ T cells.22 Therefore, we investigated the role of complement in the endocytosis and presentation of FVIII by human APCs in vitro. The use of heat-treated serum, wherein the complement system is inactivated, was associated with baseline levels of FVIII endocytosis by MO-DCs, as previously described.7,23,24 Similar levels of endocytosis were observed when the serum was immune depleted from the C3 component. In contrast, the use of normal serum that allows activation of complement leads to an increased uptake of FVIII in the case of both MO-DCs and circulating blood DCs. In line with these data, normal serum enhanced presentation of FVIII to an FVIII-specific T-cell hybridoma, as compared to serum lacking active C3. Since heating of serum may affect proteins other than complement, we reconstituted the C3-convertase in vitro using purified proteins. In vitro reconstitution of the ...
The third component of complement (C3) is an important mediator of inflammation. Murine and human genomic cosmid clones were isolated, characterized and sequenced 5′ to the complement C3 gene transcriptional initiation sites to determine cis elements that participate in constitutive and regulated C3 gene expression. The murine and human 5′ flanking regions are 51% identical overall, with positions -36 to -1 and -146 to -68 showing 80% identity. Four TATA boxes were identified upstream of the murine transcriptional initiation site, but deletion and transfection analysis using reporter gene constructs in HepG2 cells indicated that only the TATA element at position -30, together with sequences -395 to -111, are essential for constitutive expression of murine C3 in hepatocytes. Deletion analysis also suggested that sequences between -1457 and -800 contain regulatory elements that are involved in suppressing basal expression. Sequences between -90 to -41 confer both enhancer activity and ...
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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.
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.
Complement C9 Polyclonal Antibody from Invitrogen for Western Blot and Immunohistochemistry (Paraffin) applications. This antibody reacts with Human samples. Supplied as 100 µg purified antibody (1 mg/ml) in PBS with 1% BSA and 0.02% sodium azide; pH 7.4.
Complement C6 Polyclonal Antibody from Invitrogen for Western Blot and Immunohistochemistry (Frozen) applications. This antibody reacts with Mouse samples. Supplied as 100 µg purified antibody (0.1 mg/ml) in PBS with 0.1% BSA and 0.02% sodium azide.
No, rituximab reactions are anaphylactoid reactions, so-called because they resemble anaphylaxis, but they have a quite different cause. When antibody reacts with its antigen - eg rituximab reacts with the CD20 on the surface of the tumor cell - it attracts a protein known as complement. Actually complement is not a single protein but a series of more than a dozen proteins. They operate as a cascade - activation of one protein activates the next in the chain and so on down the line. If the chain is completed as far as C9 complement punches a hole in the cell to kill it, but often the chain is incomplete and the activation results in the deposition of C3 on the surface of the cells, which has the effect of making the tumor cell more appetizing to the big eater cells (or macrophages). When the complement components are activated bits of the proteins break off and are released into the fluid around the cell. Some of these broken off bits have activities of their own. In particular, C3a and C5a ...
Complement C7 deficiency is an autosomal recessive disorder well known to be associated with increased susceptibility to meningococcal infection and has mostly been reported in Caucasians. In the Korean population, no case of C7 deficiency has been reported to date. Recently we experienced an 11-yr-...
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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.
KAF156 is an antimalarial agent, which was designed to eradicate both blood-stage and liver-stage malaria parasites, providing a potentially new treatment of malaria prophylaxis (Kuhen et al., 2014; Diagana, 2015). To facilitate the understanding of metabolism and disposition of KAF156 in humans, ADME studies in rats and in vitro across species metabolism studies were conducted.. After intravenous or oral dosing of [14C]KAF156-1, mass balance was achieved in rats. The radioactivity was excreted equally via urinary and fecal pathways. KAF156 showed high clearance, large volume of distribution and long terminal half-life in rats. After oral dosing, KAF156 was well absorbed and extensively metabolized in rats such that unchanged KAF156 accounted for only ∼8-21% of the dose in feces by either dosing route. The prominent radioactive components in rat plasma were KAF156 and three oxidative metabolites (M31, M35.8, and M37). Several metabolites were identified in urine and feces by LC-MS/MS ...
Complement, C3 Convertase, Regulation, Cells, Disease, Complement Factor H, Inhibition, Therapeutic, Transplant, Allograft, Donor, Donors, and Graft
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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?. ...
Each laboratory should check if the reference ranges are transferable to its own patient population and determine own reference ranges if necessary. For diagnostic purposes, the results should always be assessed with the patients medical history, clinical examinations and other findings ...
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 ...
Learn about the signs, symptoms, and treatment of Complement 3 Deficiency, C3 Deficiency, and what to do if your dog has this health condition.
T02487 (aalt,achr,acta,amyb,cmos,cthd,cyl,ehl,fek,hta,kak,kpnk,lei,lfb,lsh,lys,mcol,noe,oor,phs,pje,ptd,rpln,sclo,scou,seny,sera,sfz,slw,sphc,sphy,srub,taj : calculation not yet completed ...
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chr08:complement(join(8594165..8594329,8592744..8592818,8592340..8592396,8592099..8592259,8591848..8591988,8591180..8591282,8590996..8591095,8590688..8590899 ...
chr04:complement(join(34150379..34150670,34150237..34150289,34150030..34150153,34149819..34149940,34148628..34148735,34148427..34148528 ...
Human Proximal Tubular Epithelial Cells from Creative Bioarray are isolated from normal human proximal tubular tissue. Human Proximal Tubular Epithelial Cells are grown in T25 tissue culture flasks pre-coated with gelatin-based coating solution for 2 min and incubated in Creative Bioarrays Culture Complete Growth Medium generally for 3-7 days. Cultures are then expanded. Prior to shipping, cells at passage 3 are detached from flasks and immediately cryo-preserved in vials. Each vial contains at least 0.5x10^6 cells per ml. Cells can be expanded for 3-7 passages at a split ratio of 1:2 or 1:3 under the cell culture conditions specified by Creative Bioarray. Repeated freezing and thawing of cells is not recommended ...
AMD is strongly associated with the over-activation of complement pathways [16]. Supporting evidence comes from the detection of various complement proteins in the drusen of patients with AMD [9] and the close association between AMD and the alternative pathway. Furthermore, the association of genetic variants in complement genes, including the human factor B gene, is a risk factor for all forms of AMD [5,9,22,24]. In addition, it has been shown that polymorphisms of genes encoding the alternative pathway proteins CFH, factor B, and C3, as well as the classical pathway protein C2, are also associated with AMD [23,46]. Studies in animal models of choroidal neovascularization (CNV), a major pathologic association with wet AMD, also supports a role for complements in AMD. Furthermore, a targeted inhibitor specific for the AP of complement significantly reduces CNV and the physiologic consequences of CNV on retinal function [11,47]. Additional evidence for a role of the AP pathway in AMD exists. For ...
AMYNDAS is developing a novel peptidic complement inhibitor AMY-101, based on the third-generation compstatin analogue Cp40. AMY-101 is a selective inhibitor of complement activation in humans and in NHP. It binds to the complement component C3, the central functional hub that controls the upstream activation/amplification and downstream effector functions of complement. By binding to C3, AMY-101 inhibits the cleavage of native C3 to its active fragments C3a and C3b. As a consequence, the deposition of C3b, amplification via the alternative pathway and all downstream complement responses are prevented. AMY-101 is being developed to treat complement-mediated diseases, which are largely driven by aberrant C3 activation.. This first-in-human study of the C3-targeting complement inhibitor AMY-101 investigates the safety and PK/PD profile of AMY-101 in healthy male volunteers after Single Ascending Dose (SAD) and Multiple Doses (MD) using subcutaneous (SQ) or intravenous (IV) administration. The ...
Activation of the complement cascade is clearly implicated in the pathology of multiple sclerosis (MS). However, the extent and nature of its involvement in specific athological processes remains uncertain. We describe a detailed immunohistochemical study to localise a strategically selected set of complement proteins, activation products and regulators in brain and spinal cord tissue of 17 patients with progressive MS, examining 35 different plaques, and 16 control donors, including 9 with CNS disease. Plaques were consistently positive for complement proteins (C3, factor B, C1q), activation products (C3b, iC3b, C4d, TCC) and regulators (factor H, C1-inhibitor, clusterin), suggesting continuing local complement synthesis, activation and regulation despite no other evidence of on-going inflammation. Complement immunolabelling was most apparent in plaque and peri-plaque areas but also present in normal appearing white matter and cortical areas to a greater extent than in control tissue. Cellular ...
The complement system provides a fundamental component of the body's immune response to invading microorganisms. This chapter highlights the various roles of the complement system in the orchestration of the immune response towards microbial infections, gives examples of microbial strategies to evade complement-mediated clearance, and discusses how acquired and inherited complement deficiencies may predispose an organism to infectious disease. Complement is activated by three pathways: the classical pathway, the alternative pathway, and the lectin pathway. The lectin pathway is activated by carbohydrate recognition molecules that bind to polysaccharide on the surface of a pathogen. Factor B, factor D, and properdin (factor P) are specific components of the alternative pathway of complement activation. The complement activation is tightly regulated by membrane-bound and fluid-phase regulatory components to avoid runaway activation of the enzymatic cascade that could lead to excess host tissue damage
Each pathway follows a sequence of reactions to generate a protease called a C3 convertase. The active protease is retained at the pathogen surface, and this ensures that the next complement zymogen in the pathway is also cleaved and activated at the pathogen surface. By contrast, the small peptide fragment is released from the site of the reaction and can act as a soluble mediator.. The early events of all three pathways of complement activation involve a series of cleavage reactions that culminate in the formation of an enzymatic activity called a C3 convertase, more The C3 convertases formed by these early events of complement activation are bound covalently to the pathogen surface. Here they cleave C3 to generate large amounts of C3bthe main effector molecule of the complement system, and C3a, a peptide mediator of inflammation.. The C3b molecules act as opsonins; they bind covalently to the pathogen and thereby target it for destruction by phagocytes equipped with receptors for C3b. These ...
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 ...
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
Properdin or complement factor P is a conserved serum glycoprotein of the immune defence. It plays a role in strengthening the activation of complement, a system of proteins essential in the first line defence against infection. Properdin is the only positive regulator and plays a major role in regulating the alternative pathway of the complement system, an effector system of the innate immune response, by binding and stabilising two specific converting enzyme complexes, which are normally labile (C3bBb and C3bBbC3b). Mouse models have shown that complement, in particular complement receptor 3 (CR3) and complement 5 (C5), contributes to survival of infection with Listeria monocytogenes. The purpose of the project was to characterise the contribution of properdin in the response to L. monocytogenes (EGD-e), a Gram-positive, intracellular pathogen, which can cause severe infectious disease in human and animals, by using in vitro and in vivo methods. In vitro assays for the first time point to the ...
The present invention provides modified IgG3 containing human constant regions which has a shorter total-hinge region compared with normal human IgG3. Also described is a method for assaying an antibody against a specific antigen or hapten for its effectiveness in complement activation in an animal species, wherein the antibody is contacted with the immobilized antigen or hapten to form an immobilized antibody/antigen or hapten complex which is then contacted with complement from the relevant animal species, followed by assay of components of the complement complex thereby formed; whereby the extent and nature of complement activation by the antibody in the sample may be determined.
The complement system is a biochemical cascade that helps, or complements, the ability of antibodies to clear pathogens from an organism. It is part of the immune system called the innate immune system that is not adaptable and does not change over the course of an individuals lifetime. However, it can be recruited and brought into action by the adaptive immune system. The Classical pathway of activation of the complement system is a group of blood proteins that mediate the specific antibody response. [source: Wikipedia] The Classical Pathway begins with circulating C1Q binding to an antigen on the surface of a pathogen, which goes on to active and recruit 2 copies of each C1R and C1S, forming a C1 complex. The activated C1 complex cleaves C2 and C4. Activated cleavage products C2A and C4B combine to form C3 convertase, which cleaves C3. The cleavage product C3B joins the complex to form C5 convertase, which cleaves C5. The cleavage product C5B joins C6, C7, C8 and multiple copies of C9 to form ...
Age-related macular degeneration (AMD) and Alzheimer disease (AD) are both neurodegenerative diseases of aging, with loss of photoreceptors and CNS neurons, respectively. A number of recent studies have shown that polymorphisms of several complement proteins in the alternative pathway of complement activation (CFB, C2, and CFH) enhance susceptibility to AMD. Somewhat similarly, in AD there is a profound increase in the levels of the initiating protein of the complement cascade called C1q, a prominent upregulation of which has also recently been reported to accompany glaucoma, which is a neurodegenerative retinal disease of aging. All of these changes, in AMD and AD, ultimately lead to activation of the pivotal complement protein called C3. Upon activation, C3 is fragmented into several pieces. One is called C3a, a small cytokine-like molecule that activates microglia and stimulates angiogenesis, whereas a larger fragment, called C3b, opsonizes the cell or debris where it was generated, leading ...
Abcams Complement C4 ELISA Kit (ab108825) suitable for Cell culture supernatant, Saliva, Milk, Urine, Cerebral Spinal Fluid in human. Reliably quantify 0.07…
Increased exposure of the tubular epithelium to filtered protein is a proposed mechanism of progressive renal failure associated with glomerular disease, but how this protein overload translates into tubular damage remains unclear. We have examined a model of adriamycin-induced proteinuria to determine the effect of locally synthesized C3, the central proinflammatory protein of the complement cascade. C3(-/-) kidney isografts placed in wild-type C3+/+ mice were protected from proteinuria-associated complement activation, tubular damage, and progressive renal failure despite the presence of abundant circulating C3. The quantity of urinary protein was unaffected by the absence of C3, and thus the influence of C3 was not explained by alteration in the filtered protein load. These results suggest that local synthesis of complement from renal epithelial cells is a critical mediator of tubular damage in proteinuria-associated renal disease. Our results concur with previous findings of increased ...
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.
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).
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.
Walk-In Labs complement C3 serum test helps determine causes of recurrent infections, autoimmune disorders & more. A cheap, convenient online blood test.
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.
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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
Health update on me: All my blood work came back excellent and my doctor was very impressed. The only things to slightly worry about was my C3 blood test, my ANA blood test and protein urine test. The Complement C3 blood test, according to the national library of medicine, is a blood test that measures the activity of a certain protein that is part of the complement system. The complement system is a group of proteins that move freely through your bloodstream. The proteins work with your immune system and play a role in the development of inflammation. My C3 was low which is common with SLE lupus patients. My ANA score came back elevated, which just means that my lupus is very so slightly active and I still had protein in my urine (but only 30mg!). All in all, nothing to worry about ...
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Lokki AInkeri; Kaartokallio T; Holmberg V; Onkamo P; Koskinen LL; Saavalainen P; Heinonen S; Kajantie E; Kere J; Kivinen K; Pouta A; Villa PM; Hiltunen L; Laivuori H; Meri S ...
Molecular, biochemical and functional characterizations of C1q/TNF family members: adipose-tissue-selective expression patterns, regulation by PPAR-gamma agonist, cysteine-mediated oligomerizations, combinatorial associations and metabolic functions ...
Assignment of complement components C4 binding protein (C4BP) and factor H (FH) to human chromosome 1q, using cDNA probes (pages 117-122). S. HING, A. J. DAY, S. J. LINTON, J. RIPOCHE, R. B. SIM, K. B. M. REID and E. SOLOMON. Version of Record online: 28 SEP 2007 , DOI: 10.1111/j.1469-1809.1988.tb01086.x. ...
AccessGUDID - Anti Human Properdin FITC (B1761082)- Fluorescein conjugated polyclonal goat antiserum to Human Complement Properdin
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Definition: Total complement of genes contained in a cell or virus; commonly used to refer to all genes present in one complete haploid set of chromosomes in eukaryotes. Source: Essential Genetics: A genomics perspective (2006) 4th Ed. ...
Complement (complementary DNA) -- In genetics, complementary DNA (cDNA) is DNA synthesized from a mature mRNA template in a reaction catalyzed by the enzyme reverse transcriptase. cDNA is often used to clone eukaryotic genes in prokaryotes. cDNA is also produced by retroviruses (such. fact lexicon with terms going straight to the point. Facts are sorted by community importance and you can build your personalized lexicon
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
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.
Ganesalingam J, An J, Shaw CE, Shaw G, Lacomis D, Bowser R. Combination of neurofilament heavy chain and complement C3 as CSF biomarkers for ALS ...
may be part of the humoral arm of innate immunity and behave as functional ancestor of antibodies by mediating agglutination, complement activation and opsonization (Martinez de la Torre 2010 ...
this suit was fun to wear and i got a lot of complements on the fringe beads. the beads didnt get annoying in the water either! throw on some shorts and it becomes a cute top ...
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 ...
Human umbilical vein endothelial cells grown in vitro under standard conditions contain a high level of mRNA specific for the complement regulatory factors H and I. An additional 1.8-kb mRNA encoding a truncated form of factor H is also present. IFN-gamma stimulation of the cells causes a 6-7 fold increase in both factor H mRNA species, and a greater than 10-fold increase in factor I mRNA. IL-1 and LPS slightly suppressed factor H mRNA, while TNF had no effect. mRNA for factor B is also detectable in IFN-gamma-stimulated cells, but messengers for C1q, C4bp, and CR3 beta chain were not found. Secretion of factor H protein was also stimulated by IFN-gamma. The presence of mRNA for factors H, B, and I, together with C3 secretion, demonstrated by others, suggests that endothelial cells can assemble the complete alternative complement pathway. Endothelial cell complement may be involved in leukocyte-endothelium interactions mediated by leukocyte C3 receptors. ...
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 ...
TY - JOUR. T1 - Complement activation in acquired and hereditary amyloid neuropathy. AU - Hafer-Macko, Charlene E.. AU - Dyck, Peter J. AU - Koski, Carol Lee. PY - 2000. Y1 - 2000. N2 - The pathogenesis of the axonal degeneration in acquired or hereditary amyloidosis is unknown. In this immunohistochemistry study, we examined 20 sural nerve biopsies from individuals with amyloid neuropathy (14 acquired and 6 hereditary) for evidence of complement activation. Complement activation products were detected on and around amyloid deposits within peripheral nerves. We found no difference in the extent, location or pattern of complement activation products between the 2 forms of amyloidosis. The presence of early classical pathway activation markers in the absence of antibody in hereditary cases suggests an antibody-independent activation of the classical pathway through binding of C1q. The lack of Factor Bb-suggested alternative pathway activation was not significant in these cases. The detection of ...
Background: Vascular endothelial cells (ECs) express and release protein components of the complement pathways, as well as secreting and anchoring ultra-large von Willebrand factor (ULVWF) multimers in long string-like structures that initiate platelet adhesion during hemostasis and thrombosis. The alternative complement pathway (AP) is an important nonantibody- requiring host defense system. Thrombotic microangiopathies can be associated with defective regulation of the AP (atypical hemolytic-uremic syndrome) or with inadequate cleavage by ADAMTS-13 of ULVWF multimeric strings secreted by/anchored to ECs (thrombotic thrombocytopenic purpura). Our goal was to determine if EC-anchored ULVWF strings caused the assembly and activation of AP components, thereby linking two essential defense mechanisms. Methodology/Principal Findings: We quantified gene expression of these complement components in cultured human umbilical vein endothelial cells (HUVECs) by real-time PCR: C3 and C5; complement factor ...
Looking for online definition of Complement factor b in the Medical Dictionary? Complement factor b explanation free. What is Complement factor b? Meaning of Complement factor b medical term. What does Complement factor b mean?
Membranoproliferative glomerulonephritis (MPGN) is a relatively-rare, immune-mediated glomerular disease. There is no accepted therapy and all current therapies are inadequate. Current therapeutic options include immunosuppression with corticosteroids alone or in combination with alkylating agents, antiplatelet therapy with aspirin and/or dipyridamole and/or warfarin, and angiotensin converting enzyme inhibitors and/or angiotensin receptor blockers. As with other glomerular diseases the amount of protein in the urine correlates well with the long-term prognosis. Thus, this parameter has been used in previous studies, and will be used in this study, as the primary indicator of therapeutic efficacy. We propose a pilot study to test the hypothesis that selective B lymphocyte depletion will result in disappearance of pathogenic antibodies and induce remission of proteinuria in patients with idiopathic membranoproliferative glomerulonephritis. Our population will be 10 adults with MPGN involving ...
Kőhalmi, Kinga Viktória and Veszeli, Nóra and Luczay, Andrea and Varga, Lilian and Farkas, Henriette (2017) A danazolkezelés hatása C1-inhibitor-hiány okozta hereditaer angiooedemás gyermekek növekedésére , Effect of danazol treatment on growth in pediatric patients with hereditary angioedema due to C1-inhibitor deficiency. Orvosi Hetilap, 158 (32). pp. 1269-1276. ISSN 0030-6002 Csuka, Dorottya and Veszeli, Nóra and Varga, Lilian and Prohászka, Zoltán and Farkas, Henriette (2017) The role of the complement system in hereditary angioedema. Molecular Immunology, 89. pp. 59-68. ISSN 0161-5890 Horváth, Zsófia and Csuka, Dorottya and Vargova, Katarina and Kovács, Andrea and Lee, Sarolta and Varga, Lilian and Prohászka, Zoltán and Kiss, Róbert Gábor and Préda, István and Tóth Zsámboki, Emese (2016) Alternative complement pathway activation during invasive coronary procedures in acute myocardial infarction and stable angina pectoris. CLINICA CHIMICA ACTA, 463. pp. 138-144. ISSN ...

Evaluation and treatment of membranoproliferative glomerulonephritisEvaluation and treatment of membranoproliferative glomerulonephritis

Acquired and genetic complement abnormalities play a critical role in dense deposit disease and other C3 glomerulopathies. ... These issues will be reviewed here with the exception of MPGN due to complement-mediated disease (C3 glomerulopathies, ... See C3 glomerulopathies: Dense deposit disease and C3 glomerulonephritis and C4 glomerulopathy and Recurrence of ... C3 glomerulonephritis: clinicopathological findings, complement abnormalities, glomerular proteomic profile, treatment, and ...
more infohttps://www.uptodate.com/contents/evaluation-and-treatment-of-membranoproliferative-glomerulonephritis

Factor H deficiencyFactor H deficiency

Laboratory features usually include decreased serum levels of factor H, complement component C3 ({120700}), and a decrease in ... Complement factor H (CFH) is a negative regulator of the alternative pathway of complement, and properdin is the sole positive ... the convertase of the alternative pathway of the complement cascade. C3NeF prolongs the half-life of C3 convertase. Patients ... develop uncontrolled C3 activation and spontaneous renal disease characterized by accumulation of C3 along the glomerular ... ...
more infohttp://diseaseinfosearch.org/Factor+H+deficiency/8366

Anti-Complement C3, Mouse - MP BiomedicalsAnti-Complement C3, Mouse - MP Biomedicals

GOAT F(AB)2 FRAGMENT TO MOUSE COMPLEMENT C3. Product is the lyophilized powder of goat F(ab)2 fragment to mouse complement C3 ... GOAT IGG FRACTION TO MOUSE COMPLEMENT C3. Product is the lyophilized powder of goat IgG fraction to mouse complement C3 and ... FLUORESCEIN-CONJUGATED GOAT IGG F(AB)2 FRAGMENT TO MOUSE COMPLEMENT C3. Product is the lyophilized powder of fluorescein-5- ... PEROXIDASE-CONJUGATED GOAT IGG FRACTION TO MOUSE COMPLEMENT C3. Product is the lyophilized powder of horseradish peroxidase ( ...
more infohttps://www.mpbio.com/index.php?cPath=2873_1_4_20_2708_2684_2743&country=223

Anti-Complement C3, Rabbit - MP BiomedicalsAnti-Complement C3, Rabbit - MP Biomedicals

Unless specified otherwise, MP Biomedicals products are for laboratory research use only, not for human or clinical use. For more information, please contact our customer service department ...
more infohttp://www.mpbio.com/index.php?cPath=2873_1_4_20_2708_2684_2744&country=223

Complement C3 and Autophagy Keep the β Cell Alive.  - PubMed - NCBIComplement C3 and Autophagy Keep the β Cell Alive. - PubMed - NCBI

Complement Component C3 Is Highly Expressed in Human Pancreatic Islets and Prevents β Cell Death via ATG16L1 Interaction and ... Complement C3 and Autophagy Keep the β Cell Alive.. Toledo M1, Singh R2. ... 2018) show that intracellular complement component C3 interacts with autophagy protein ATG16L1 and protects against β cell ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/30625308

Complement C3 Genotype Variants and Risk of Lung Cancer MortalityComplement C3 Genotype Variants and Risk of Lung Cancer Mortality

... Poul Suadicani,1 Hans Ole Hein,1,2 and Finn Gyntelberg1 ... J. R. Yates, T. Sepp, B. K. Matharu et al., "Complement C3 variant and the risk of age-related macular degeneration," New ... J. E. Finn, L. Zhang, S. Agrawal, D. R. W. Jayne, D. B. G. Oliveira, and P. W. Mathieson, "Molecular analysis of C3 allotypes ... M. M. Markiewski and J. D. Lambris, "Is complement good or bad for cancer patients? A new perspective on an old dilemma," ...
more infohttps://www.hindawi.com/journals/isrn/2011/423571/ref/

Complement C3 | Blood Test | Life ExtensionComplement C3 | Blood Test | Life Extension

... of the complement system. Deficiency of C4 is closely linked to development of autoimmune diseases such as Lupus and Rheumatoid ... Complement component C3 is the most important and abundant protein in the complement system. These various components travel ... This blood test measures component 3 (C3) of the complement system. Deficiency of C3 may be associated with active Lupus, ... The complement system is a group of proteins that are important in your defense against infection and play a role in the ...
more infohttp://www.lifeextension.com/Vitamins-Supplements/itemLC006452/Complement-C3

Complement C3 | Blood Test - Life ExtensionComplement C3 | Blood Test - Life Extension

... of the complement system. Deficiency of C4 is closely linked to development of autoimmune diseases such as Lupus and Rheumatoid ... Complement component C3 is the most important and abundant protein in the complement system. These various components travel ... This blood test measures component 3 (C3) of the complement system. Deficiency of C3 may be associated with active lupus, ... Complement component C3 is the most important and abundant protein in the complement system. ...
more infohttps://www.lifeextension.com/lab-testing/itemlc006452/complement-c3

Complement C3 antibody | acris-antibodies.comComplement C3 antibody | acris-antibodies.com

The complement system is an important part of the humoral response in innate immunity, consisting of three different pathways. ... Alternative names for Complement C3 antibody. CPAMD1, Complement component 3, C3 and PZP-like alpha-2-macroglobulin domain- ... Rabbit Polyclonal antibody to Complement C3 (complement component 3). Rabbit. IgG. Aff - Purified. Hu, Ms. ICC/IF, P, WB. 0.1 ... Background of Complement C3 antibody. The complement system is an important part of the humoral response in innate immunity, ...
more infohttps://www.acris-antibodies.com/target/complement-c3-antibody.htm

JCI -
Hyperfunctional complement C3 promotes C5-dependent atypical hemolytic uremic syndrome in miceJCI - Hyperfunctional complement C3 promotes C5-dependent atypical hemolytic uremic syndrome in mice

... to the complement-activation protein C3 results in aHUS. Homozygous C3 p.D1115N (C3KI) mice developed spontaneous chronic ... Thus, our data provide in vivo modeling evidence that gain-of-function changes in complement C3 drive aHUS. They also show that ... Therapeutic blockade or genetic deletion of C5, a protein downstream of C3 in the complement cascade, protected homozygous C3KI ... Hyperfunctional complement C3 promotes C5-dependent atypical hemolytic uremic syndrome in mice. ...
more infohttps://jci.org/articles/view/99296/figure/5

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 5 Convertase; Complement C3 Convertases; Complement C5 Convertases; Activator, C3; C3 Convertases, Complement; C3-C5 ... C3; Convertase, C3-C5; Convertase, Complement 3; Convertases, Complement C3; Convertases, Complement C3-C5; Convertases, ...
more infohttp://www.curehunter.com/public/keywordSummaryD050577-Complement-C3-C5-Convertases-C3-Convertase.do

Complement C3 Antibody for ELISA LS-C128294Complement C3 Antibody for ELISA LS-C128294

Complement C3 antibody LS-C128294 is an unconjugated sheep polyclonal antibody to human Complement C3. Validated for ELISA and ... Complement C3 antibody LS-C128294 is an unconjugated sheep polyclonal antibody to human Complement C3. Validated for ELISA and ... Complement C3 antibody LS-C128294 is an unconjugated sheep polyclonal antibody to human Complement C3. Validated for ELISA and ... Complement C3 antibody was raised against purified C3d from pooled activated serum. ...
more infohttps://www.lsbio.com/antibodies/complement-c3-antibody-elisa-ls-c128294/131914

Complement C3 and its polymorphism: biological and clinical consequencesComplement C3 and its polymorphism: biological and clinical consequences

Complement 3 (C3) is a crucial component of the innate immune system, which in association with other complement proteins, ... Complement C3 and its polymorphism: biological and clinical consequences. Joris Delanghe (UGent) , Reinhart Speeckaert (UGent) ... immune system, Complement C3, polymorphism, HEMOLYTIC-UREMIC SYNDROME, DENSE DEPOSIT DISEASE, SYSTEMIC-LUPUS-ERYTHEMATOSUS, NON ... article{6538750, abstract = {Complement 3 (C3) is a crucial component of the innate immune system, which in association with ...
more infohttps://biblio.ugent.be/publication/6538750

Kamiya Biomedical Company - Clinical Diagnostics - Complement C3 ReagentKamiya Biomedical Company - Clinical Diagnostics - Complement C3 Reagent

x = INCSTAR Complement C3 Test Kit. y = K-ASSAY ® Complement C3 assay. x min = 78 y min = 74 ... A comparison of the K-ASSAY ® Complement C3 assay and an INCSTAR Complement C3 Test Kit was performed using a Hitachi 717. The ... For the quantitative determination of human complement C3 (3rd complement component) in serum by immunoturbidimetric assay. ... The precision for the K-ASSAY ® Complement C3 assay was determined using packaged reagents, pooled human serum, and a Hitachi ...
more infohttp://kamiyabiomedical.com/03ClinicalDiagnosticsProducts/Datasheets/KAI-009.php?language=english

Prognostic Significance of Preoperative and Postoperative Complement C3 Depletion in Gastric Cancer: A Three-Year Survival...Prognostic Significance of Preoperative and Postoperative Complement C3 Depletion in Gastric Cancer: A Three-Year Survival...

Y. Yuan, D. Yan, G. Han, G. Gu, and J. Ren, "Complement C3 depletion links to the expansion of regulatory T cells and ... J. R. Delanghe, R. Speeckaert, and M. M. Speeckaert, "Complement C3 and its polymorphism: Biological and clinical consequences ... Prognostic Significance of Preoperative and Postoperative Complement C3 Depletion in Gastric Cancer: A Three-Year Survival ... S. Ostrand-Rosenberg, "Cancer and complement," Nature Biotechnology, vol. 26, no. 12, pp. 1348-1349, 2008. View at Publisher · ...
more infohttps://www.hindawi.com/journals/bmri/2017/2161840/ref/

Complement C3 and Complement C4 | definition of Complement C3 and Complement C4 by Medical dictionaryComplement C3 and Complement C4 | definition of Complement C3 and Complement C4 by Medical dictionary

What is Complement C3 and Complement C4? Meaning of Complement C3 and Complement C4 medical term. What does Complement C3 and ... Looking for online definition of Complement C3 and Complement C4 in the Medical Dictionary? Complement C3 and Complement C4 ... Complement C3 and Complement C4. Complement C3 and Complement C4. Synonym/acronym: C3 and C4. ... Complement C3 and Complement C4 , definition of Complement C3 and Complement C4 by Medical dictionary https://medical- ...
more infohttps://medical-dictionary.thefreedictionary.com/Complement+C3+and+Complement+C4

Complement C3 is a novel modulator of the anti-factor VIII immune response | HaematologicaComplement C3 is a novel modulator of the anti-factor VIII immune response | Haematologica

Complement C3 participates in FVIII endocytosis by MO-DCs leading to presentation to CD4+ T cells. Because the complement C3 ... Complement human proteins Factor B, Factor D, C3, C3b and C3-depleted serum were purchased from Complement Technology (Comptech ... generating an initial C3 convertase, C3(H2O)Bb, that activates complement by cleaving C3 into its active fragments, C3a and C3b ... we show a novel role for complement C3 in enhancing the immune response against therapeutic FVIII. In vitro, complement C3 and ...
more infohttp://www.haematologica.org/content/103/2/351

Inhibiting complement C3 activation by gene therapy reduces glaucoma progression | IOVS | ARVO JournalsInhibiting complement C3 activation by gene therapy reduces glaucoma progression | IOVS | ARVO Journals

All three complement activation pathways converge at C3 cleavage. Here, we test the therapeutic effect of limiting C3 ... Inhibiting complement C3 activation by gene therapy reduces glaucoma progression Alejandra Bosco; Sarah Anderson; Kevin T Breen ... Inhibiting complement C3 activation by gene therapy reduces glaucoma progression You will receive an email whenever this ... Methods : We utilized CR2-Crry, which is the soluble rodent-specific complement inhibitor (sCrry) linked to a complement ...
more infohttps://iovs.arvojournals.org/article.aspx?articleid=2638391

Anti-Complement C3 Antibody | Goat anti-Human Polyclonal Serum | LSBioAnti-Complement C3 Antibody | Goat anti-Human Polyclonal Serum | LSBio

Complement C3 antibody LS-C187808 is an unconjugated goat polyclonal antibody to human Complement C3. Validated for ... Complement C3 antibody LS-C187808 is an unconjugated goat polyclonal antibody to human Complement C3. Validated for ... Recognizes human C3, a secreted protein that plays a central role in the activation of the complement system. This reagent is ...
more infohttps://www.lsbio.com/antibodies/complement-c3-antibody-ls-c187808/195711

INABIS 98 -  Activation and Deposition of Human Breast-milk Complement C3 Opsonins on a Serum Sensitive BacteriaINABIS '98 - Activation and Deposition of Human Breast-milk Complement C3 Opsonins on a Serum Sensitive Bacteria

Activation and Deposition of Human Breast-milk Complement C3 Opsonins on a Serum Sensitive Bacteria Contact Person: Michael O. ... Ogundele, M.O.; (1998). Activation and Deposition of Human Breast-milk Complement C3 Opsonins on a Serum Sensitive Bacteria. ... 7. Ballow-M; Donshik-PC; Mendelson-L(1985) Complement proteins and C3 anaphylatoxin in the tears of patients with ... I. Complement-mediated bactericidal activity of antibodies to a serum susceptible strain of E. coli of the serotype O 111. ...
more infohttp://www.mcmaster.ca/inabis98/immunology/ogundele0177/six.html

JCI Insight -
Serum Gp96 is a chaperone of complement-C3 during graft-versus-host diseaseJCI Insight - Serum Gp96 is a chaperone of complement-C3 during graft-versus-host disease

Finally, experimental induction of GvHD in complement C3-deficient mice confirms the link between Gp96 and complement C3 in the ... This model was used to identify complement C3 as a main partner of Gp96 in the serum. Our biolayer interferometry, yeast two- ... Accordingly, in vitro experiments with purified proteins demonstrate that Gp96 downregulates several complement C3 functions. ... Serum Gp96 is a chaperone of complement-C3 during graft-versus-host disease. ...
more infohttps://insight.jci.org/articles/view/90531/figure/1

C3 Complement Blood TestC3 Complement Blood Test

Complement C3 blood testing can help evaluate a variety of immune system issues. Order discounted lab testing from Request A ... C3 Complement Blood Test. This test measures levels of Complement C3 in the blood. The complement system includes over 30 ... C3 Complement Blood Test. This test measures levels of Complement C3 in the blood. The complement system includes over 30 ... C3 Complement Blood Test. This test measures levels of Complement C3 in the blood. The complement system includes over 30 ...
more infohttps://requestatest.com/C3-complement-blood-test

Serum immunoglobulin and complement (C3) levels | NeurologySerum immunoglobulin and complement (C3) levels | Neurology

Serum immunoglobulin and complement (C3) levels. John N. Whitaker, Joseph Sciabbarrasi, W. King Engel, John R. Warmolts, Warren ... Serum immunoglobulin and complement (C3) levels. A study in adults with idiopathic, chronic polyneuropathies and motor neuron ...
more infohttps://n.neurology.org/content/23/11/1164

Mouse monoclonal to Complement C3 beta chainMouse monoclonal to Complement C3 beta chain

Lately, we confirmed that cultured stromal cells of the limbus and peripheral cornea Mouse monoclonal to Complement C3 beta ... immune Adenosine Deaminase Imatinib Mesylate, Mouse monoclonal to Complement C3 beta chain ...
more infohttp://www.immune-source.com/tag/mouse-monoclonal-to-complement-c3-beta-chain/

Alternative-complement-pathway C3/C5 convertase - WikipediaAlternative-complement-pathway C3/C5 convertase - Wikipedia

Alternative-complement-pathway C3/C5 convertase (EC 3.4.21.47, complement component C3/C5 convertase (alternative), proenzyme ... C3 convertase, C3b,Bb,CVF,Bb,C5 convertase, (C3b)n,Bb, complement C 3(C 5) convertase (amplification), alternative complement ... Alternative-complement-pathway C3/C5 convertase at the US National Library of Medicine Medical Subject Headings (MeSH) ... This enzyme catalyses the following chemical reaction Cleavage of Arg-Ser bond in complement component C3 alpha-chain to yield ...
more infohttps://en.wikipedia.org/wiki/Alternative-complement-pathway_C3/C5_convertase
  • Our biolayer interferometry, yeast two-hybrid and in silico modeling data allowed us to determine that Gp96 binds to a complement C3 fragment encompassing amino acids 749-954, a functional complement C3 hot spot important for binding of different regulators. (jci.org)
  • Here, using in vitro assays for FVIII endocytosis by human monocyte-derived dendritic cells and presentation to T cells, as well as in vivo complement depletion in FVIII-deficient mice, we show a novel role for complement C3 in enhancing the immune response against therapeutic FVIII. (haematologica.org)
  • Complement is activated and responsive to bacteria , fungi and some immune complexes. (healthtap.com)
  • The complement RNAseq data were incorporated into a gene network showing interactions among C3-generating renal tubular cells and other immune competent migratory cells. (iupui.edu)
  • 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)
  • Here, we test the therapeutic effect of limiting C3 activation during glaucoma progression in D2 mice using ocular gene therapy. (arvojournals.org)
  • Thus, aHUS provides an archetypal complement-mediated disease with which to model new therapeutic strategies and treatments. (jci.org)
  • Complement depletion deteriorates clinical outcomes of severe abdominal sepsis: a conspirator of infection and coagulopathy in crime? (hindawi.com)
  • Complement activation and polymorphonuclear neutrophil leukocyte elastase in sepsis: correlation with severity of disease. (springer.com)
  • Murine and human genomic cosmid clones were isolated, characterized and sequenced 5′ to the complement C3 gene transcriptional initiation sites to determine cis elements that participate in constitutive and regulated C3 gene expression. (biochemj.org)
  • Four TATA boxes were identified upstream of the murine transcriptional initiation site, but deletion and transfection analysis using reporter gene constructs in HepG2 cells indicated that only the TATA element at position -30, together with sequences -395 to -111, are essential for constitutive expression of murine C3 in hepatocytes. (biochemj.org)
  • Collectively, these results localize cis-acting elements involved in constitutive and IL-1/IL-6-regulated murine C3 gene expression and provide evidence for specific transacting factors. (biochemj.org)
  • Thus, our data provide in vivo modeling evidence that gain-of-function changes in complement C3 drive aHUS. (jci.org)
  • Lower than normal complement levels are associated with a number of conditions such as increased bacterial infections, rheumatoid arthritis, cirrhosis, hepatitis, kidney disease, malnutrition, and septicemia. (requestatest.com)
  • In DI there were significant increases in renal mRNA encoding C3, C4, C5, C6, C8, and C9 over sham-operated lean normal controls (LS). (iupui.edu)
  • C3, C4, and C9 proteins were demonstrated in renal tubules and glomeruli. (iupui.edu)
  • Here we question this by examining an aged mouse model where both complement factor H and C3 have been knocked out (CFH -/- .C3 -/- ) compared with CFH -/- alone and normal aged C57Bl/6 wild type (WT) controls. (arvojournals.org)
  • Contrary to expectation, these results point to a beneficial/protective role of C3 in this AMD mouse. (arvojournals.org)
  • To order both tests, please order the C3 and C4 Blood Test . (requestatest.com)
  • The normal range for a complement C3 blood test is 80 to 160 milligrams per deciliter (mg/dL), or 0.8 to 1.6 grams per liter (g/L). (lomalindahealth.org)
  • Complement C3 and C4 are the ones which are most commonly tested. (requestatest.com)