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.

Complement activation and expression of membrane regulators in the middle ear mucosa in otitis media with effusion. (1/225)

The aetiopathogenesis of chronic otitis media with effusion (OME) in children is not yet fully understood. OME is characterized by metaplasia of the epithelium and accumulation of sticky, glue-like effusion in the middle ear containing different mediators of inflammation, including activation fragments of the complement system. Here we examined whether the fluid phase complement activation is reflected in the middle ear mucosa and how the mucosa is protected against the cytolytic activity of complement. Mucosal biopsies from 18 middle ears of children with a history of chronic OME were taken. The biopsies were analysed by immunofluorescence microscopy after staining for complement fragments iC3b/C3c, C3d and C9, and regulators membrane cofactor protein (MCP; CD46), decay-accelerating factor (DAF; CD55) and protectin (CD59). There was a strong staining for iC3b/C3c, and a weaker one for C3d and C9 on the surface of the middle ear epithelial cells of OME patients but not in controls without OME. MCP was expressed on the hyperplastic three to four outer cell layers of the epithelium, while CD59 was expressed throughout the middle ear mucosa. The results suggest a strong ongoing complement activation and consequent inflammation in the middle ear cavity. Unrestricted complement damage of the epithelial lining is prevented by the strong expression of MCP and CD59.  (+info)

Function of the factor I modules (FIMS) of human complement component C6. (2/225)

In order to elucidate the function of complement component C6, truncated C6 molecules were expressed recombinantly. These were either deleted of the factor I modules (FIMs) (C6des-748-913) or both complement control protein (CCP) modules and FIMs (C6des-611-913). C6des-748-913 exhibited approximately 60-70% of the hemolytic activity of full-length C6 when assayed for Alternative Pathway activity, but when measured for the Classical Pathway, C6des-748-914 was only 4-6% as effective as C6. The activity difference between C6 and C6des-748-913 for the two complement pathways can be explained by a greater stability of newly formed metastable C5b* when produced by the Alternative Pathway compared with that made by the Classical Pathway. The half-lives of metastable C5b* and the decay of (125)I-C5b measured from cells used to activate the Alternative Pathway were found to be about 5-12-fold longer than those same parameters derived from cells that had activated the Classical Pathway. (125)I-C5 binds reversibly to C6 in an ionic strength-dependent fashion, but (125)I-C5 binds only weakly to C6des-FIMs and not at all to C6des-CCP/FIMs. Therefore, although the FIMs are not required absolutely for C6 activity, these modules promote interaction of C6 with C5 enabling a more efficient bimolecular coupling ultimately leading to the formation of the C5b-6 complex.  (+info)

On the mechanism of cytolysis by complement: evidence on insertion of C5b and C7 subunits of the C5b,6,7 complex into phospholipid bilayers of erythrocyte membranes. (3/225)

The doughnut hypothesis of cytolysis by complement [Mayer, M. M. (1972) Proc. Nat. Acad. Sci. USA 69, 2954-2958] describes an annular structure made up of C5b-9 (complement factors C5b, C6, C7, C8, and C9) which becomes inserted in the lipid bilayer of the cell membrane, thus creating a hole. We now present initial explorations of this hypothesis. EAC1-6 and EAC1-7 (sheep erythrocytes carrying rabbit antibody and complement factors C1 through C6 or C1 through C7, respectively), prepared with either 125I-C3 or 125I-C5 were incubated with trypsin and the release of bound 125I was measured. In the case of 125I-C3, all of the radioactivity was released by trypsin from both intermediates. With 125I-C5, trypsin released all of the 125I from EAC1-6, but only 40-55% from EAC1-7. Possible reasons for resistance of the C5b subunit in EAC1-7 to tryptic digestion are discussed; in terms of the doughnut hypothesis it would be due to shielding by lipid molecules as a consequence of insertion into the lipid bilayer. In accord with this interpretation we have also found that C5b in EAC1-7, but not in EAC1-6, resists elution by 0.3 M NaC1. Similarly, we have found that 125I-C7 in EAC1-7 resists stripping by trypsin. Hence, we now propose the hypothesis that hydrophobic polypeptide chains from the C5b and the C7 subunits of C5b,6,7 complex become inserted in the phospholipid bilayer and that subsequent reactions with C8 and C9 open a channel across the membrane.  (+info)

Increased ion permeability of planar lipid bilayer membranes after treatment with the C5b-9 cytolytic attack mechanism of complement. (4/225)

The ion permeability of planar lipid bilayers, as measured electrically, was found to increase modestly upon treatment with purified complement complex C5b,6 and complement components C7 and C8. The subsequent addition C9 greatly amplified this change. No permeability changes occurred when components were added individually to the membrane, or when they were used in paired combinations, or when C5b, C7, C8, and C9 were admixed prior to addition. Thus, there is a significant parallel between the permeability changes induced in the model membrane and damage produced in biological membranes by the C5b-9 complement attack sequence. The efficiency of membrane action by C5b-9 was critically dependent on the order in whcih components were added to the membrane. There were also differences in the electrical properties of membranes treated with C5b-8 and C5b-9, though in both cases the enhanced bilayer permeability is best attributed to the formation of trans-membrane channels. Collectively, the data are consistent with the hypothesis that the mechanism of membrane action by complement involves the production of a stable channel across the lipid bilayer, resulting in cell death by colloid-osmotic lysis.  (+info)

Molecular aspects of complement-mediated bacterial killing. Periplasmic conversion of C9 from a protoxin to a toxin. (5/225)

As part of the membrane attack complex complement protein C9 is responsible for direct killing of bacteria. Here we show that in the periplasmic space of an Escherichia coli cell C9 is converted from a protoxin to a toxin by periplasmic conditions missing in spheroplasts. This conversion is independent of the pathway by which C9 enters the periplasm. Both, C9 shocked into the periplasm and plasmid-expressed C9 targeted to the periplasm via a signal sequence are toxic. Toxicity requires disulfide-linked C9 because export into the periplasm of cells defective in disulfide bond synthesis (dsbA and dsbB mutants) is not toxic unless N-acetylcysteine is added externally to promote cystines. A N-terminal fragment, C9[1-144], is not toxic nor is cytoplasmically expressed C9, even in trxB mutants that are able to form disulfide bonds in the cytoplasm. Importantly, expression of full-length C9 in complement-resistant cells has no effect on their viability. Expression and translocation into the periplasm may provide a novel model to identify molecular mechanisms of other bactericidal disulfide-linked proteins and to investigate the nature of bacterial complement resistance.  (+info)

Acute phase proteins and C9 in patients with Behcet's syndrome and aphthous ulcers. (6/225)

Estimation of the concentration of C9, C-reactive protein (CRP) and alpha1-antitrypsin in forty sera from patients with Behcet's syndrome and recurrent oral ulcers showed significantly increased amounts of C9 and CRP in Behcet's syndrome. The concentration of C9 was also significantly raised in recurrent oral ulceration, though to a lesser extent than in Behcet's syndrome. The assay C9 and CRP might be useful in the differential diagnosis of Behcet's syndrome, especially from recurrent oral ulcers. It is suggested that during epithelial inflammation in recurrent oral ulcers some of the acute phase proteins are increased and in some patients these may modulate the immunological mechanism in such a way as to induce a transition from focal oral ulceration to the multifocal Behcet's syndrome.  (+info)

Free radicals upregulate complement expression in rabbit isolated heart. (7/225)

Both free radicals and complement activation can injure tissue. Our study determined whether free radicals alter complement production by the myocardium. Isolated hearts from New Zealand White rabbits were perfused on a Langendorff apparatus and exposed to xanthine (X; 100 microM) plus xanthine oxidase (XO; 8 mU/ml) (X/XO). The free radical-generating system significantly (P < 0.05) increased C1q and also increased C1r, C3, C8, and C9 transcription compared with controls. Immunohistological examination revealed augmented membrane attack complex deposition on X/XO-treated tissue. X/XO-treated hearts also exhibited significant (P < 0.05) increases in coronary perfusion pressure and left ventricular end-diastolic pressure and a decrease in left-ventricular developed pressure. N-(2-mercaptopropionyl)-glycine (3 mM), in conjunction with the superoxide dismutase mimetic SC-52608 (100 microM), significantly (P < 0.05) reduced the upregulation of C1q, C1r, C3, C8, and C9 mRNA expression elicited by X/XO. The antioxidants also ameliorated the deterioration in function caused by X/XO. Local complement activation may represent a mechanism by which free radicals mediate tissue injury.  (+info)

CD59 protects rat kidney from complement mediated injury in collaboration with crry. (8/225)

BACKGROUND: As previously reported, the membrane-bound complement regulator at the C3 level (Crry/p65) is important in maintaining normal integrity of the kidney in rats. However, the role of a complement regulator at the C8/9 level (CD59) is not clear, especially when activation of complement occurs at the C3 level. The aim of this work was to elucidate the in vivo role of CD59 under C3 activating conditions. METHODS: Two monoclonal antibodies, 5I2 and 6D1, were used to suppress the function of Crry and CD59, respectively. In order to activate alternative the pathway of complement, the left kidney was perfused with 5I2 and/or 6D1 and was recirculated. RESULTS: In the kidneys perfused with 5I2 alone, deposition of C3 and membrane attack complex (MAC) was observed in the peritubular capillaries, vasa recta, and tubular basement membranes. Cast formation, tubular dilation and degeneration, and cellular infiltration were observed at days 1 and 4, and they recovered by day 7. Further suppression of CD59 by 6D1 significantly enhanced the deposition of MAC and worsened the already exacerbated tubulointerstitial injury. These effects of 6D1 were dose dependent. Perfusion with 6D1 alone did not induce histologic damage or MAC deposition in the tubulointerstitium. CONCLUSIONS: In rats, CD59 maintains normal integrity of the kidney in collaboration with Crry in rats against complement-mediated damage in vivo.  (+info)

*MACPF

"Nonsense mutation in exon 4 of human complement C9 gene is the major cause of Japanese complement C9 deficiency". Hum. Genet. ... Archetypal members of the family are complement C9 and perforin, both of which function in human immunity. C9 functions by ... Complement proteins C6-C9 all contain a MACPF domain and assemble into the membrane attack complex. C6, C7 and C8β appear to be ... 1997). "The human complement C9 gene: identification of two mutations causing deficiency and revision of the gene structure". J ...

*Pore-forming toxin

Eukaryote MACPF proteins function in immune defence and are found in proteins such as perforin and complement C9. Bacteria ... 1] Tschopp J, Masson D, Stanley KK (1986). "Structural/functional similarity between proteins involved in complement- and ...

*Complement membrane attack complex

Stanley KK, Luzio JP, Tschopp J, Kocher HP, Jackson P (1985). "The sequence and topology of human complement component C9". ... Multiple molecules of C9 can join spontaneously in concentrated solution to form polymers of C9. These polymers can also form a ... C5b-6-7-8 subsequently binds to C9 and acts as a catalyst in the polymerization of C9. MAC is composed of a complex of four ... "Nucleotide sequence of cDNA and derived amino acid sequence of human complement component C9". Proc. Natl. Acad. Sci. U.S.A. 81 ...

*Perforin

... has structural and functional similarities to complement component 9 (C9). Like C9, this protein creates transmembrane ... Shinkai Y, Takio K, Okumura K (1988). "Homology of perforin to the ninth component of complement (C9)". Nature. 334 (6182): 525 ... Young JD, Cohn ZA, Podack ER (1986). "The ninth component of complement and the pore-forming protein (perforin 1) from ... 1990). "Localization and molecular modelling of the membrane-inserted domain of the ninth component of human complement and ...

*Membranous glomerulonephritis

The immune complex serves as an activator that triggers a response from the C5b - C9 complements, which form a membrane attack ... Immunofluorescence microscopy will reveal typical granular deposition of immunoglobulins and complement along the basement ...

*Outline of immunology

C6 C7 C8 C9 Complement pathway inhibitors C1-inhibitor - Classical, Lectin, Alternate Decay-accelerating factor (CD59) - ... system Complement system Classical complement pathway Mannan-binding lectin pathway Alternate complement pathway Complement ... Secreted PRRs Complement system (see complement proteins section) Collectins Mannan-binding lectin (MBL) Surfactant protein A ( ... Complement receptor CR1 (CD35) CR2 (CD21) CR3 - Heterodimer: CD11b / CD18 CR4 - Heterodimer: CD11c / CD18 CRIg (Complement ...

*Complement component 9

... (C9) is a protein involved in the complement system, which is part of the innate immune system. C9 is a ... There are 10-16 molecules of C9 in a single membrane attack complex (MAC), along with one of each of the complement components ... 2001). "The complement system and innate immunity". Immunobiology: The Immune System in Health and Disease. New York: Garland ... Lint TF, Zeitz HJ, Gewurz H (November 1980). "Inherited deficiency of the ninth component of complement in man". J. Immunol. ...

*C9

... , C09 or C-9 may refer to: C9 (Complement component 9), a protein ATC code C09, a subgroup of the Anatomical Therapeutic ... C-9), a US Navy cruiser C9, the IATA code for Cirrus Airlines Sauber C9, a Le Mans racing car C9 engine, by Caterpillar Inc. C9 ... ICD-10 code for malignant neoplasm of tonsil Hi-Point Models C9 and C9 Comp handguns C9 LMG, a Canadian light machine gun C9, ... C9 League, a Chinese association of universities Cierva C.9, a 1927 British experimental autogyro HMS C9, a British submarine ...

*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 ...

*Terminal complement pathway deficiency

Initial complement tests often include C3 and C4, but not C5 through C9. Instead, the CH50 result may play a role in diagnosis ... Terminal complement pathway deficiency is a genetic condition affecting the complement membrane attack complex (MAC). It ... While C9 is part of the MAC, and deficiencies have been identified, it is not required for cell lysis.) People with this ... Suspect terminal complement pathway deficiency with patients who have more than one episode of Neisseria infection. ...

*CD59

When complement activation leads to deposition of C5b678 on host cells, CD59 can prevent C9 from polymerizing and forming the ... Ninomiya H, Sims PJ (1992). "The human complement regulatory protein CD59 binds to the alpha-chain of C8 and to the "b"domain ... Huang Y, Qiao F, Abagyan R, Hazard S, Tomlinson S (September 2006). "Defining the CD59-C9 binding interaction". J. Biol. Chem. ... 1992). "Complement regulatory proteins at the feto-maternal interface during human placental development: distribution of CD59 ...

*Meningococcal disease

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

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

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

*Complement system

... and polymeric C9. MAC is the cytolytic endproduct of the complement cascade; it forms a transmembrane channel, which causes ... Polymorphisms of complement component 3, complement factor B, and complement factor I, as well as deletion of complement factor ... Three biochemical pathways activate the complement system: the classical complement pathway, the alternative complement pathway ... The complement system is a part of the immune system that enhances (complements) the ability of antibodies and phagocytic cells ...

*Total complement activity

C5-C9; absence of hemolysis in both CH50 and AH50), classic pathway deficiencies (C1, C2, C4; absence of lysis in CH50) and ... Total complement activity is a test performed to assess the level of functioning of the complement system. The terms "CH50" or ... "Complement: MedlinePlus Medical Encyclopedia". medlineplus.gov. Retrieved 11 February 2017. ...

*Alternative complement pathway

C5b binds sequentially to C6, C7, C8 and then to multiple molecules of C9 to form membrane attack complex. Since C3b is free ... Inhibition of the alternative complement pathway by antisense oligonucleotides targeting complement factor B improves lupus ... cells from complement-mediated damage. CFHR5 (Complement Factor H-Related protein 5) is able to bind to act as a cofactor for ... there are several different kinds of regulatory proteins that disrupt the complement activation process: Complement Receptor 1 ...

*List of MeSH codes (D12.776.124)

... complement c7 MeSH D12.776.124.486.274.750 -- complement c8 MeSH D12.776.124.486.274.850 -- complement c9 MeSH D12.776.124.486. ... complement c4a MeSH D12.776.124.486.274.024.270 -- complement c5a MeSH D12.776.124.486.274.024.270.255 -- complement c5a, des- ... complement c1r MeSH D12.776.124.486.274.050.290 -- complement c1s MeSH D12.776.124.486.274.150 -- complement c2 MeSH D12.776. ... complement c2b MeSH D12.776.124.486.274.250 -- complement c3 MeSH D12.776.124.486.274.250.250 -- complement c3a MeSH D12.776. ...

*CD9

Ninomiya H, Sims PJ (1992). "The human complement regulatory protein CD59 binds to the alpha-chain of C8 and to the "b"domain ... of C9". J. Biol. Chem. 267 (19): 13675-80. PMID 1377690. Miyake M, Koyama M, Seno M, Ikeyama S (1992). "Identification of the ...

*Classical complement pathway

Subsequent interactions between C5b and other terminal components C6, C7, C8, and C9 form the membrane attack complex or the ... Alternative complement pathway - another complement system pathway Lectin pathway - another complement system pathway Noris, ... The classical complement pathway is one of three pathways which activate the complement system, which is part of the immune ... Activation of the complement pathway through the classical, lectin or alternative complement pathway is followed by a cascade ...

*Autoimmune hemolytic anemia

Cases may also arise with complement alone or with IgA, IgM or a combination of these three antibody classes and complement. ... C9) either can form the membrane attack complex (MAC) or can bind the antibody, aiding phagocytosis by macrophages (C3b). This ... Antibodies are produced against the RBCs, which leads to complement activation. Complement fragments, such as C3a, C4a and C5a ... IgM is a potent activator of the classical complement pathway, thus, AIHA involving IgM is characterized by complement mediated ...

*Steyr M

In 2010 the C (Compact) sized C-A1 series was introduced in 9×19mm Parabellum and .40 S&W chamberings as the C9-A1 and C40-A1. ... In 2013 the Steyr M (Medium) and S (Small) form factors were complemented by the L (Large) sized series and the C (Compact) ... For Italy only the C9-A1 is offered in the 9×21mm chambering. In 2013 the Steyr M (Medium), Steyr C (Compact) and S (Sub- ... Third generation' Steyr C9-A1. 'Third generation' Steyr M9-A1. 'Third generation' Steyr L9-A1. 'Third generation' Steyr ...

*CD59 antigen

CD59 associates with C9, inhibiting incorporation into C5b-8 preventing terminal steps in polymerization of the (MAC) in plasma ... thus protecting cells from complement-mediated lysis. It has a signaling role, as a GPI anchored molecule, in T cell activation ...

*Primary immunodeficiency

Complement deficiencies are the result of a lack of any of these proteins. They may predispose to infections but also to ... C8a deficiency C8b deficiency C9 deficiency (Neisserial infections) C1-inhibitor deficiency (hereditary angioedema) Factor I ... The complement system is part of the innate as well as the adaptive immune system; it is a group of circulating proteins that ... MASP2 deficiency Complement receptor 3 (CR3) deficiency Membrane cofactor protein (CD46) deficiency Membrane attack complex ...

*C3b

The C1 complement complex binds to these antibodies resulting in its activation via cross proteolysis. This activated C1 ... C5b associates with C6, C7, C8, and C9, all of which form a complex that results in a pore through the pathogen's membrane. ... C3b is the larger of two elements formed by the cleavage of complement component 3, and is considered an important part of the ... The key to the success of the complement system in clearing antigens is regulating the effects of C3b to pathogens alone and ...

*Pattern recognition receptor

C5, C6, C7, C8 and C9 form the membrane attack complex (MAC). This is another large superfamily of CLRs that includes The ... Complement receptors, collectins, ficolins, pentraxins such as serum amyloid and C-reactive protein, lipid transferases, ... Once bound to the ligands MBL and Ficolin oligomers recruit MASP1 and MASP2 and initiate the lectin pathway of complement ... "/"self turned nonself" type pathogen pattern are also identified and destroyed (e.g. by complement fixation or other cytotoxic ...

*HealthLine

Complementing the HealthLine is a set of bike lanes on the outer edges of the stretch Euclid Avenue that connects Cleveland ... A low sulfur diesel engine (Caterpillar C-9) generates electrical power to run smaller electric motors mounted on each of the ...
A novel cell surface antigen has been identified on a wide range of lymphoid cells and erythrocytes. A mAb YTH 53.1 (CD59) against this antigen enhanced the lysis of human red cells and lymphocytes by homologous complement. Studies of reactive lysis using different species of C56, and of whole serum used as a source of C7-9, indicated that the inhibitory activity of the CD59 antigen is directed towards the homologous membrane attack complex. CD59 antigen was purified from human urine and erythrocyte stroma by affinity chromatography using the mAb YTH 53.1 immobilized on Sepharose, and, following transient expression of a human T cell cDNA library in COS cells, the corresponding cDNA also identified using the antibody. It was found that the CD59 antigen is a small protein (approximately 20 kD as judged by SDS-PAGE, 11.5 kD predicted from the isolated cDNA) sometimes associated with larger components (45 and 80 kD) in urine. The sequence of CD59 antigen is unlike that of other complement ...
TY - JOUR. T1 - The membrane attack complex of complement. T2 - Relation of C7 to the metastable membrane binding site of the intermediate complex C5b-7. AU - Preissner, K. T.. AU - Podack, E. R.. AU - Muller-Eberhard, H. J.. PY - 1985/1/1. Y1 - 1985/1/1. N2 - Isolated C7 (m.w. 120,000) in 1% deoxycholate (DOC) forms dimers with an apparent m.w. of 230,000 and a DOC-binding capacity of 82 mol per mol of dimer. Dimerization of C7 also occurs in the presence of DOC-phospholipid mixed micelles and eventuates in the insertion of C7 dimers into the lipid bilayer upon the removal of the detergent, C5b-7 complex formation in the fluid phase or on lipid vesicles likewise involves polymerization, C5b-7 sedimented with 17-40S, which suggests a dimeric to hexameric composition. In avidin-biotin binding experiments in which two differentially labeled forms of C5b,6 (biotinyl 125I-C5b,6, and 131I-C5b,6) were used in equimolar amounts to assemble C5b-7, more than 50% of the biotinyl 125I-C5b,6-containing ...
Alloantibodies in pre-sensitized transplant candidates deposit complement membrane attack complexes (MAC) on graft endothelial cells (ECs), increasing risk of CD8+ T cell-mediated acute rejection. We recently showed (a) human ECs endocytose MAC into Rab5+ endosomes, creating a signaling platform that stabilizes NF-κB-inducing kinase (NIK) protein; (b) endosomal NIK activates both non-canonical NF-κB signaling to synthesize pro-IL-1β and an NLRP3 inflammasome to process and secrete active IL-1β; and (c) IL-1β activates ECs, increasing recruitment and activation of alloreactive effector memory CD4+ T (TEM) cells. Here, we report IFN-γ priming induced nuclear expression of IL-15/IL-15Rα complexes in cultured human ECs and that MAC-induced IL-1β stimulated translocation of IL-15/IL-15Rα complexes to the EC surface in a canonical NF-κB-dependent process, where IL-15/IL-15Rα transpresentation increased activation and maturation of alloreactive CD8+ TEM. Blocking NLRP3 inflammasome assembly, ...
Herein reported is the case of a 15-year-old female without a relevant medical history, who developed severe headaches, speech problems, dizziness, weakness, inability to walk, depressed consciousness, confusion, amnesia and vomiting, 14 days after receiving her first qHPV vaccine injection. After the second vaccine booster, her symptoms worsened and she expired 15 days later. Autopsy revealed cerebral oedema and cerebellar herniation indicative of a focally disrupted blood-brain barrier.. There was no evidence of an active brain infection. Immunohistochemistry (IHC) examination of the brainstem, hippocampus and the cerebellum showed prominent infiltration of T-lymphocytes and macrophages in all brain areas examined. Notably, marked activation of the complement membrane attack complex (MAC) was detected in the cerebellar Purkinje cells, hippocampal neurons and portions of the brainstem. This pattern of MAC activation in the absence of an active brain infection indicates an abnormal triggering of ...
Regenesance is developing nanoparticle formulations of inhibitors of the complement membrane attack complex (MAC) for the treatment of peripheral neuropathy.
Constituent of the membrane attack complex (MAC) that plays a key role in the innate and adaptive immune response by forming pores in the plasma membrane of target cells (PubMed:9634479, PubMed:9212048, PubMed:26841934). C9 is the pore-forming subunit of the MAC (PubMed:4055801, PubMed:26841934, PubMed:30111885).
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.
Die genetische Anfälligkeit für Meningokokken-Infektionen liegt vor allem in Störungen des Komplementsystems begründet, vor allem der terminale membrane attack complex (MAC), der von C8 und C9 gebildet wird, aber auch Teile des Komplementsystems, die die Bildung des MAC steuern, können betroffen sein (C3, C5, C6, C7).. ...
Name:C.I.Reactive Black 8,C.I.18207 Molecular Structure: Single azo,Metal Complexes C.I.Reactive Black 8,C.I.18207,CAS 12225-26-2,656.90,C19H11ClN8Na2O10S2,Reactive Black K-BR,Black HN C.I.Reactive Black 8,C.I.18207,CAS 12225-26-2,656.90,C19H11ClN8Na2O10S2,Reactive Black K-BR,Black HN Molecular Formula:C19H11ClN8Na2O10S2 Molecular Weight: CAS Registry Number:12225-26-2
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.
Isolated C7 (m.w. 120,000) in 1% deoxycholate (DOC) forms dimers with an apparent m.w. of 230,000 and a DOC-binding capacity of 82 mol per mol of dimer. Dimerization of C7 also occurs in the presence of DOC-phospholipid mixed micelles and eventuates in the insertion of C7 dimers into the lipid bilayer upon the removal of the detergent. C5b-7 complex formation in the fluid phase or on lipid vesicles likewise involves polymerization. C5b-7 sedimented with 17-40S, which suggests a dimeric to hexameric composition. In avidin-biotin binding experiments in which two differentially labeled forms of C5b,6 (biotinyl 125I-C5b,6, and 131I-C5b,6) were used in equimolar amounts to assemble C5b-7, more than 50% of the biotinyl 125I-C5b,6-containing complexes also contained 131I label; again suggesting that C5b-7 consisted of oligomers rather than monomers. The conformation of C7 in C5b-7 and in dimeric C7 appeared similar by the following criteria. On formation of C5b-7 from C5b,6 and C7, a 20% increase in ...
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.
Complex C DailyFoods Vitamin Formula All The C Factors As Nature Intended In Nature, Vitamin C is only found as a complex food with all the beneficial factors, such as bioflavonoids, intact. This formula contains 250 mg of Cold Fusion FoodState Vitamin C in its optimal form ~ FOOD. Cold Fusion FoodState Vitamin C is 10 times less acidic than regular Vitamin C (ascorbic acid), therefore it is Naturally Buffered and gentler on the stomach. Complex C DailyFoods is formulated with 100% Cold Fusion FoodState nutrients, developed by Durham Research, Inc. Cold Fusion FoodState nutrients have the inherent benefits of Vital Food Factors, known as Nutrient Chaperones. Nutrient Chaperones contain the plant intelligence necessary for all nutrient delivery and utilization. These nutrients have Food Chaperones, which facilitate utilization and reduce the potential for side-effects. Benefits are enhanced with the addition of phytonutrient rich concentrated fruit and vegetable extracts. Cold Fusion
Complement C6, 50 µg. C6 is a component of complement cascade. It is part of the membrane attack complex which can insert into the cell membrane and cause cell to lyse.
Granulocytic infiltrate occurs in the absence of demyelination, terminal complement complex formation, and overt tissue destruction in NMO white matter. a H&
The complement system (Chap. 308) consists of a group of serum proteins functioning as a cooperative, self-regulating cascade of enzymes that adhere to- and in some cases disrupt-the surface of invading organisms. Some of these surface-adherent proteins (e.g., C3b) can then act as opsonins for destruction of microbes by phagocytes. The later, "terminal" components (C7, C8, and C9) can directly kill some bacterial invaders (notably, many of the neisseriae) by forming a membrane attack complex and disrupting the integrity of the bacterial membrane, thus causing bacteriolysis. ...
Membrane attack complex (MAC) is formed under the combined stimulation of amyloid beta (Aβ) and normal human serum (NHS), immunolabeled with a monoclonal mouse anti-human C5b-9 antibody and subsequently visualized by Cy3 (red). RPE cell nuclei are counter-stained with DAPI. Scale bars: 20 μm. See full article online. Read More ...
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Background In the rat brain, a single intracerebroventricular injection of neuraminidase from Clostridium perfringens induces ependymal detachment and death. This injury occurs before the infiltration of inflammatory blood cells; some reports implicate the complement system as a cause of these injuries. Here, we set out to test the role of complement. Methods The assembly of the complement membrane attack complex on the ependymal epithelium of rats injected with neuraminidase was analyzed by immunohistochemistry. Complement activation, triggered by neuraminidase, and the participation of different activation pathways were analyzed by Western blot. In vitro studies used primary cultures of ependymal cells and explants of the septal ventricular wall. In these models, ependymal cells were exposed to neuraminidase in the presence or absence of complement, and their viability was assessed by observing beating of cilia or by trypan blue staining. The role of complement in ependymal damage induced by ...
Dr. Elias Reichel, of Tufts University School of Medicine and a founder of Hemera Biosciences, Inc., of Boston, MA, presented on a new approach to treating the dry form of age-related macula degeneration. His paper was based on the research being done by Hemera Biosciences on HMR59, a naturally occurring protein that protects retinal cells from damage by MAC (Membrane Attack Complex), that can be delivered for long-lasting activity via a gene therapy approach. ...
Please ask any questions you may have about this specific product in the field below.. Your question(s) and our corresponding answer(s) will not be confidential and will be posted publically on this specific product page.. Additionally, PureFormulas is unable to directly recommend products in relation to specific health conditions. Please contact your trusted healthcare practitioner for direct product recommendations.. If you have any general questions regarding orders or our policies and programs, please contact our Customer Happiness Team @ 1.800.383.6008. If you are pregnant, nursing, taking any medications or have any medical condition, consult your doctor before use. Your healthcare professional is the best source for guidance before beginning an exercise or nutritional supplement program.. ...
Please ask any questions you may have about this specific product in the field below.. Your question(s) and our corresponding answer(s) will not be confidential and will be posted publically on this specific product page.. Additionally, PureFormulas is unable to directly recommend products in relation to specific health conditions. Please contact your trusted healthcare practitioner for direct product recommendations.. If you have any general questions regarding orders or our policies and programs, please contact our Customer Happiness Team @ 1.800.383.6008. If you are pregnant, nursing, taking any medications or have any medical condition, consult your doctor before use. Your healthcare professional is the best source for guidance before beginning an exercise or nutritional supplement program.. ...
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?. ...
W poprzednich kilku tematach omówione i udowodnione bylo działanie kreatyny powodujące wzrost siły,mocy,wzrost wykononanej pracy,wzrost wytrzymałości i masy mieśniowej; r
It was Mihikas low weight that prompted doctors to operate on her right in the NICU. "The journey from her hospital room to the operation theatre could be fatal for such micro-preemies due to the difference in temperature," said Dr Mohanty. Hence, the team of surgeons and anesthetists gathered in Mishikas room to fix the hole in her heart vessels. "It wasnt an open heart surgery, but it was a difficult procedure because no instruments are designed for operation on such small children," he said. ...
The C5b-9 complex (Terminal Complement Complex-TCC) is the final product of the terminal complement pathway. In this study, using the monoclonal antibody MCaE11 (specific for a C9 neoantigen) and an immunohistochemical technique, we examined the TCC deposits in synovial tissues from 4 patients affected by rheumatoid arthritis (RA) and 6 patients affected by osteoarthritis (OA). Synovial tissues from 8 patients affected by acute joint trauma were examined as controls. Furthermore, plasma TCC levels were measured in 44 RA patients and 51 controls, using the above mentioned antibody and a sandwich ELISA. Eight synovial fluids were also included in this study. Abundant TCC deposits were detected in the cytoplasm of the synovial lining cells and of large stromal mononuclear cells in all the RA and in 3 out of 6 OA synovial tissues characterized by histological signs of inflammation. No TCC deposits were found in non-inflamed synovial tissues from patients with joint trauma. In agreement with previous ...
[A type of glomerulonephritis that is characterized by the accumulation of immune deposits ( COMPLEMENT MEMBRANE ATTACK COMPLEX) on the outer aspect of the GLOMERULAR BASEMENT MEMBRANE. It progresses from subepithelial dense deposits, to basement membrane reaction and eventual thickening of the basement membrane., A slowly progressive inflammation of the glomeruli characterized by immune complex deposits at the glomerular basement membrane, resulting in a thickened membrane, and nephrotic syndrome.]
A casein kinase released from activated human platelets has been shown to phosphorylate a number of plasma proteins. When platelets are activated they release substantial amounts of ATP and divalent cations which are necessary for phosphorylation of proteins. The aim of this study was to elucidate the optimal conditions for phosphorylation of the human complement component C4, identify phosphorylation site in the molecule and to investigate possible impact on the functions of phosphorylated C4. For this purpose, C4 must be prepared from human plasma, which was done using a modification of a previously published method. The results showed a pure and 100 % active protein. C4 was incubated with [g-32P]ATP and cations. After SDS-PAGE and autoradiography it was shown that C4 was phosphorylated in the a-chain. Maximal phosphorylation was achieved when C4 was phosphorylated in the presence of 20 mM Ca2+. Incubation of phosphorylated and unphosphorylated C4 with trypsin showed that phosphorylated C4 was ...
The key event in complement activation is the proteolytic cleavage of C3 to C3a and C3b. Three pathways can lead to C3 cleavage, namely, classical, alternative, and mannose-binding lectin (MBL) pathways. C3 cleavage leads on to the activation of the terminal complement pathway, causing the generation of the membrane attack complex (MAC), which assembles…
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.
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These studies suggested that cell lysates and supernatant collected from cultured PMNs that were exposed to cytokines or C. albicans hyphae opsonized with normal human serum had elevated levels of C6 and C7 proteins [18,19]; however, it was not conclusive that these proteins were produced by PMNs in culture because (1) the rise in C6 or C7 in culture could have been released by C. albicans hyphae or derived from normal human serum, (2) the inhibition of protein biosynthesis by cycloheximide did not affect the rise in C6 or C7 in PMN cultures [18], and (3) conclusive evidence showing that PMNs are actively expressing these terminal complement mRNAs or proteins has been lacking in the literature ...
Objective: Complement proteins have been associated with atherosclerosis and cardiovascular risk factors. Recent data suggest a potential role of complement protein C3 in clot stability with hypofibrinolytic and prothrombotic features. Women after menopause are at greater risk of cardiovascular disease and have significantly higher levels of C3 compared with younger women. To better understand the association between complement proteins and atherosclerosis we evaluated the cross-sectional associations between complement proteins C3 and C4 and hemostatic markers (factor VIIc, fibrinogen, plasminogen activator inhibitor-1 (PAI-1) antigen and tissue plasminogen activator (tPA) antigen) in a sample of midlife women.. Design: Pilot data from the Study of Womens Health Across the Nation (SWAN) Pittsburgh site were used. Both C3 and C4 were measured using frozen serum specimens by immunoturbidimetric assay. Data for hemostatic markers were available in SWAN Core data (factor VIIc and fibrinogen were ...
Background/Purpose: The influence of complement-mediated innate immune responses on cartilage and bone homeostasis in the ageing joint have not been studied. Inappropriate complement-mediated cell damage is prevented by membrane regulators such as CD59. Synovial tissue expression of CD59 is altered during inflammatory arthritis; elevated CD59 levels may be necessary to protect joint tissues. Roles of CD59 in maintaining tissue equilibrium and structural architecture within the synovial joint have not been described previously. Since CD59a is the primary regulator of membrane attack complex assembly in mice; we used CD59a-gene-deleted mice (CD59a-/-) as tools to unravel the function of CD59a in modulating age-related joint degeneration. Methods: Hind limbs were collected from C57BL/6J wild type (WT) and CD59a-/- mice at 8-, 20- and 50- weeks of age (6 to 10 mice/group). The Mankin score was used to classify the histopathological severity of osteoarthritic (OA) lesions. Three dimensional ...
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 ...
When the complement system is activated, it triggers a variety of events leading to cleavage of one component known as C5. Once C5 is cleaved, a variety of events occur that propagate the formation of the membrane attack complex. This member attack complex generates pores, or holes, in cells ultimately leading to the cells demise. So when you have such a powerful system, regulators of the system are needed. These regulators sit on the outer membrane of cells, so the complement system recognizes that these cells are of the self. When those regulators are missing, as is the case in PNH, this leads to the destructions of the cells that are missing these protein shields.. Some of those shields, (2 proteins known as CD 55 and CD 59) are anchored the cell surface by a tail. We call this tail a GPI anchor - but in PNH this GPI anchor is missing because of a mutation in a gene called PIG-A. This defective gene leads to cause the cells inability to form this GPI anchor. So the complement regulator ...
2QOS: Crystal structure of complement protein C8gamma in complex with a peptide containing the C8gamma binding site on C8alpha: Implications for C8gamma ligand binding.
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 ...
The presence of lytic antibodies in the circulation of patients with chronic Chagas disease might lead to their cure. It has been shown that amastigotes of Trypanosoma cruzi activate complement and accumulate large amounts of the terminal complement components, but without killing the parasites. One plausible explanation for this observation is that the insertion of the membrane attack complex of complement is prevented by inhibitors present in the parasite membrane. To explore this possibility, we raised a panel of monoclonal antibodies (MAbs) against the surface molecules of T. cruzi amastigotes. One of these, MAb M4C12, induced complement-mediated lysis of amastigotes as detected with a 86Rb-release assay. The antigen molecule from the membrane lysate of amastigotes that was recognized by MAb M4C12 was purified, characterized, and designated M4C12Ag. It is a 92-kD molecule structurally related to Ssp4, a previously characterized amastigote surface molecule. However, M4C12Ag is more basic (pI 6.9-7.1
During sublytic complement attack on human neutrophils, plasma-membrane vesicles are shed from the cell surface as a cell-protection mechanism. By using surface-iodinated neutrophils it was found that less than 2% of surface label was recovered in shed vesicles under conditions where 40% of complement component C9 was shed. SDS/PAGE of 125I-labelled shed vesicles and plasma membranes showed differences in iodination pattern, demonstrating the sorting of membrane proteins into the shed vesicles. Analysis of 32P-labelled phospholipids after labeling of neutrophils with [32P]Pi before sublytic complement attack showed the presence of phosphatidic acid, phosphatidylcholine, phosphatidyl-ethanolamine, phosphatidylinositol and polyphosphoinositides in shed vesicles. Quantitative analysis using [3H]acetic anhydride-labelling method showed that the molar proportions of phosphatidylethanolamine, phosphatidylinositol, phosphatidylserine and sphingomyelin were the same in shed vesicles as in plasma ...
Cerebral IR injury produces a profound inflammatory response characterized by neutrophil, macrophage, and platelet accumulation, upregulation of adhesion molecules, blood-brain barrier destruction, and cytokine production.5 During central nervous system inflammation, complement activation plays a direct role in neuronal cell death6 and has been implicated in many disease processes, including subarachnoid hemorrhage,9 Alzheimer disease,10 trauma,11 and stroke.12,13 In a study of patients who died after ischemic stroke, Lindsberg et al9 demonstrated complement deposition within areas of necrosis and concluded that activation of the terminal complement pathway with membrane attack complex assembly occurs within cerebral infarct zones. Others have shown that complement depletion before cerebral IR injury may have neuroprotective effects in animal models.12,14 Huang et al12 used a mouse model of middle cerebral artery occlusion and reperfusion to demonstrate that administering a potent inhibitor of ...
c-C3BP or rGAPDH was observed (Figure 3c, d). The H.c-C3BP or rGAPDH interaction with C3 was specific and strong, which was evident from the fact that the column-bound C3 was eluted at high salt wash (0·5 m NaCl) or by lowering the pH to 2·2. To test whether H.c-C3BP or rGAPDH binding to C3 would influence complement function, a simple haemolytic assay was performed where the lysis of sensitized sheep erythrocytes by serum complement proteins was measured. As shown in Figure 3(e, f), a dose-dependent inhibition of erythrocyte lysis by H.c-C3BP and rGAPDH was observed. To rule out that the observed inhibition was not due to suppression of the classical pathway, binding of C1q protein by H.c-C3BP was. measured. No interaction among these proteins was evident in the microtitre plate assay (not shown). To confirm check details whether the inhibition of erythrocyte lysis by H.c-C3BP or rGAPDH was due to suppression of C3 activation, the formation of membrane attack complex (MAC) was measured on the ...
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.
In addition to being a component of innate immunity and an ancient defense mechanism against invading pathogens, complement activation also participates in the adaptive immune response, inflammation, hemostasis, embryogenesis, and organ repair and development. Activation of the complement system via classical, lectin, or alternative pathways generates anaphylatoxins (C3a and C5a) and membrane attack complex (C5b-9) and opsonizes targeted cells. Complement activation end products and their receptors mediate cell-cell interactions that regulate several biological functions in the extravascular tissue. Signaling of anaphylatoxin receptors or assembly of membrane attack complex promotes cell dedifferentiation, proliferation, and migration in addition to reducing apoptosis. As a result, complement activation in the tumor microenvironment enhances tumor growth and increases metastasis. In this Review, I discuss immune and nonimmune functions of complement proteins and the tumor-promoting effect of ...
In addition to being a component of innate immunity and an ancient defense mechanism against invading pathogens, complement activation also participates in the adaptive immune response, inflammation, hemostasis, embryogenesis, and organ repair and development. Activation of the complement system via classical, lectin, or alternative pathways generates anaphylatoxins (C3a and C5a) and membrane attack complex (C5b-9) and opsonizes targeted cells. Complement activation end products and their receptors mediate cell-cell interactions that regulate several biological functions in the extravascular tissue. Signaling of anaphylatoxin receptors or assembly of membrane attack complex promotes cell dedifferentiation, proliferation, and migration in addition to reducing apoptosis. As a result, complement activation in the tumor microenvironment enhances tumor growth and increases metastasis. In this Review, I discuss immune and nonimmune functions of complement proteins and the tumor-promoting effect of ...
CH50 and CH100 measures the integrity of the classical and terminal complement pathways. Indicated in the investigation of suspected immune deficiency associated with recurrent pyogenic infections, recurrent/atypical meningococcal infections and atypical immune complex disorders.AP100 measures the integrity of the alternative and terminal complement pathways. Rare deficiencies of AP components predispose to neisserial infections.AP100 measures the integrity of the alternative and terminal complement pathways. Rare deficiencies of AP components predispose to neisserial infections ...
This study demonstrates that anti-ganglioside Abs, including experimental mAbs and GBS patient serum, induce sequential nodal and/or axonal injury in a new passive transfer mouse model that recapitulates the salient pathologic features found in axonal GBS (Griffin et al., 1996b). We found that the breakdown of BNB induced by L5SNT was essential for Ab-mediated nerve injury. Furthermore, this anti-ganglioside Abs-mediated neuropathy (injury to intact nerve fibers) depends on activating FcγRs bearing macrophages/microglia-mediated inflammation triggered by ICs formed by anti-ganglioside Abs and their target antigens on the nerves. Notably, we found that the terminal complement complex was not involved in the anti-ganglioside Abs-mediated axonal degeneration in this animal model. Overall, our study supports the notion that cellular elements of innate immunity are required for Ab-mediated nerve injury and involved in the pathogenesis of GBS. The identification of activating FcγRs in ...
Eggs are part of The Paleo Diet, as humans have consumed eggs during the paleolithic era, although not in a year round basis (because bird eggs appear only seasonally), hence Dr. Cordain has advocated eggs, specially those rich in omega-3 fatty acids, in his three books. One of the egg white functions is to protect the yolk against microbal attack using proteolytic enzymes, besides being storage of nutrients for the growing embryo and transport of nutrients into the growing embryo. Except for ovoalbumen, most of the proteins in egg white have antimicrobial, antibacterial or antiviral activity, some of these proteins are called ovomucoid, ovomucin and lysozyme, among others. These proteins may disrupt the integrity of the gut lining leading to increased intestinal permeability and lysozyme is the most harmful of these proteins in terms of membranolytic activity (breakdown of cell membranes). We recommend that patients suffering from autoimmune diseases to avoid egg white at the beginning as ...
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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 ...
Abstract: : Purpose: Terminal complement components (C5,C5b-9)and several complement inhibitors are ubiquitous drusen components. This implies that complement activation may be a key element in drusen formation; but the specific complement activator(s) and activation pathway are unknown. The classical pathway is triggered by the binding of immune complexes to C1q. Alternative and lectin pathways that are antibody-independent also exist. Other molecules that interact with, or substitute for, C1q can also activate complement directly. Methods: The RPE/choroid was excised from human donor eyes with and without drusen. Vibratome sections were examined using differential interference contrast (DIC) and confocal microscopy (CM). Some sections were re-embedded and examined by electron microscopy (TEM). For CM, sections were probed with: a.) monoclonal antibodies (Ab) raised against activation-specific fragments of complement C3, HLA-DR antigen, and IgG; b.) Abs to mitochondrial, Golgi, and lysosomal ...
Background Glaucoma is an age-related neurodegenerative disorder involving the loss of retinal ganglion cells (RGCs), which results in blindness. Studies in animal models have shown that activation of inflammatory processes occurs early in the disease. In particular, the complement cascade is activated very early in DBA/2J mice, a widely used mouse model of glaucoma. A comprehensive analysis of the role of the complement cascade in DBA/2J glaucoma has not been possible because DBA/2J mice are naturally deficient in complement component 5 (C5, also known as hemolytic complement, Hc), a key mediator of the downstream processes of the complement cascade, including the formation of the membrane attack complex. Methods To assess the role of C5 in DBA/2J glaucoma, we backcrossed a functional C5 gene from strain C57BL/6J to strain DBA/2J for at least 10 generations. The prevalence and severity of glaucoma was evaluated using ocular examinations, IOP measurements, and assessments of optic nerve damage and RGC
Radioimmune assays were developed to assay the binding of complement components C1q, C1s and C4 to antibody aggregates and to cell-bound antibody. The binding of the components was compared with the haemolytic activity and with the capacity to form the C3 convertase activity in the presence of excess C2. The destruction of whole complement and of C4 activity is similar per 1,000 molecules of antibody in aggregates and cell-bound antibody, as is the binding of C1g and C1s, the latter being in a 1:2 molar ratio. The binding of C4 is about 12 times greater, per 1,000 molecules of antibody, on cells than in aggregates. However, the effective C4 molecules, as judged by the formation of C3 convertase activity, are much more similar on cells and aggregates. An assembly mechanism of the early components of complement on antibody-coated cells, which is compatible with these results, is suggested. ...
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. . ...
This gene encodes a plasma glycoprotein that positively regulates the alternative complement pathway of the innate immune system. This protein binds to many microbial surfaces and apoptotic cells and stabilizes the C3- and C5-convertase enzyme complexes in a feedback loop that ultimately leads to formation of the membrane attack complex and lysis of the target cell. Mutations in this gene result in two forms of properdin deficiency, which results in high susceptibility to meningococcal infections. Multiple alternatively spliced variants, encoding the same protein, have been identified.[provided by RefSeq, Feb 2009 ...
Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterised by the production of IgG autoantibodies that are specific for self-antigens, such as DNA, nuclear proteins and certain cytoplasmic components, in association with a diverse array of clinical manifestations. The primary pathological findings in patients with SLE are those of inflammation, vasculitis, immune complex deposition, and vasculopathy. Immune complexes comprising autoantibody and self-antigen is deposited particulary in the renal glomeruli and mediate a systemic inflammatory response by activating complement or via Fc{gamma}R-mediated neutrophil and macrophage activation. Activation of complement (C5) leads to injury both through formation of the membrane attack complex (C5b-9) or by generation of the anaphylatoxin and cell activator C5a. Neutrophils and macrophages cause tissue injury by the release of oxidants and proteases ...
Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterised by the production of IgG autoantibodies that are specific for self-antigens, such as DNA, nuclear proteins and certain cytoplasmic components, in association with a diverse array of clinical manifestations. The primary pathological findings in patients with SLE are those of inflammation, vasculitis, immune complex deposition, and vasculopathy. Immune complexes comprising autoantibody and self-antigen is deposited particulary in the renal glomeruli and mediate a systemic inflammatory response by activating complement or via Fc{gamma}R-mediated neutrophil and macrophage activation. Activation of complement (C5) leads to injury both through formation of the membrane attack complex (C5b-9) or by generation of the anaphylatoxin and cell activator C5a. Neutrophils and macrophages cause tissue injury by the release of oxidants and proteases ...
The general aim of this study was to evaluate the disease spectrum in patients presenting with a pure polymyositis (pPM) phenotype. Specific objectives were to characterize clinical features, autoantibodies (aAbs), and membrane attack complex (MAC) in muscle biopsies of patients with treatment-responsive, statin-exposed necrotizing autoimmune myositis (NAM). Patients from the Centre hospitalier de lUniversité de Montréal autoimmune myositis (AIM) Cohort with a pPM phenotype, response to immunosuppression, and follow-up ≥3 years were included. Of 17 consecutive patients with pPM, 14 patients had a NAM, of whom 12 were previously exposed to atorvastatin (mean 38.8 months). These 12 patients were therefore suspected of atorvastatin-induced AIM (atorAIM) and selected for study. All had aAbs to 3-hydroxy-3-methylglutaryl coenzyme A reductase, and none had overlap aAbs, aAbs to signal recognition particle, or cancer. Three stages of myopathy were recognized: stage 1 (isolated serum creatine ...
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 ...
Behcets syndrome is a rare condition where blood vessels all throughout the body become abnormally inflamed, explains Mayo Clinic. The disease is variable in where it produces symptoms and can...
IgG antibody accounts for the vast majority of all antibody mediated protection even though it is the slowest to be produced after the initial insult. Its primary means of protection is to identify the pathogen by attaching to it and marking it for destruction by other immune cells. It can also burst cells by fixing complement. Complement is a group of proteins that build on one another after the initial component has been "fixed", much like the first domino must be tipped over to topple the whole row. Once the "row" has been completed, the complement has the ability to pierce the cell wall of the antigen. Typically only gram negative bacteria can be pierced (lysed) by a particular chain of complement known as the membrane attack (MAC). Gram positives can fall prey to the complement cascade but through the identification route ...
|strong|Mouse anti Human C3d antibody, clone 053A-514.3.1.4|/strong| recognizes human complement component 3d (C3d) neoantigen, a ~33 kDa polypeptide fragment generated over the course of complem…
Serum levels rise for other proteins, cialis 5mg wirkungseintritt such as ceruloplasmin, complement proteins, haptoglobin, fibrinogen, and C-reactive
TY - JOUR. T1 - Interaction of complement and clusterin in renal injury. AU - Correa-Rotter, Ricardo. AU - Hostetter, Thomas H.. AU - Nath, Karl A. AU - Manivel, J. Carlos. AU - Rosenberg, Mark E.. PY - 1992/11. Y1 - 1992/11. N2 - Clusterin is a heterodimeric glycoprotein that has been associated with such diverse biologic functions as reproduction, cell regression, cell aggregation, and regulation of the cytolytic activity of the membrane attack complex of complement. Clusterin is a component of glomerular immune deposits in the kidney, and increased Clusterin expression occurs in a number of renal injury states. To further explore the interaction between Clusterin and complement, the requirement for an intact complement system for renal Clusterin induction in an acute (folic acid nephropathy) and a chronic (subtotal renal ablation) model of renal injury was examined. After it was first demonstrated that folic acid increased renal clusterin mRNA in the rat, a species in which renal clusterin ...
Forty strains of Aeromonas hydrophila and Aeromonas veronii recovered from invasive and non-invasive infections were tested for their susceptibility to complement-mediated lysis by 65% pooled human serum (PHS). Based upon the results of this assay, two major populations could be defined. The first group (n = 20) consisted of serogroup 0:11 strains, all of which possessed a paracrystalline surface layer (S layer); all of these strains were refractory to the bactericidal activity of 65% PHS with the exception of A. hydrophila strain AH-121, which was composed of mixed subpopulations of serum-susceptible and serum-resistant clones. A second collection of isolates (n = 20), all of which were S-layer-negative, contained a subgroup of strains (n = 7) that were highly susceptible to complement-mediated lysis, showing a greater than 100-fold reduction of viable progeny within 30 min of exposure to 65% PHS. Serum-resistant strains from both groups could not be lysed by exposure of bacterial cells to polyclonal
... is produced by our E.coli expression system and the target gene encoding Asn679-Arg755 is expressed.
Complement, C3 Convertase, Regulation, Cells, Disease, Complement Factor H, Inhibition, Therapeutic, Transplant, Allograft, Donor, Donors, and Graft
Main / Vitamins/Supplements / Can you take valtrex and antibiotics He had me on Metagenics Ultraclear rice based and honestly it tastes terrible and I was too wimpy to take the higher potency. Since Ive been taking Amoxicillin, my symptoms from the This material does not endorse drugs, diagnose patients, or recommend therapy. For good health - Have a diet rich in fresh vegetables, fruits, whole grains, milk and milk products, nuts, beans, legumes, lentils and small amounts of lean meats.. These medications are not usually taken together. February 18, psychologyforum. Valtrex valacyclovir may diminish the presence of virus in the skin or mucous membranes lesions and lessen the chances of a viral culture being positive, but will not in any way alter the antibody test on a blood specimen. ...
C1QB - C1QB (Myc-DDK-tagged)-Human complement component 1, q subcomponent, B chain (C1QB) available for purchase from OriGene - Your Gene Company.

Complement C9 Antibody
		        
	Complement C9 Antibody

Complement C9 Polyclonal Antibody from Invitrogen for Western Blot and Immunohistochemistry (Paraffin) applications. This ... Cite Complement C9 Polyclonal Antibody. The following antibody was used in this experiment: Complement C9 Polyclonal Antibody ... Protein Aliases: C5b-9 complex component; Complement component C9; Membrane Attack Complex component ... PA5-19826 targets C9 in IHC (P) and WB applications and shows reactivity with Human samples.. The PA5-19826 immunogen is ...
more infohttps://www.thermofisher.com/antibody/product/C9-Antibody-Polyclonal/PA5-19826

Complement C9 antibody | acris-antibodies.comComplement C9 antibody | acris-antibodies.com

The three distinct activation pathways of complement converge with the formation of a C5 convertase. The cleavage of C5 by this ... Background of Complement C9 antibody. The three distinct activation pathways of complement converge with the formation of a C5 ... Immunohistochemical analysis of Complement C9 staining in human liver cancer formalin fixed paraffin embedded tissue section. ... Lane 1 : Complement factor C9 isolated from human plasma. Lane 2 : Human plasma.. *MAB0780 ...
more infohttps://www.acris-antibodies.com/target/complement-c9-antibody.htm?ab_ag_reactivity=Hu&ab_applications=E

Complement C9 antibody | acris-antibodies.comComplement C9 antibody | acris-antibodies.com

The three distinct activation pathways of complement converge with the formation of a C5 convertase. The cleavage of C5 by this ... Background of Complement C9 antibody. The three distinct activation pathways of complement converge with the formation of a C5 ... Immunohistochemical analysis of Complement C9 staining in human liver cancer formalin fixed paraffin embedded tissue section. ... Lane 1 : Complement factor C9 isolated from human plasma. Lane 2 : Human plasma.. *MAB0780 ...
more infohttps://www.acris-antibodies.com/target/complement-c9-antibody.htm?ab_ag_presentation=Aff+-+Purified&ab_applications=E

Complement C9, Human CAS 80295-59-6 | 204910Complement C9, Human CAS 80295-59-6 | 204910

Complement C9, Human, CAS 80295-59-6, is a native, single-chain glycoprotein present in normal human serum at 60 µg/ml. - Find ... human C9 complement component. Single-chain glycoprotein present in normal human serum at 60 µg/ml. On activation of complement ... human C9 complement component. Single-chain glycoprotein present in normal human serum at 60 µg/ml. On activation of complement ... Complement C9, Human, CAS 80295-59-6, is a native, single-chain glycoprotein present in normal human serum at 60 µg/ml.. More,, ...
more infohttp://www.emdmillipore.com/US/en/product/Complement-C9-Human,EMD_BIO-204910

Complement C9 Antibody (FITC) for IHC, WB/Western LS-C693053Complement C9 Antibody (FITC) for IHC, WB/Western LS-C693053

Complement C9 antibody LS-C693053 is an FITC-conjugated guinea pig polyclonal antibody to rabbit Complement C9. Validated for ... C9 Antibody, Complement C9 Antibody, Complement component 9 Antibody, Complement component C9 Antibody ... Complement C9 antibody LS-C693053 is an FITC-conjugated guinea pig polyclonal antibody to rabbit Complement C9. Validated for ... Complement C9 antibody LS-C693053 is an FITC-conjugated guinea pig polyclonal antibody to rabbit Complement C9. Validated for ...
more infohttps://www.lsbio.com/antibodies/complement-c9-antibody-fitc-ihc-wb-western-ls-c693053/718481

Complement C9 Antibody (aa22-265, HRP) for IHC, WB/Western LS-C710425Complement C9 Antibody (aa22-265, HRP) for IHC, WB/Western LS-C710425

Complement C9 antibody LS-C710425 is an HRP-conjugated rabbit polyclonal antibody to human Complement C9. Validated for IHC and ... C9 Antibody, Complement C9 Antibody, Complement component 9 Antibody, Complement component C9 Antibody ... Complement C9 antibody LS-C710425 is an HRP-conjugated rabbit polyclonal antibody to human Complement C9. Validated for IHC and ... Complement C9 antibody LS-C710425 is an HRP-conjugated rabbit polyclonal antibody to human Complement C9. Validated for IHC and ...
more infohttps://www.lsbio.com/antibodies/complement-c9-antibody-aa22-265-hrp-ihc-wb-western-ls-c710425/735853

Complement component C9 (P79755) | InterPro | EMBL-EBIComplement component C9 (P79755) | InterPro | EMBL-EBI

Membrane attack complex component/perforin/complement C9 (IPR001862)*Complement component C9 (IPR037567) ...
more infohttp://www.ebi.ac.uk/interpro/protein/P79755

Complement C9 deficiencyComplement C9 deficiency

... Complement component 9 deficiency is caused by mutations of the C9 gene. If both alleles are altered ... Recurrent meningitis in a patient with congenital deficiency of the C9 component of complement. First case of C9 deficiency in ... Abbott C et al. (1989) The gene for human complement component C9 mapped to chromosome 5 by polymerase chain reaction. ... Witzel-Schlömp K et al. (1997) The human complement C9 gene: identification of two mutations causing deficiency and revision of ...
more infohttp://moldiag.com/en/id/D0376

Complement Component C9 Lysates: Novus BiologicalsComplement Component C9 Lysates: Novus Biologicals

Browse our Complement Component C9 Lysate catalog backed by our Guarantee+. ... Complement Component C9 Lysates available through Novus Biologicals. ... Complement Component C9 Lysates. We offer Complement Component C9 Lysates for use in common research applications: Western Blot ... Our Complement Component C9 Lysates can be used in a variety of model species. Use the list below to choose the Complement ...
more infohttps://www.novusbio.com/lysates/complement-component-c9?related_pathways=Cell%20Proliferation

Monoclonal antibody targeting complement C9 binding domain of Trichinella spiralis paramyosin impairs the viability of...Monoclonal antibody targeting complement C9 binding domain of Trichinella spiralis paramyosin impairs the viability of...

Previous studies demonstrated that Ts-Pmy bound to complement components C8 and C9 and inhibited the polymerization of C9 ... The binding of mAb 9G3 to Ts-Pmy efficiently blocked the binding of Ts-Pmy to human complement C9, resulting in a significant ... mAb 9G3 is a specific antibody that binds to the C9 binding domain of Ts-Pmy and interferes with Ts-Pmys complement-binding ... In this study, a monoclonal antibody against the complement C9 binding domain of Ts-Pmy (mAb 9G3) was produced using hybridoma ...
more infohttps://parasitesandvectors.biomedcentral.com/articles/10.1186/1756-3305-7-313

C9 - Complement component C9 precursor - Homo sapiens (Human) - C9 gene & proteinC9 - Complement component C9 precursor - Homo sapiens (Human) - C9 gene & protein

C9 is the pore-forming subunit of the MAC (PubMed:4055801, PubMed:26841934, PubMed:30111885). ... "The architecture of complement component C9 and poly(C9).". DiScipio R.G., Hugli T.E.. J. Biol. Chem. 260:14802-14809(1985) [ ... "The architecture of complement component C9 and poly(C9).". DiScipio R.G., Hugli T.E.. J. Biol. Chem. 260:14802-14809(1985) [ ... "The architecture of complement component C9 and poly(C9).". DiScipio R.G., Hugli T.E.. J. Biol. Chem. 260:14802-14809(1985) [ ...
more infohttps://www.uniprot.org/uniprot/P02748

Complement Component C9  - 产品: Leica BiosystemsComplement Component C9 - 产品: Leica Biosystems

Complement component C9 acts in a similar way to perforin, a pore forming protein found in cytotoxic T cells. Male and female ... Complement component C9 binds to the C5b-8 complex as the final protein of the membrane attack complex. After binding, it ... The detection of complement component C9 has been reported in cases of acute myocardial damage at necropsy. Detection of ... Human myocardium: immunohistochemical staining for complement component C9 using NCL-CCC9. Note staining of partially necrotic ...
more infohttps://www.leicabiosystems.com/cn/ihc-ish-fish/immunohistochemistry-ihc-antibodies-novocastra-reagents/primary-antibodies/products/complement-component-c9/

R-PLEX Human Complement C9 Antibody Set | Meso Scale DiscoveryR-PLEX Human Complement C9 Antibody Set | Meso Scale Discovery

R-PLEX Human Complement C9 Antibody Set Calibration Curve. Complement C9 Analyte. Description - Complement C9 (C9D, ARMD15, C9 ... R-PLEX Human Complement C9 Antibody Set .testRadioBox { padding-left:40%; } R-PLEX Human Complement C9 Antibody Set Overview. ... R-PLEX Human Complement C9 Antibody Set Features. *Measures human Complement C9 in plasma ... Calibration curve for the R-PLEX Human Complement C9 Antibody Set was assessed and representative data is presented below. ...
more infohttps://www.mesoscale.com/en/products/r-plex-human-complement-c9-antibody-set-f21xz/

C9 Complement, Functional, Serum -
Munson Healthcare LaboratoriesC9 Complement, Functional, Serum - Munson Healthcare Laboratories

Test Code C9FX C9 Complement, Functional, Serum Reporting Name. C9 Complement, Functional, S ... The total complement (CH50) assay (COM / Complement, Total, Serum) should be used as a screen for suspected complement ... A deficiency of an individual component of the complement cascade will result in an undetectable total complement level. ... Investigation of a patient with a low total (hemolytic) complement (CH50) level ...
more infohttps://mhc.testcatalog.org/show/C9FX

Complement Component C9  - 製品情報: Leica BiosystemsComplement Component C9 - 製品情報: Leica Biosystems

Complement component C9 binds to the C5b-8 complex as the final protein of the membrane attack complex. After binding, it ... Complement Component C9 Primary Antibodies Complement Component C9 Novocastra. *製品情報 ... Complement component C9 acts in a similar way to perforin, a pore forming protein found in cytotoxic T cells. Male and female ... Complement component C9 binds to the C5b-8 complex as the final protein of the membrane attack complex. After binding, it ...
more infohttp://www.leicabiosystems.com/jp/ihc-ish-fish/immunohistochemistry-ihc-antibodies-novocastra-reagents/primary-antibodies/products/complement-component-c9/

reagents-immunoassay-protein-complement-component-c5-c9reagents-immunoassay-protein-complement-component-c5-c9

Deficiency of complement components C5 to C9 are associated with several diseases, especially recurrent neisserial infections. ... IVD Test Reagent/Kits, Immunoassay, Protein, Complement Component, C5-C9. Definition : Immunoassay reagents intended to perform ... Home > Specialties > IVD Test Reagent/Kits, Immunoassay, Protein, Complement Component, C5-C9 ... Entry Terms : "C5-9 (Complement Component) Determination Reagents" , "Reagents, Immunoassay, Protein, Complement Component, C5- ...
more infohttp://productguide.ophthalmologymanagement.com/term/5528/reagents-immunoassay-protein-complement-component-c5-c9

MRMaid, the Web-based Tool for Designing Multiple Reaction Monitoring (MRM) Transitions | Molecular & Cellular ProteomicsMRMaid, the Web-based Tool for Designing Multiple Reaction Monitoring (MRM) Transitions | Molecular & Cellular Proteomics

Complement C9 (ENSG00000113600). 10. AIEDYINEFSVR. 13. 37.9. 5. 6. 28.3. 31.3. 1271.6 (y10). 1271.2-1272.2. 12. 27.1. ... Complement factor H (ENSG00000000971). 33. SPDVINGSPISQK. 23. 34.4. 7. 6. 16.3. 17.7. 830.4 (y8). 830.1-831.2. 17. 93.6. ...
more infohttp://www.mcponline.org/content/8/4/696/tab-figures-data

C6 - Complement component C6 precursor - Homo sapiens (Human) - C6 gene & proteinC6 - Complement component C6 precursor - Homo sapiens (Human) - C6 gene & protein

Belongs to the complement C6/C7/C8/C9 family.Curated. Keywords - Domaini. EGF-like domain, Repeat, Signal, Sushi. Phylogenomic ... "Structural homology of complement protein C6 with other channel-forming proteins of complement.". Chakravarti D.N., Chakravarti ... R-HSA-166665 Terminal pathway of complement. R-HSA-977606 Regulation of Complement cascade. ... R-HSA-166665 Terminal pathway of complement. R-HSA-977606 Regulation of Complement cascade. ...
more infohttps://www.uniprot.org/uniprot/P13671

Modulation of synaptic maintenance - The Board of Trustees of the Leland Stanford Junior UniversityModulation of synaptic maintenance - The Board of Trustees of the Leland Stanford Junior University

Alternatively, C3-activation can activate downstream complement proteins C5-C9 to eliminate unwanted cells via the formation of ... Complement. Complement is a system of plasma proteins that interacts with the cell surfaces of pathogens or cells to mark them ... Johnson et al., Perforant Path Transection Induces Complement C9 Deposition in Hippocampus. Exp Neurol. 1996;138:198-205. ... Inhibition of complement. A number of molecules are known that inhibit the activity of complement. In addition to known ...
more infohttp://www.freepatentsonline.com/9382314.html

Shop by Product Category ELISA | Lucerna-Chem AGShop by Product Category ELISA | Lucerna-Chem AG

AssayMax™ Human Complement C9 ELISA Kit Supplier: Assaypro • Format: Sandwich ELISA. Pricing Collapse ... AssayMax™ Human Complement C3 ELISA Kit (Plasma and Serum Samples) Supplier: Assaypro • Crossreactivity: Dg, Bo, Mk, Ms, Rt, Pg ...
more infohttps://lucerna-chem.ch/shop/category/57/elisa

Gene ID: 414919 | C9 Antibody ResourceGene ID: 414919 | C9 Antibody Resource

C9 , Review 7 of antibodies with 3 images, 3 of protocols, relevant gene trends, publication graphs, tissue expression data, ... Sheep anti Complement C9 Antibody (1ml). 1ml. $275. Details. Polyclonal Antibody. ARP60085_P050. C9 Antibody (ARP60085_P050). ... Dog C9 antibody; Canis familiaris C9 antibody. E2RFV9. 93.0%. ARP60085. Dog C9 antibody; Canis familiaris C9 antibody. E2RFV9. ... Horse C9 antibody; Equus caballus C9 antibody. F6UFT2. 86.0%. ARP60086. Horse C9 antibody; Equus caballus C9 antibody. P48770. ...
more infohttps://www.avivasysbio.com/sd/genepage/page/c9.php

Patente US3625214 - Drug-delivery device - Google PatentesPatente US3625214 - Drug-delivery device - Google Patentes

C9 complement inhibitor. US5843922 *. 11 Jun 1996. 1 Dic 1998. Fuisz Technologies Ltd.. Preparation of oligosaccharides and ... Compositions and methods to inhibit formation of the C5b-9 complex of complement. ...
more infohttp://www.google.es/patents/US3625214

Zur deutschen Internetseite wechselnZur deutschen Internetseite wechseln

Complement C9 Antikörper. Nicht möglich. Mouse. IgG1. 64E9. Liquid. Hu. P, WB. 50 µl / 425,00 € ...
more infohttps://www.acris-antikoerper.de/antibodies/primary-antibodies.htm?ab_ag_presentation=Liquid

Patent US6891154 - Amino acid sequence pattern matching - Google PatentsPatent US6891154 - Amino acid sequence pattern matching - Google Patents

C9 complement protein [homo sapiens]. 18ADEE16G02.1799.1799.2.dta. 1:. Chain c, crystal structure of the human. ...
more infohttp://www.google.com/patents/US6891154?dq=6,757,682
  • The binding activity of the mAb produced for recombinant or native Ts -Pmy and the blockade of Ts -Pmy binding to C9 by the mAb were assessed by Western blot analysis. (biomedcentral.com)
  • mAb 9G3 was successfully produced against the C9 binding domain of Ts -Pmy and bound specifically not only to recombinant Ts -Pmy but also to native Ts -Pmy expressed in different stages of T. spiralis , including adult worms, newborn larvae and muscle larvae. (biomedcentral.com)
  • Whereas uEVs of young patients with ADPKD and preserved kidney function already had higher levels of complement, only uEVs of patients with advanced stages of ADPKD had increased levels of villin-1, periplakin, and envoplakin. (asnjournals.org)
  • The C9 binding domain of Ts -Pmy was identified within 14 amino acid residues at the C-terminus of Ts -Pmy. (biomedcentral.com)