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.
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.
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.
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.
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.
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.
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.
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).
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.
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.
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).
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.
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.
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).
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).
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.
Molecules on the surface of some B-lymphocytes and macrophages, that recognize and combine with the C3b, C3d, C1q, and C4b components of complement.
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).
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.
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.
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.
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.
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.
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 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 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.
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.
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.
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.
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).
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.
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).
A G-protein-coupled receptor that signals an increase in intracellular calcium in response to the potent ANAPHYLATOXIN peptide COMPLEMENT C5A.
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.
Compounds that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host.
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.
Serum proteins that inhibit, antagonize, or inactivate COMPLEMENT C1 or its subunits.
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.
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.
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.
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.
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.
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).
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.
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.
Important enzymes in the CLASSICAL COMPLEMENT ACTIVATION PATHWAY. They cleave COMPLEMENT C3 and COMPLEMENT C5.
The N-terminal fragment of COMPLEMENT 2, released by the action of activated COMPLEMENT C1S.
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)
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.
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.
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).
Important enzymes in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY. They cleave COMPLEMENT C3 and COMPLEMENT C5.
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.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.
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.
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.
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.
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).
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.
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.
Proteins that are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.
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.
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.
The engulfing and degradation of microorganisms; other cells that are dead, dying, or pathogenic; and foreign particles by phagocytic cells (PHAGOCYTES).
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 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.
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.
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).
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.
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.
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.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.
The clear portion of BLOOD that is left after BLOOD COAGULATION to remove BLOOD CELLS and clotting proteins.
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.
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.
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.
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.
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.
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.
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.
Thickening of the walls of small ARTERIES or ARTERIOLES due to cell proliferation or HYALINE deposition.
Antibodies produced by a single clone of cells.
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.
Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.
Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
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 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.
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.)
Established cell cultures that have the potential to propagate indefinitely.
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.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
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.
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.
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.
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.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
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.
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 in which a polyacrylamide gel is used as the diffusion medium.
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.
Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.
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).
Proteins prepared by recombinant DNA technology.
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.
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
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.
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.
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).
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 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).
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).
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.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
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.
Plasmids containing at least one cos (cohesive-end site) of PHAGE LAMBDA. They are used as cloning vehicles.
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.
Proteins found in any species of bacterium.
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.
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.
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.
Transport proteins that carry specific substances in the blood or across cell membranes.
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.
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.
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.
An individual in which both alleles at a given locus are identical.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
Biologically active substances whose activities affect or play a role in the functioning of the immune system.
Elements of limited time intervals, contributing to particular results or situations.
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.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
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.
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.
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.
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.
Glycoproteins found on the membrane or surface of cells.
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.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
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.
The sum of the weight of all the atoms in a molecule.
The rate dynamics in chemical or physical systems.
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.
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.
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.
The presence of proteins in the urine, an indicator of KIDNEY DISEASES.
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.
The production of ANTIBODIES by proliferating and differentiated B-LYMPHOCYTES under stimulation by ANTIGENS.
Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.
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.
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.
Use of restriction endonucleases to analyze and generate a physical map of genomes, genes, or other segments of DNA.
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.
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.
A plasma protein that circulates in increased amounts during inflammation and after tissue damage.
The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.
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.
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)
Cytochrome P-450 monooxygenases (MIXED FUNCTION OXYGENASES) that are important in steroid biosynthesis and metabolism.
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.
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.
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.
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.
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.
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.
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 used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.
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.
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.
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
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.
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.
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.
The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.
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.
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.
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.
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.
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.
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.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.
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.
Immunoglobulins produced in a response to BACTERIAL ANTIGENS.
The systematic study of the complete complement of proteins (PROTEOME) of organisms.
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.
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.
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).
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.
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.
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.
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.
A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.
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.
A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.
Group of diseases mediated by the deposition of large soluble complexes of antigen and antibody with resultant damage to tissue. Besides SERUM SICKNESS and the ARTHUS REACTION, evidence supports a pathogenic role for immune complexes in many other IMMUNE SYSTEM DISEASES including GLOMERULONEPHRITIS, systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC) and POLYARTERITIS NODOSA.

Mutations of the type A domain of complement factor B that promote high-affinity C3b-binding. (1/656)

Factor B is a zymogen that carries the catalytic site of the complement alternative pathway convertases. During C3 convertase assembly, factor B associates with C3b and is cleaved at a single site by factor D. The Ba fragment is released, leaving the active complex, C3bBb. During the course of this process, the protease domain becomes activated. The type A domain of factor B, also part of Bb, is similar in structure to the type A domain of the complement receptor and integrin, CR3. Previously, mutations in the factor B type A domain were described that impair C3b-binding. This report describes "gain of function" mutations obtained by substituting factor B type A domain amino acids with homologous ones derived from the type A domain of CR3. Replacement of the betaA-alpha1 Mg2+ binding loop residue D254 with smaller amino acids, especially glycine, increased hemolytic activity and C3bBb stability. The removal of the oligosaccharide at position 260, near the Mg2+ binding cleft, when combined with the D254G substitution, resulted in increased affinity for C3b and iC3b, a C3b derivative. These findings offer strong evidence for the direct involvement of the type A domain in C3b binding, and are suggestive that steric effects of the D254 sidechain and the N260-linked oligosaccharide may contribute to the regulation of ligand binding.  (+info)

Capsular sialic acid limits C5a production on type III group B streptococci. (2/656)

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

Amplification of the antibody response by C3b complexed to antigen through an ester link. (3/656)

Complement C3 has been described as playing an important role in the cell-mediated immune response. C3b has the capacity to covalently bind Ag and then to stimulate in vitro Ag presentation to T lymphocytes. To verify this observation in vivo, we prepared and purified covalent human C3b-Ag complexes using lysozyme (HEL) as Ag. The characterization of these HEL-C3b complexes indicates that they are representative of those susceptible to be generated in physiological conditions. Mice were immunized with 0.1 to 0.6 microgram of either free HEL, HEL + C3b, HEL-C3b, or HEL + CFA. Response was assessed after two i.p. injections by quantification of specific Ab production. Immunization with either HEL-C3b complexes or HEL + CFA leads to anti-HEL IgG production whereas free HEL or HEL + C3b was ineffective. Either HEL-C3b or HEL + CFA immunizations led to a similar Ig subclass patterns, including IgG1, IgG2a, IgA, and IgM. Our experiments provide the first evidence for modulation of specific Ab response by C3b when it is bound to Ag through a physiological-like link. Taken together with previous data concerning Ab response following recombinant HEL-C3d immunization, cellular events such as processing of C3b-Ag by APC and recognition by T lymphocytes, this present result underlines the importance of C3b and its fragments in stimulation of the immune system, through the multiplicity and complementarity of its interactions.  (+info)

A novel glycosylphosphatidyl inositol-anchored protein on human leukocytes: a possible role for regulation of neutrophil adherence and migration. (4/656)

We report here a novel glycosylphosphatidyl-inositol (GPI)-anchored glycoprotein on human leukocytes. Treatment of neutrophils with a mAb (3H9) to this molecule sequentially up-regulates and down-regulates beta2 integrin-dependent adhesion of these cells as well as their transendothelial migration in vitro. In addition, this mAb simultaneously modulates the avidity of beta2 integrin for its ligand, iC3b, with kinetics similar to those observed in 3H9 modulation of neutrophil adherence. This mAb also induces beta2 integrin-dependent cytoskeletal remodeling. This novel GPI-anchored protein (GPI-80) is highly homologous with Vanin-1, a recently reported GPI-anchored protein that is expressed on perivascular thymic stromal cells and is involved in thymus homing in mice. The finding that both GPI-80 and Vanin-1 are 40% homologous with human biotinidase suggests the existence of a biotinidase superfamily of molecules that may be involved in the regulation of leukocyte trafficking.  (+info)

Binding of soluble immune complexes to Raji lymphocytes. Role of receptors for complement components, C1q and C3-C3b. (5/656)

We have found that, although the binding of particulate antigen-antibody complement complexes such as EAC to lymphoblastoid Raji cells is mediated largely through receptors for C3b, the binding of complement-containing soluble complexes such as those prepared with aggregated human IgG (AHG) occurs also via receptors for C1q. Evidence supporting this conclusion included: (1) Binding of AHG to Raji cells takes place after incubation in EDTA serum; (2) Binding of AHG does not occur in C1q deficient EDTA serum but does take place after addition of C1q; (3) The extent of binding of AHG in EDTA serum is a function of the amount of C1q present; (4) Raji cells can bind up to 5-4 times 10(5) molecules of 125I C1q per cell which can be blocked by unlabelled C1q; (5) AHG pre-incubated with C can bind to a T-cell line MOLT, which lacks receptors for C3b but possesses receptors for C1q to the same extent as Raji cells; (6) Immunoassays for immune complexes in human sera yield similar results whether Raji cells, MOLT cells or C1q precipitation is used for assay; (7) EAC-Raji cell rosettes can be inhibited with inulin-treated, C1q deficient serum containing C3b or C3d whereas binding of AHG or immune complexes in patient samples to Raji or MOLT cells is not inhibited by this reagent. We conclude that receptors for C1q on certain B and T lymphocytes may play an important role in physiologic functions of lymphocytes depending on binding of soluble immune complexes to their surfaces.  (+info)

Complement activation and increased systemic and pulmonary vascular resistance indices during infusion of postoperatively drained untreated blood. (6/656)

In nine healthy young patients, operated on for thoracic scoliosis, a pulmonary artery catheter was inserted for the study of haemodynamic variables and blood sampling during autologous transfusion of postoperatively drained blood. At 1-3 h after wound closure, 10 ml kg/body weight of drained untreated blood from the wound was collected and recirculated over a l-h period. The concentration of the complement activation product, C3bc, increased from a mean of 5.4 (SD 1.5) AU ml-1 before infusion to 11.1 (3.9) AU ml-1 during infusion and then returned to 7.8 (2.8) AU ml-1 after infusion. The concentration of the terminal complement complex (TCC) increased from 0.5 (0.2) to 1.3 (0.5) AU ml-1 and was reduced to 0.7 (0.3) AU ml-1 after infusion. Only TCC exceeded the reference values which are 14 AU ml-1 for C3bc and 1.0 AU ml-1 for TCC. Pulmonary vascular resistance index concomitantly increased from a mean of 130 (SD 52) to 195 (88) dyn s cm-5 m-2 and was reduced to 170 (86) dyn s cm-5 m-2 after infusion. Systemic vascular resistance index increased from a mean of 1238 (SD 403) to 1349 (473) dyn s cm-5 m-2 and returned to 1196 (401) dyn s cm-5 m-2 after infusion. White blood cell count (WCC) increased from 14.4 (4.3) x 10(9) litre-1 before infusion to 17.8 (7.2) x 10(9) litre-1 during and after infusion. No change in platelet count during infusion was observed. There were no differences in WCC or platelet count between mixed venous or peripheral arterial blood. Pulmonary and systemic vascular resistance indices may be influenced by activated complement in drained untreated blood when it is recirculated.  (+info)

Complement activation and expression of membrane regulators in the middle ear mucosa in otitis media with effusion. (7/656)

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)

Pneumococcal surface protein A inhibits complement activation by Streptococcus pneumoniae. (8/656)

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

Poziotinib (HM781-36B) is an irreversible pan-HER inhibitor with IC50 of 3.2 nM, 5.3 nM and 23.5 nM for HER1, HER2, and HER4, respectively. Phase 2.
Returns an iterator pointing to the first element in the container whose key is not considered to go before k (i.e., either it is equivalent or goes after ...
61840DNAVaccinia virus 1tttttattat ttgtacgatg tccaggataa catttttacg gataaataaa tatgaaggtg 60gagagcgtga cgttcctgac attgttggga ataggatgcg ttctatcatg ctgtactatt 120ccgtcacgac ccattaatat gaaatttaag aatagtgtgg agactgatgc taatgctaat 180tacaacatag gagacactat agaatatcta tgtctacctg gatacagaaa gcaaaaaatg 240ggacctatat atgctaaatg tacaggtact ggatggacac tctttaatca atgtattaaa 300cggagatgcc catcgcctcg agatatcgat aatggccaac ttgatattgg tggagtagac 360tttggctcta gtataacgta ctcttgtaat agcggatatc atttgatcgg tgaatctaaa 420tcgtattgtg aattaggatc tactggatct atggtatgga atcccgaggc acctatttgt 480gaatctgtta aatgccaatc ccctccatct atatccaacg gaagacataa cggatacgag 540gatttttata ccgatgggag cgttgtaact tatagttgca atagtggata ttcgttgatt 600ggtaactctg gtgtcctgtg ttcaggagga gaatggtccg atccacccac gtgtcagatt 660gttaaatgtc cacatcctac aatatcaaac ggatacttgt ctagcgggtt taaaagatca 720tactcataca acgacaatgt agactttaag tgcaagtacg gatataaact atctggttcc 780tcatcatcta cttgctctcc aggaaataca tggaagccgg aacttccaaa atgtgtacgc 8402244PRTVaccinia virus ...
Suramin is a competitive inhibitor of heparin binding to many proteins, including viral envelope proteins, protein tyrosine phosphatases, and fibroblast growth factors (FGFs). It has been clinically evaluated as a potential therapeutic in treatment of cancers caused by unregulated angiogenesis, triggered by FGFs. Although it has shown clinical promise in treatment of several cancers, suramin has many undesirable side effects. There is currently no experimental structure that reveals the molecular interactions responsible for suramin inhibition of heparin binding, which could be of potential use in structure-assisted design of improved analogues of suramin. We report the structure of suramin, in complex with the heparin-binding site of vaccinia virus complement control protein (VCP), which interacts with heparin in a geometrically similar manner to many FGFs. The larger than anticipated flexibility of suramin manifested in this structure, and other details of VCP-suramin interactions, might ...
TY - JOUR. T1 - Decidual endothelial cells express surface-bound C1q as a molecular bridge between endovascular trophoblast and decidual endothelium. AU - Tripodo, Claudio. AU - Agostinis, Chiara. AU - Rizzi, Lucia. AU - Tedesco, Francesco. AU - Radillo, Oriano. AU - De Seta, Francesco. AU - Ghebrehiwet, Berhane. AU - Bossi, Fleur. AU - Bulla, Roberta. AU - Debeus, Alessandra. PY - 2008. Y1 - 2008. N2 - This study was prompted by the observation that decidual endothelial cells (DECs), unlike endothelial cells (ECs) of blood vessels in normal skin, kidney glomeruli and brain, express surface-bound C1q in physiologic pregnancy. This finding was unexpected, because deposits of C1q are usually observed in pathologic conditions and are associated with complement activation. In the case of DECs, we failed to detect immunoglobulins and C4 co-localized with C1q on the cell surface. Surprisingly, DECs expressed mRNA for the three chains of C1q and secreted detectable level of this component in serum-free ...
Anti-CFI / Complement Factor I Antibody (Internal), Rabbit Anti Human Polyclonal Antibody validated in WB, IHC-P (ALS17749), Abgent
There are two concepts behind the alternative pathway of complement: what occurs when a non-self cell is absent; and what occurs when a non-self cell is present. When a non-self cell is absent (meaning the tissue is healthy) then there is fluid-phase activation. Fluid-phase activation occurs continuously, spontaneously and very slowly. In fluid-phase activation, C3 spontaneously activates via hydrolysis to form C3H2O -- since it is unstable, C3H2O usually reverts to C3. However, if C3H2O encounters Factor B, then the two molecules bind to form a more stable C3H2OB molecule. Factor D then cleaves C3H2OB molecule to yield the enzyme C3H2OBb (aka fluid-phase C3 convertase). C3H2OBb has an active site on Bb; to culminate fluid-phase activation, this active site cleaves C3 into C3a and C3b. Fluid-phase activation is depicted in the figure to the left.. When a non-self cell is present, then a much faster process occurs. C3b binds to the surface of the non-self cell, then Factor B binds to the C3b. ...
The complement system labels microbes and host debris for clearance. Degradation of surface-bound C3b is pivotal to direct immune responses and protect host cells. How the serine protease factor I (FI), assisted by regulators, cleaves either two or three distant peptide bonds in the CUB domain of C3b remains unclear. We present a crystal structure of C3b in complex with FI and regulator factor H (FH; domains 1-4 with 19-20). FI binds C3b-FH between FH domains 2 and 3 and a reoriented C3b C-terminal domain and docks onto the first scissile bond, while stabilizing its catalytic domain for proteolytic activity ...
Factor I antibody [OX-21] (complement factor I) for ELISA, IP, RIA, WB. Anti-Factor I mAb (GTX41626) is tested in Human samples. 100% Ab-Assurance.
Complete information for CFI gene (Protein Coding), Complement Factor I, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
The SCOP classification for the Complement control module/SCR domain family. Additional information, provided for both this family and the superfamily it belongs to, includes SUPERFAMILY links to genome assignments, alignments, domain combinations, taxonomic visualisation and hidden Markov model information.
Complement control module/SCR domain alignments. Alignments can be refined by adding alignments from other genomes, adding your own sequences and/or aligning to other models from the same superfamily. The display of alignments can also be customised.
Alectinib (CH5424802) is a potent ALK inhibitor with IC50 of 1.9 nM in cell-free assays, sensitive to L1196M mutation and higher selectivity for ALK than PF-02341066, NVP-TAE684 and PHA-E429.
β重型海洋性貧血4一般所說的重症海洋性貧血就是指「β重型海洋性貧血「3是β血紅蛋白鏈合成嚴重的不足》剛出生時3患有β重型海洋性貧血的寶寶在外觀上跟正常者沒有任何差別》但是漸漸地到了三到六個月大時3這時候因為β血紅蛋白鏈不夠3沒有辦法合成「成人血紅素「情況產生3因此會有臉色蒼白 食慾 活力變差...等貧血的症狀產生》一旦寶寶發病3後果嚴重3必須每隔二至三週輸血一次》長期的輸血會造成體內鐵質的沉積3導致體內器官逐漸喪失功能3最後常因心臟衰竭而在孩童時即死亡》另一方面3由於長期輸血3容易引起病毒的感染3例如B型 C型肝炎3和愛滋病等》真正要根治這種疾病3需要骨髓移植》我國目前在骨髓移植的成功率大約在60%3其餘40%的失敗者可能因併發症死亡3或者回復原來長期輸血打排鐵劑的狀況》 ...
第一卷(共115分)第一部分听力(共两节,满分30分)第一节(共5小题;每小题1.5分,满分7.5分)听下面5段对话。每段对话后有一个小题,从题中所给的A、B、C三个选项中选出最佳选项,并标在试卷的相应位置。听完每段对话后,你都有10秒钟的时间来回答有关小题和阅读下一小题。每段对话仅读一遍
Persistent pathogens have evolved to avoid elimination by the mammalian immune system including mechanisms to evade complement. Infections with African trypanosomes can persist for years and cause human and animal disease throughout sub-Saharan Africa. It is not known how trypanosomes limit the action of the alternative complement pathway. Here we identify an African trypanosome receptor for mammalian factor H, a negative regulator of the alternative pathway. Structural studies show how the receptor binds ligand, leaving inhibitory domains of factor H free to inactivate complement C3b deposited on the trypanosome surface. Receptor expression is highest in developmental stages transmitted to the tsetse fly vector and those exposed to blood meals in the tsetse gut. Receptor gene deletion reduced tsetse infection, identifying this receptor as a virulence factor for transmission. This demonstrates how a pathogen evolved a molecular mechanism to increase transmission to an insect vector by exploitation of a
Cells expressing a membrane C receptor (CR(3)) specific for C3b-inactivator- cleaved C3b (C3bi) were identified by rosette assay with C3bi-coated sheep erythrocytes (EC3bi) or C3bi-coated fluorescent microspheres (C3bi-ms). C3bi- ms, probably because of their smaller size, bound to a higher proportion of cells than did EC3bi. C3bi-ms bound to greater than 90 percent of mature neutrophils, 85 percent of monocytes, 92 percent of erythrocytes, and 12 percent of peripheral blood lymphocytes. Binding of C3bi-ms to neutrophils, monocytes, and erythrocytes was inhibited by fluid-phase C3bi, Fab anti-C3c, or Fab anti-C3d but was not inhibited by F(ab)(2) anti-CR(1) (C3b receptor) or F(ab)(2) anti-CR(2) (C3d receptor) nor by fluid-phase C3b, C3c, or C3d. This indicated that monocytes, neutrophils, and erythrocytes expressed C3bi receptors (CR(3)) that were separate and distinct from CR(1) and CR(2) and specific for a site in the C3 molecule that was only exposed subsequently to cleavage of C3b by C3b ...
The role of cell membrane-associated human factor H for the binding of cell-bound C3b to complement receptor-carrying (CR+) cells was investigated. Pretreatment of CR+ cells with antibodies to factor H inhibited the adherence of C3b-coated red cells to human tonsil lymphocytes (TL) and peripheral bl …
Decay-accelerating factor (CD55), a regulator of the alternative and classical pathways of complement activation, is expressed on all serum-exposed cells. It is used by pathogens, including many enteroviruses and uropathogenic Escherichia coli, as a receptor prior to infection. We describe the x-ray structure of a pathogen-binding fragment of human CD55 at 1.7 A resolution containing two of the three domains required for regulation of human complement. We have used mutagenesis to map biological functions onto the molecule; decay-accelerating activity maps to a single face of the molecule, whereas bacterial and viral pathogens recognize a variety of different sites on CD55.
1G40: Crystal structure of a complement control protein that regulates both pathways of complement activation and binds heparan sulfate proteoglycans.
TGR-1202 is a novel PI3Kδ inhibitor, with IC50 and EC50 of 22.2 nM and 24.3 nM, respectively; Also active against CK1ε, with an EC50 value of 6.0 μM. ...Quality confirmed by NMR,HPLC & MS.
The short consensus repeat domain (SCR, complement control protein module, sushi-domain) is a structural unit found in multiple adjacent copies in more than 40 human proteins. Each bead-like domain is composed of approximately 60 residues and the adjacent domains are connected in a head-to-tail fash …
The alternative pathway is continuously activated at a low level, analogous to a car engine at idle, as a result of spontaneous C3 hydrolysis due to the breakdown of the internal thioester bond (C3 is mildly unstable in aqueous environment). The alternative pathway does not rely on pathogen-binding antibodies like the other pathways.[2] C3b that is generated from C3 by a C3 convertase enzyme complex in the fluid phase is rapidly inactivated by factor H and factor I, as is the C3b-like C3 that is the product of spontaneous cleavage of the internal thioester. In contrast, when the internal thioester of C3 reacts with a hydroxyl or amino group of a molecule on the surface of a cell or pathogen, the C3b that is now covalently bound to the surface is protected from factor H-mediated inactivation. The surface-bound C3b may now bind factor B to form C3bB. This complex in the presence of factor D will be cleaved into Ba and Bb. Bb will remain associated with C3b to form C3bBb, which is the alternative ...
The alternative pathway is continuously activated at a low level, analogous to a car engine at idle, as a result of spontaneous C3 hydrolysis due to the breakdown of the internal thioester bond (C3 is mildly unstable in aqueous environment). The alternative pathway does not rely on pathogen-binding antibodies like the other pathways.[2] C3b that is generated from C3 by a C3 convertase enzyme complex in the fluid phase is rapidly inactivated by factor H and factor I, as is the C3b-like C3 that is the product of spontaneous cleavage of the internal thioester. In contrast, when the internal thioester of C3 reacts with a hydroxyl or amino group of a molecule on the surface of a cell or pathogen, the C3b that is now covalently bound to the surface is protected from factor H-mediated inactivation. The surface-bound C3b may now bind factor B to form C3bB. This complex in the presence of factor D will be cleaved into Ba and Bb. Bb will remain associated with C3b to form C3bBb, which is the alternative ...
若限制補體活化的調節蛋白缺陷(ex. Complement H、Complement factor I、CD46等),會造成補體不正常的活化,造成血管內皮和腎臟細胞的傷害。此狀況可能為先天性,也可能是後天產生(產生自體抗體). ...
MUC5B molecule. Computer model showing the structure of a molecule of the protein MUC5B (mucin 5 subtype B). Mucins key characteristic is their ability to form gels. They are therefore a key component in most gel-like secretions, serving functions from lubrication to cell signalling to forming chemical barriers. - Stock Image C015/4507
Patterns of Chemical Reactions Synthesis reaction (A+BAB) Atoms or molecules combine Energy is absorbed for bond formation Decomposition reaction (ABA+B) Molecule is broken down Chemical energy is released Slide 2.18
Tideglusib is an irreversible GSK-3 inhibitor with IC50 of 5 nM and 60 nM for GSK-3βWT (1 h preincubation) and GSK-3βC199A (1 h preincubation), respectively....Quality confirmed by NMR,HPLC & MS.
nbspHayato Murakoshi a, Madoka Koyanagi a, Tomohiro Akahoshi a, Takayuki Chikata a, Nozomi Kuse a, Hiroyuki Gatanaga a, d, Sarah L. Rowland-Jones b c, et al ...
The opportunistic human pathogenic fungus Aspergillus fumigatus is a major cause of fungal infections in immunocompromised patients. Innate immunity plays an important role in the defense against infections. The complement system represents an essential part of the innate immune system. This cascade system is activated on the surface of A. fumigatus conidia and hyphae and enhances phagocytosis of conidia. A. fumigatus conidia but not hyphae bind to their surface host complement regulators factor H, FHL-1, and CFHR1, which control complement activation. Here, we show that A. fumigatus hyphae possess an additional endogenous activity to control complement activation. A. fumigatus culture supernatant efficiently cleaved complement components C3, C4, C5, and C1q as well as immunoglobulin G. Secretome analysis and protease inhibitor studies identified the secreted alkaline protease Alp1, which is present in large amounts in the culture supernatant, as the central molecule responsible for this ...
Hemolytic uremic syndrome (HUS) is a disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure. Recent studies have identified a factor H-associated form of HUS, caused by gene mutations that cluster in the C-terminal region of the complement regulator factor H. Here we report how three mutations (E1172Stop, R1210C, and R1215G; each of the latter two identified in three independent cases from different, unrelated families) affect protein function. All three mutations cause reduced binding to the central complement component C3b/C3d to heparin, as well as to endothelial cells. These defective features of the mutant factor H proteins explain progression of endothelial cell and microvascular damage in factor H-associated genetic HUS and indicate a protective role of factor H for tissue integrity during thrombus formation.. ...
Hemolytic uremic syndrome (HUS) is a disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure. Recent studies have identified a factor H-associated form of HUS, caused by gene mutations that cluster in the C-terminal region of the complement regulator factor H. Here we report how three mutations (E1172Stop, R1210C, and R1215G; each of the latter two identified in three independent cases from different, unrelated families) affect protein function. All three mutations cause reduced binding to the central complement component C3b/C3d to heparin, as well as to endothelial cells. These defective features of the mutant factor H proteins explain progression of endothelial cell and microvascular damage in factor H-associated genetic HUS and indicate a protective role of factor H for tissue integrity during thrombus formation.. ...
Mark, L, Spiller, OB, Okroj, M, Chanas, S, Aitken, JA, Wong, SW, Damania, B, Blom, AM and Blackbourn, DJ (2007) Molecular characterization of the rhesus rhadinovirus (RRV) ORF4 gene and the RRV complement control protein it encodes ...
The complement control protein (CCP) modules (also known as short consensus repeats) are defined by a consensus sequence within a stretch of about 60 amino acid residues. These modules have been identified more than 140 times in over 20 proteins, including 12 proteins of the complement system. The solution structure of the 16th CCP module from human complement factor H has been determined by a combination of 2-dimensional nuclear magnetic resonance spectroscopy and restrained simulated annealing. In all, 548 structurally important nuclear Overhauser enhancement cross-peaks were quantified as distance restraints and, together with 41 experimentally measured angle restraints, were incorporated into a simulated annealing protocol to determine a family of closely related structures that satisfied the experimental observations. The CCP structure is shown to be based on a beta-sandwich arrangement; one face made up of three beta-strands hydrogen-bonded to form a triple-stranded region at its centre ...
The complement control protein (CCP) modules (also known as short consensus repeats) are defined by a consensus sequence within a stretch of about 60 amino acid residues. These modules have been identified more than 140 times in over 20 proteins, including 12 proteins of the complement system. The solution structure of the 16th CCP module from human complement factor H has been determined by a combination of 2-dimensional nuclear magnetic resonance spectroscopy and restrained simulated annealing. In all, 548 structurally important nuclear Overhauser enhancement cross-peaks were quantified as distance restraints and, together with 41 experimentally measured angle restraints, were incorporated into a simulated annealing protocol to determine a family of closely related structures that satisfied the experimental observations. The CCP structure is shown to be based on a beta-sandwich arrangement; one face made up of three beta-strands hydrogen-bonded to form a triple-stranded region at its centre ...
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Looking for online definition of Complement factor b in the Medical Dictionary? Complement factor b explanation free. What is Complement factor b? Meaning of Complement factor b medical term. What does Complement factor b mean?
4AYI: Structure of a complex between CCPs 6 and 7 of Human Complement Factor H and Neisseria meningitidis FHbp Variant 3 Wild type
Candida albicans is a major cause of invasive fungal infections worldwide. Upon infection and when in contact with human plasma as well as body fluids the fungus is challenged by the activated complement system a central part of the human innate immune response. C. albicans controls and evades host complement attack by binding several human complement regulators like Factor H, Factor H-like protein 1 and C4BP to the surface. Gpm1 (Phosphoglycerate mutase 1) is one fungal Factor H/FHL1 -binding protein. As Gpm1 is surface exposed, we asked whether Gpm1 also contributes to host cell attachment. Here, we show by flow cytometry and by laser scanning microscopy that candida Gpm1 binds to human umbilical vein endothelial cells (HUVEC) to keratinocytes (HaCaT), and also to monocytic U937 cells. Wild type candida did bind, but the candida gpm1Δ/Δ knock-out mutant did not bind to these human cells. In addition Gpm1 when attached to latex beads also conferred attachment to human endothelial cells. When ...
SR GROUP - Exporter, Importer, Manufacturer, Distributor, Supplier, Trading Company of Rat CFH(Complement Factor H) ELISA Kit based in Delhi, India
Complement receptor type 1 (CR1 or CD35) is a peripheral glycosylated membrane protein that regulates the complement activation in the control of immune responses. The author would like to overview the folding and binding properties of the soluble form of CR1, so-called as sCR1, introducing our development of the high-yield overexpression and purification methods as well as the investigation to its molecular structure. Although sCR1 prepared through our method showed the highest binding affinity against C3b, it is quite difficult to be crystallized for X-ray structure analysis. In spite of many attempts, only microcrystals have been obtained so far. Considering the usefulness to understand factors within the difficulty, the primary sequence of sCR1 has been reexamined from the viewpoints both of secondary structure predictions and recent findings of intrinsically disordered proteins (IDPs) or natively unfolded proteins (NUPs). As an example, the theoretically predicted structure of a short consensus
The IUPHAR/BPS Guide to Pharmacology. complement factor B - S1: Chymotrypsin. Detailed annotation on the structure, function, physiology, pharmacology and clinical relevance of drug targets.
Maus Monoklonal Complement Factor I Antikörper für ELISA, WB. Jetzt diesen anti-Complement Factor I Antikörper bestellen. | Produkt ABIN4264851
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Complement, C3 Convertase, Regulation, Cells, Disease, Complement Factor H, Inhibition, Therapeutic, Transplant, Allograft, Donor, Donors, and Graft
The three distinct activation pathways of complement converge with the formation of a C5 convertase. The cleavage of C5 by this convertase initiates…
TY - JOUR. T1 - First-line therapy in atypical hemolytic uremic syndrome. T2 - consideration on infants with a poor prognosis. AU - Szarvas, Nóra. AU - Szilágyi, Ágnes. AU - Tasic, Velibor. AU - Nushi-Stavileci, Valbona. AU - Sofijanova, Aspazija. AU - Gucev, Zoran. AU - Szabó, Miklós. AU - Szabó, Attila. AU - Szeifert, Lilla. AU - Reusz, György. AU - Rusai, Krisztina. AU - Arbeiter, Klaus. AU - Müller, Thomas. AU - Prohászka, Zoltán. PY - 2014/12/11. Y1 - 2014/12/11. N2 - BACKGROUND: Atypical hemolytic uremic syndrome (aHUS) is a rare and heterogeneous disorder. The first line treatment of aHUS is plasma therapy, but in the past few years, the recommendations have changed greatly with the advent of eculizumab, a humanized monoclonal anti C5-antibody. Although recent recommendations suggest using it as a primary treatment for aHUS, important questions have arisen about the necessity of immediate use of eculizumab in all cases. We aimed to draw attention to a specific subgroup of aHUS ...
Human complement factor H Y402H polymorphism causes an age-related macular degeneration phenotype and lipoprotein dysregulation in mice.
Purpose: Complement activation and oxidative stress have been increasingly implicated in the pathogenesis of AMD. Complement activation products have been detected in Bruchs membrane and drusen from patients, indicating that in AMD, complement attack likely occurs primarily on the RPE basal surface. Herein, we describe a model used to investigate the effect of oxidative stress on complement-mediated RPE cell injury, whereby complement attack was initiated with an RPE-specific priming antibody on the basal surface of differentiated human RPE cells.. Methods: ARPE-19 cells and RPE cells from 2 donors were cultured for one month on collagen-coated porous supports in DMEM-F12 containing 1% FBS. Transepithelial resistance (TER) was recorded, apical microvilli and tight junctions were identified by transmission electron microscope, and ZO-1 was examined by immuno-fluorescent staining. Cytokeratin-18 staining was used to confirm the epithelial nature of RPE cells. The cells were basally exposed for 2 ...
Abstract. Abstract 2085Introduction:. Atypical hemolytic uremic syndrome (aHUS) is a rare chronic disorder characterized by persistent uncontrolled complement
This is a Phase 3, multicenter study of OMS721 in adults and adolescents with atypical hemolytic uremic syndrome (aHUS). The uncontrolled, open-label study will evaluate the effect of OMS721 in subjects with plasma therapy-resistant aHUS and plasma therapy-responsive aHUS. This study has four periods: Screening, Treatment Induction, Treatment Maintenance, and Follow-up. Approximate enrollment is 80 subjects. An interim analysis will be performed after 40 subjects have completed 26 weeks of treatment for potential registration ...
Activation of the complement cascade is clearly implicated in the pathology of multiple sclerosis (MS). However, the extent and nature of its involvement in specific athological processes remains uncertain. We describe a detailed immunohistochemical study to localise a strategically selected set of complement proteins, activation products and regulators in brain and spinal cord tissue of 17 patients with progressive MS, examining 35 different plaques, and 16 control donors, including 9 with CNS disease. Plaques were consistently positive for complement proteins (C3, factor B, C1q), activation products (C3b, iC3b, C4d, TCC) and regulators (factor H, C1-inhibitor, clusterin), suggesting continuing local complement synthesis, activation and regulation despite no other evidence of on-going inflammation. Complement immunolabelling was most apparent in plaque and peri-plaque areas but also present in normal appearing white matter and cortical areas to a greater extent than in control tissue. Cellular ...
Assembly of the terminal C5b-C9 complement components into the cytolytic C5b-9 complex is accompanied by exposure of characteristic neoantigens on the macromolecule. We report the production and characterization of mouse monoclonal antibodies to C9-dependent neoantigens of human C5b-9. Binding-inhibition assays with EDTA-human plasma and micro-ELISA assays with purified C9 showed that the antibodies did not react with native complement components and thus confirmed the specificity of the antibodies for the neoantigens. The monoclonal antibodies did, however, cross-react with cytolyticaIly inactive, fluid-phase C5b-9 complexes, Thus, expression of the neoantigenic determinants was not dependent on the formation of high molecular weight C9 polymers with the complex, since these are absent in fluid-phase C5b-9. Radioiodinated antibodies could be utilized in immunoradiometric assays for the detection and quantitation of C5b-9 on cell membranes. Cross-reactivities of the antibodies with C9-dependent ...
MalaCards based summary : Complement Component 3 Deficiency, also known as c3 deficiency, is related to complement factor i deficiency and neisseria meningitidis infection, and has symptoms including recurrent bacterial infections An important gene associated with Complement Component 3 Deficiency is C3 (Complement C3), and among its related pathways/superpathways are Innate Immune System and Creation of C4 and C2 activators. Affiliated tissues include t cells, skin and brain, and related phenotypes are Increased shRNA abundance (Z-score > 2) and Increased shRNA abundance (Z-score > 2) ...
Objective: The expression of complement receptor type 1 on different cells is associated with autoimmunity. Erythrocyte-Complement Receptor Type 1 (E-CR1) is a candidate ..
The reduction in C in this study was accomplished, as in our previous study (44), by use of CVF, which activates the alternative pathway of the C cascade (10). It forms a complex with factor B, CVF Bb, which is functionally analogous to C3b Bb, the natural C3 convertase that cleaves catalytically the α-chain of C3. The difference between the two compounds is that CVF Bb is highly resistant to the normal control mechanisms that limit the activity of C3b Bb, so that fluid-phase C activation continues unabated, drastically depleting C. Consequently, absent the substrates from which they are produced, all the subsequent C components are also depleted; hence, hypocomplementemia results. Since the present data showed, in confirmation of our earlier observations (44), that CVF-induced hypocomplementemia, as indicated by a decreased serum CH100 activity, impaired the febrile response of conscious guinea pigs to systemic LPS, some or all of the fragments from C3 to C9 must be important for fever ...
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Information for healthcare professionals for diagnosing and treating Atypical Hemolytic Uremic Syndrome. Soliris is the only therapy approved for the treatment of aHUS.
KEGG Orthology (KO) [BR:hsa00001] 09150 Organismal Systems 09151 Immune system 04662 B cell receptor signaling pathway [PATH:hsa04662] 974 CD79B; CD79b molecule K06507 CD79B; CD79B antigen 09180 Brite Hierarchies 09183 Protein families: signaling and cellular processes 04090 CD molecules [BR:hsa04090] 974 CD79B; CD79b molecule K06507 CD79B; CD79B antigen CD molecules [BR:hsa04090] Proteins 974 CD79B; CD79b molecule K06507 CD79B; CD79B antigen ...
Maus Monoklonal Complement Factor H Antikörper für ELISA, WB. Jetzt diesen anti-Complement Factor H Antikörper bestellen. | Produkt ABIN4264777
Read about a case report study describing the clinical case of a patient with atypical hemolytic uremic syndrome (aHUS) associated with heart disease.
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নিজেকে এত বেশী সমালোচনা করার কোন প্রয়োজন নেই। উইকিপিডিয়াতে সব রকম মানুষই দরকার। বৈচিত্রের মধ্যেই এর ঐক্য। একেক জনের দোষ-গুণ একে অপরে complement করে নেবার মধ্যেই যৌথ উদ্যোগের মজা। প্রশাশক হওয়া স্বেচ্ছামূলক। তাই তা নিয়ে আর বিব্রত করব না। তবে একটা কথা বলতে পারি- নিজেকে যা ভাববে বা বলবে (auto-suggestion) নিজ আদিতে তাই না হলেও তাই হয়ে পড়বে। উইকিপিডিয়াতে কিছু যায় আসে না। কিন্তু আসল জী্বনে শুধু ...
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... is produced when complement factor I cleaves C3b. Complement receptors on white blood cells are able to bind iC3b, so iC3b ... Unlike intact C3b, iC3b cannot associate with factor B, thus preventing amplification of the complement cascade through the ... Complement factor I can further cleave iC3b into a protein fragment known as C3d. Robbins Basic Pathology 8th ed 2007. R Cotran ... iC3b is a protein fragment that is part of the complement system, a component of the vertebrate immune system. ...
C3b and thus form the alternative pathway C5 convertase.CVFBb is a noncovalent association product of CVF3 and the complement ... First of all, C5 has to bind to C3b fragment. The capacity to bind C3b is a stable feature of component C5, as C5b also has ... Cell-bound C3 and C5 convertase differ in their C3b requirement. C3-convertase (C3bBb) need only one molecule of C3b to form, ... whereas two or more C3b are required for generation of C5 convertase (C3bBb). It means, when C3b is randomly distributed on the ...
... also cleaves IgG and complement component C3b, inhibiting phagocytosis. The full length of mature staphylokinase ...
These receptors recognise targets coated in C3b, C4b and C3bi from plasma complement. The extracellular domain of the receptors ... Recognition by complement receptors is not enough to cause internalisation without additional signals. In macrophages, the CR1 ... Complement coated targets are internalised by 'sinking' into the phagocyte membrane, without any protrusions. Mannose and other ... Among these are receptors that recognise the Fc part of bound IgG antibodies, deposited complement or receptors, that recognise ...
Microbes may activate the complement system directly and complement component C3b bind to microbes. After C3b is degraded into ... Frank K, Atkinson JP (2001). "Complement system." In Austen KF, Frank K, Atkinson JP, Cantor H. eds. Samter's Immunologic ... Co-stimulation for B cells is provided alternatively by complement receptors. ... B cells express complement receptor CR2 (CD21) to bind to iC3b, C3dg, or C3d. This additional binding makes the B cells 100- to ...
They bear membrane receptors for opsonins, such as IgG and the fragment C3b of complement. They express LCAs (leucocyte common ...
"Staphylococcus aureus clumping factor A binds to complement regulator factor I and increases factor I cleavage of C3b". The ... ClfA also has been shown to bind to complement regulator I protein. It is responsible for the clumping of blood plasma observed ...
The S-layer prevents complement-mediated bacterial killing by impairing the binding of C3b to the surface of the bacteria. The ... Aside from complement-mediated mechanisms, C. fetus has also evolved variation in its S-layer proteins (SLPs) of the S-layer to ... Additionally, Cfv has long LPS side chains (O-antigens) that may resist complement-mediated bacterial killing. ...
The complement system is used to enhance the effect of antibodies and phagocytic cells, which engulf and destroy other cells. ... Microfilariae block this pathway by cleaving C3b-an important protein in this process-to form iC3b. iC3b cannot go on to ... "Onchocerca volvulus microfilariae avoid complement attack by direct binding of factor H". The Journal of Infectious Diseases. ...
Porins are also recognized by TLR2, they bind complement factors (C3b, C4b, factor H, and C4bp (complement factor 4b-binding ... fHbp protects meningococci from complement-mediated death in human serum experiments, but has also been shown to protect ... Porins are also an important factor for complement inhibition for both pathogenic and commensal species. Porins are important ... and complement deficiency. The incubation period is short, from 2 to 10 days. In susceptible individuals, N. meningitidis may ...
SpeB degrades immunoglobulins and cytokines, as well as through cleavage of C3b, inhibiting recruitment of phagocytic cells and ... the complement activation pathway. This results in decreased inflammation and neutrophil levels around the site of infection, ...
... aureus protein Sbi acts as a complement inhibitor and forms a tripartite complex with host complement Factor H and C3b". PLoS ... sbi protein interferes with the host's innate immune response by binding Factor H, Complement component 3 and IgG. Protein A ... June 2008). "Interaction of human complement with Sbi, a staphylococcal immunoglobulin-binding protein: indications of a novel ... mechanism of complement evasion by Staphylococcus aureus". J. Biol. Chem. 283 (25): 17579-17593. doi:10.1074/jbc.M800265200. ...
Besides complement particles C1q and C3b which help to opsonize the apoptotic cells, also thrombospondin, pentraxins (C- ... components of complement pathways (e.g. C1q, C3b) and other molecules found in extracellular space. Collectins (e.g. mannose- ... Non-apoptotic cells also express complement inhibitors, preventing the assembly of C3 convertase or the lytic pore. Among ... or complement receptors (CR3 and CR4). There is a variety of receptors which recognize the externalized phosphatidylserine. ...
"Structures of C3b in complex with factors B and D give insight into complement convertase formation". Science. 330 (6012): 1816 ... Factor D is involved in the alternative complement pathway of the complement system where it cleaves factor B. The protein ... Factor D (EC 3.4.21.46, C3 proactivator convertase, properdin factor D esterase, factor D (complement), complement factor D, ... Before cleavage of the scissile bond in Factor B can occur, Factor B must first bind with C3b before to form the C3bB complex. ...
... a complement protein that is formed from the breakdown of C3b. C3d binds to the CR2 receptor. This disambiguation page lists ...
Complement+C4b-Binding+Protein at the US National Library of Medicine Medical Subject Headings (MeSH) v t e. ... It also has ability to bind C3b. C4BP accelerates decay of C3-convertase and is a cofactor for serine protease factor I which ... The genes coding for C4BP α-chain (C4BPA) and β-chain (C4BPB) are located in the regulators of complement activation (RCA) gene ... C4b-binding protein (C4BP) is a protein complex involved in the complement system where it acts as inhibitor. C4BP has an ...
2000). "Functional properties of complement factor H-related proteins FHR-3 and FHR-4: binding to the C3d region of C3b and ... Complement factor H-related protein 4 is a protein that in humans is encoded by the CFHR4 gene. GRCh38: Ensembl release 89: ... "Entrez Gene: CFHR4 complement factor H-related 4". Hageman GS, Hancox LS, Taiber AJ, et al. (2007). "Extended Haplotypes in the ... Diaz-Guillen MA, Rodriguez de Cordoba S, Heine-Suner D (Jul 1999). "A radiation hybrid map of complement factor H and factor H- ...
... which activate the classical pathway of the complement system. The cascade begins to work from C1 to C3b through C4b, C3b being ... Because primate erythrocytes express complement receptor 1 (CR1) on their surface and having binding specificity to C4b, C3b, ... London: Mosby, ISBN 0-7234-2918-9. Frank K, Atkinson JP (2001). "Complement system." In Austen KF, Frank K, Atkinson JP, Cantor ... Bala Subramanian V, Liszewski MK, Atkinson JP (2000). "The complement system and autoimmunity." In Lahita RG, Chiorazzi N, ...
C3b and C5) to avoid opsonisation. It can also recruit complement regulators such as Factor H, C4b-binding protein, factor H- ... It also secretes proteases to degrade complement proteins such as C3. It can bind to thrombin that decreases the fibrin ... They also bind to several human proteins such as complement proteins, thrombin, fibrinogen, and plasminogen using surface ...
... such as when C3b binds to C3-convertase, or they can facilitate the formation of the Complement membrane attack complex (MAC) ... Should the microbe be coated with opsonising antibodies or C3b complement, the co-stimulation of endocytic PRR and opsonin ... complex also creates byproducts like C3b and C4b which are important components for the efficient function of the complement ... As well as endocytic PRRs, phagocytes furthermore express opsonin receptors such as Fc receptor and complement receptor 1 (CR1 ...
It has pneumococcal surface proteins that inhibit complement-mediated opsonization, and it secretes IgA1 protease that will ... Polysaccharide capsule-prevents phagocytosis by host immune cells by inhibiting C3b opsonization of the bacterial cells ... an adhesin that can interact with carbohydrates on the cell surface of pulmonary epithelial cells and can inhibit complement- ... Pneumolysin (Ply)-a 53-kDa pore-forming protein that can cause lysis of host cells and activate complement Autolysin (LytA)- ...
... complement c3 MeSH D12.776.124.486.274.250.250 - complement c3a MeSH D12.776.124.486.274.250.260 - complement c3b MeSH D12.776. ... complement c3b inactivator proteins MeSH D12.776.124.486.274.920.325.200 - complement factor h MeSH D12.776.124.486.274.920. ... complement c1 MeSH D12.776.124.486.274.050.270 - complement c1q MeSH D12.776.124.486.274.050.280 - complement c1r MeSH D12.776. ... complement c2 MeSH D12.776.124.486.274.150.500 - complement c2a MeSH D12.776.124.486.274.150.750 - complement c2b MeSH D12.776. ...
C3 is cleaved into its a and b subunits, and C3b binds the convertase. These together are called the C5 convertase. Similarly ... 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 ...
... where the C3b-tagged immune complex is then destroyed. In both cases C3b interacts with the C3b receptor, complement receptor 1 ... C3b is the larger of two elements formed by the cleavage of complement component 3, and is considered an important part of the ... Furthermore, if C3b does bind to a host-cell surface, regulators of complement activity (RCAs), a group of genetically-, ... The key to the success of the complement system in clearing antigens is regulating the effects of C3b to pathogens alone and ...
All three pathways converge at a step in which complement protein C3 is cleaved into proteins C3a and C3b, which results in a ... Complement component 4A Complement component 4B HLA A1-B8-DR3-DQ2 haplotype Complement system Complement deficiency Sekar A, ... Complement component 4 (C4), in humans, is a protein involved in the intricate complement system, originating from the human ... Complement peptide C5a, C4a, and C3a receptors". Pharmacological Reviews. 65 (1): 500-43. doi:10.1124/pr.111.005223. PMID ...
Complement C3b/C4b Receptor 1, CR1 (CD35) Complement Regulator of the Immunoglobulin Superfamily, CRIg Soluble complement ... Complement control protein are proteins that interact with components of the complement system. The complement system is ... Complement proteins protect against malignant cells- both by direct complement attack and through initiation of Complement- ... are the enzymes that drive complement activation by activating C3b, a central component of the complement system. Some CCPs, ...
... cleaving most C3 molecules in the serum into C3a and C3b fragments, which depletes the amount of intact C3. C3 deficiency makes ... Complement 3 deficiency is a genetic condition affecting complement component 3 (C3). People can suffer from either primary or ... C3 is the most abundant complement component and is a particularly important complement component because there are three ways ... Complement component 3 (C3) is a protein involved in both the innate and adaptive immune response. C3 is one of over 30 ...
C3b contributes to further downstream complement activation. C3b binds to the C3 convertase (C4b2b), to form C5 convertase ( ... 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 ...
Since C3b is free and abundant in the plasma, it can bind to either a host cell or a pathogen surface. To prevent complement ... Factor I requires a C3b-binding protein cofactor such as complement factor H, CR1, or Membrane Cofactor of Proteolysis (MCP or ... Pangburn MK, Schreiber RD, Müller-Eberhard HJ (July 1977). "Human complement C3b inactivator: isolation, characterization, and ... C3b)2BbP or C4b2a3b from the classical pathway), the complement system follows the same path regardless of the means of ...
"Phagocytosis of Mycobacterium tuberculosis is mediated by human monocyte complement receptors and complement component C3". J. ... iC3b is generated by proteolysis of C3b and binding to the receptor causes phagocytosis and destruction of the foreign cell ... CR3 and CR4 have been shown to be 87% homologous via sequence analysis of human cDNA of the α chains; however, the complement ... Wagner C, Hänsch GM, Stegmaier S, Denefleh B, Hug F, Schoels M (April 2001). "The complement receptor 3, CR3 (CD11b/CD18), on T ...
Tekkinud C3b seondub omakorda C4b-ga, mille tulemusena tekib C5-konvertaas. C3b ja selle edasised seondumisproduktid- iCb3 ja ... Zipfel, P. F., Hallström, T., & Riesbeck, K. (2013). Human complement control and complement evasion by pathogenic microbes- ... 1,0 1,1 1,2 1,3 Rus, H., Cudrici, C., & Niculescu, F. (2005). The role of the complement system in innate immunity. Immunologic ... 7,0 7,1 Lambris, J. D., Ricklin, D., & Geisbrecht, B. V. (2008). Complement evasion by human pathogens. Nature Reviews. ...
"Bacterial resistance to complement killing mediated by the Ail protein of Yersinia enterocolitica". Proc. Natl. Acad. Sci. U.S ... "Role of the YadA protein in prevention of opsonization of Yersinia enterocolitica by C3b molecules". Infect. Immun. 61 (8): ...
... (EC 3.4.21.42, C1 esterase, activated complement C1s, complement C overbar 1r, C1s) is a protein ... complement activation, lectin pathway. • complement activation. • regulation of complement activation. Sources:Amigo / QuickGO ... complement activation, classical pathway. • immune system process. • innate immune response. • ... Sim RB (1981). "The human complement system serine proteases C1r and C1s and their proenzymes". Methods in Enzymology. 80 Pt C ...
This newly bound C3b recruits more B, D and P activity and greatly amplifies the complement activation. When complement is ... complement factor B, and complement factor I, as well as deletion of complement factor H-related 3 and complement factor H- ... Complement deficiencyEdit. Main article: Complement deficiency. It is thought that the complement system might play a role in ... In the alternative pathway, C3b binds to Factor B. Factor D releases Factor Ba from Factor B bound to C3b. The complex of C3b(2 ...
Media related to Complement membrane attack complex at Wikimedia Commons. *Complement+Membrane+Attack+Complex at the US ... The membrane attack complex (MAC) or terminal complement complex (TCC) is a structure typically formed on the surface of ... Reid K. B. M., The complement system, in: B. D. Hames and D. M. Glover (eds.), Molecular Immunology, Oxford: IRL Press, 1988, ... MAC is composed of a complex of four complement proteins (C5b, C6, C7, and C8) that bind to the outer surface of the plasma ...
Cleaves to produce C3a and C3b. C3a stimulates histamine release by mast cells, thereby producing vasodilation. C3b is able to ... The combination and activation of this range of complement proteins forms themembrane attack complex, which is able to insert ... A complex of the complement proteins C5b, C6, C7, C8, and multiple units of C9. ... Able to break down fibrin clots, cleave complement protein C3, and activate Factor XII. ...
Maller JB, Fagerness JA, Reynolds RC, Neale BM, Daly MJ, Seddon JM (2007). "Variation in Complement Factor 3 is Associated with ... CFH je uključen u inhibiciju upalnog odgovora posredovanog sa C3b (sa alternativnim putem komplementa) i ponašajući se kao ... kofaktor za cijepanje C3b u njegov inaktivni oblik C3bi, i za slabljenje aktivnog kompleksa koji tvore sa C3b i faktor B. C- ... "Complement C3 Variant and the Risk of Age-Related Macular Degeneration". N Engl J Med. 357 (6): 553-561. doi:10.1056/ ...
Sengeløv H (1996). "Complement receptors in neutrophils.". Crit. Rev. Immunol. 15 (2): 107-31. PMID 8573284. ... C3 (C3a, C3b/iC3b) - C5 (C5a). C3-konvertaza - C5-konvertaza. Kasno. MAC (C6, C7, C8, C9) ... "Function, structure and therapeutic potential of complement C5a receptors". British Journal of Pharmacology 152 (4): 429-48. ...
Proteîna C3 bi tena serê xwe, xwe dike du parçeyan[4], C3a û C3b. Heke di nav laş de hokarên nexweşiyê tune be, C3b bi zûka ve ... a b https://www.britannica.com/science/complement-immune-system-component *↑ a b c d e f g h i OpenStax, Microbiology, openstax ... Sîstema temamker an jî sîstema tewawker (bi îngilîzî: complement system)[1] beşek ji sîstema bergiriya giştî ye. Sîstema ... Lê heke di nav laş de hokarên nexweşiyên dagirker hebe, wê gavê C3b bi rûyê hokara nexweşiyê ve tê girêdan û gazî li proteînên ...
... is a member of the immunoglobulin superfamily, with a structure related to the putative primordial form of the family. As members of the immunoglobulin superfamily play fundamental roles in intercellular recognition involved in various immunologic phenomena, differentiation, and development, basigin is thought also to play a role in intercellular recognition (Miyauchi et al., 1991; Kanekura et al., 1991).[9][10] It has a variety of functions. In addition to its metalloproteinase-inducing ability, basigin also regulates several distinct functions, such as spermatogenesis, expression of the monocarboxylate transporter and the responsiveness of lymphocytes.[6] Basigin is a type I integral membrane receptor that has many ligands, including the cyclophilin (CyP) proteins Cyp-A and CyP-B and certain integrins.[11][12][13] It is expressed by many cell types, including epithelial cells, endothelial cells and leukocytes. The human basigin protein contains 269 amino acids that form two heavily ...
Beeken WL, Northwood I, Beliveau C, Baigent G, Gump D (1987). "Eosinophils of human colonic mucosa: C3b and Fc gamma receptor ... complement complex (C5-C6-C7), interleukin 5, and histamine (though this has a narrow range of concentration). Harm resulting ...
Browse our Complement C3b ELISA Kits all backed by our Guarantee+. ... Complement C3b ELISA Kits available through Novus Biologicals. ...
Complement 3c/metabolism, Complement 3d/metabolism, Complement 5/metabolism, Complement Factor B/metabolism, Complement Factor ... After enzymatic C3b coupling or standard amine C3b coupling, we analyzed and compared the binding of four C3b ligands to the ... Complement C3b interactions studied with surface plasmon resonance technique. Jokiranta, T S ... In this study, we have used this technique to study interactions between the central complement component C3b and its multiple ...
... immediately faces innate immune reactions such as the activated complement system. Here, a novel innate immune evasion strategy ... which in turn leads to degradation of complement C3 and C3b. Efb and to a lesser extend Sbi enhance plasmin cleavage of C3/C3b ... Staphylococcus aureus proteins Sbi and Efb recruit human plasmin to degrade complement C3 and C3b PLoS One. 2012;7(10):e47638. ... together with C3 and its activation product C3b for efficient degradation of these complement components in the local microbial ...
The alternative pathway of complement is thought to be activated following hydrolysis of C3, generation of C3b, and formation ... Properdin: binding to C3b and stabilization of the C3b-dependent C3 convertase. J. Exp. Med. 142: 856-863. ... Properdin Binds to Late Apoptotic and Necrotic Cells Independently of C3b and Regulates Alternative Pathway Complement ... Properdin Binds to Late Apoptotic and Necrotic Cells Independently of C3b and Regulates Alternative Pathway Complement ...
Complement C3b in standards and samples is sandwiched by the immobilized antibody and biotinylated polyclonal antibody specific ... A polyclonal antibody specific for human complement C3b has been pre-coated onto a 96-well microplate with removable strips. ... This assay employs a quantitative sandwich enzyme immunoassay technique that measures human complement C3b in less than 4 hours ... kit is designed for detection of human complement C3b in plasma, serum, urine, milk, saliva, CSF, and cell culture supernatant ...
... key components of the complement system.: In all three complement pathways, the central molecule is C3, which, upon activation ... forms the major opsonin C3b - the key component of complement. C3b is also essential for propagation of the complement cascade ... C3b and factor H: key components of the complement system.. Authors * Jokiranta, T Sakari1 ... In order to prevent damage to self cells and tissues and restrict overconsumption of the complement components, C3b molecules ...
The present invention concerns antibodies to C3b and the prevention and treatment of complement-associated disorder using such ... 102000016550 Complement Factor H Human genes 0 description 17 * 108010034753 Complement Membrane Attack Complex Proteins 0 ... c3b. complement. s77. method. Prior art date. 2007-06-07. Legal status (The legal status is an assumption and is not a legal ... C3b antibodies and methods for the prevention and treatment of complement- associated disorders - Google Patents. C3b ...
... is a native C3b complement component. It is a glycoprotein composed of the modified C3-α chain (αʹ) (M.W. 105,000) and the ... More,, Complement C3b, Human, is a native C3b complement component. It is a glycoprotein composed of the modified C3-α chain (α ... Complement C3b, Human, is a native C3b complement component. It is a glycoprotein composed of the modified C3-α chain (αʹ) (M.W ... Native, human C3b complement component. Cleavage of the C3-α chain at peptide bond 77 by either of the complement C3 convertase ...
CD35 is caTagorized as a regulator of complement avtivation. It binds complement components C3b and C4b, composed of four ... CD35 is caTagorized as a regulator of complement avtivation. It binds complement components C3b and C4b, composed of four ... CD35 is caTagorized as a regulator of complement avtivation. It binds complement components C3b and C4b, composed of four ... CD35 is caTagorized as a regulator of complement avtivation. It binds complement components C3b and C4b, mediating phagocytosis ...
... where the C3b-tagged immune complex is then destroyed. In both cases C3b interacts with the C3b receptor, complement receptor 1 ... C3b is the larger of two elements formed by the cleavage of complement component 3, and is considered an important part of the ... Furthermore, if C3b does bind to a host-cell surface, regulators of complement activity (RCAs), a group of genetically-, ... The key to the success of the complement system in clearing antigens is regulating the effects of C3b to pathogens alone and ...
iC3b is produced when complement factor I cleaves C3b. Complement receptors on white blood cells are able to bind iC3b, so iC3b ... Unlike intact C3b, iC3b cannot associate with factor B, thus preventing amplification of the complement cascade through the ... Complement factor I can further cleave iC3b into a protein fragment known as C3d. Robbins Basic Pathology 8th ed 2007. R Cotran ... iC3b is a protein fragment that is part of the complement system, a component of the vertebrate immune system. ...
Pretreatment of CR+ cells with antibodies to factor H inhibited the adherence of C3b-coated red cells to human tonsil ... The role of cell membrane-associated human factor H for the binding of cell-bound C3b to complement receptor-carrying (CR+) ... The role of cell membrane-associated human factor H for the binding of cell-bound C3b to complement receptor-carrying (CR+) ... Importance of factors H and I for the adherence of C3b-coated erythrocytes to cells Immunobiology. 1983 Aug;165(2):211-24. doi ...
Binding of C3b to platelets and CHO cells. For assessing the binding of C3b to cells, purified C3b (Advanced Research ... C3b binds to activated platelets. To study the molecular events involved in the initiation and propagation of the complement ... B) Binding of C3b-FITC to the monocytic cells, THP-1, which constitutively express the complement receptor CR1. (C) Cleavage of ... We confirmed that C3b binds to the surface of activated platelets. Consistent with the activation of complement on platelets, ...
This protein plays a key role in a part of the bodys immune response known as the complement system. Learn about this gene and ... The C3 gene provides instructions for making a protein called complement component 3 (or C3). ... One of these pieces, called C3b, interacts with several other proteins on the surface of cells to trigger the complement ... This protein plays a key role in a part of the bodys immune response known as the complement system. The complement system is ...
We then assessed complement activation by detecting the deposition of complement activation products C3b/iC3b on the PC12 cells ... Thus, complement KO rats should be superior to complement KO mice for studying the role of complement in human pathological ... Complement activation was assessed by detecting C3b/iC3 deposition on the cells using flow cytometry. Dotted lines, isotype ... Although complement has been implicated in other pain models, the potential role of complement in CIPN was not clear. It has ...
complement component;. iC3b,. inactivated C3b;. PE,. phosphatidylethanolamine;. photoox-A2E,. photooxidized A2E;. RPE,. retinal ... To this end, we established an in vitro assay by using human serum as a source of complement, and we measured products of C3 ... Complement activation by photooxidation products of A2E, a lipofuscin constituent of the retinal pigment epithelium. Jilin Zhou ... In an investigation of a potential trigger for complement activation in AMD, we explored the notion that the complex mixture of ...
complement C3b/C4b receptor 1 (Knops blood group). Enable Javascript to view the expand/collapse boxes.. Open All Close All ... This gene is a member of the receptors of complement activation (RCA) family and is located in the cluster RCA region of ... Membrane immune adherence receptor that plays a critical role in the capture and clearance of complement-opsonized pathogens by ... The protein mediates cellular binding to particles and immune complexes that have activated complement. Decreases in expression ...
Complement receptor 1 (CR1) has factor H-like activity, permitting factor I to cleave C3b. Membrane cofactor protein also has ... encoded search term (Complement-Related Disorders) and Complement-Related Disorders What to Read Next on Medscape. Related ... Table 3. Proteins of the Human Complement (C) System, Lectin Pathway *Table 4. Proteins of the Human Complement (C) System, C3 ... C3bBb complex then acts as the C3 convertase and generates more C3b through an amplification loop. Binding of factor H to C3b ...
Gerdes, J; Naiem, M; Mason, D Y.; and Stein, H, "Human complement (c3b) receptors defined by a mouse monoclonal antibody." ( ...
Of the 8 plasma membrane receptors for complement, only deficiencies of CR3 and CR4 due to CD18 deficiency have been described ... The complement system exerts many of its effects through complement receptors (CRs). ... C3b/C4b. RBC, polymorphonuclear cell, macrophage, B cell, follicular dendritic cell. Immune adherence, phagocytosis ... encoded search term (Pediatric Complement Receptor Deficiency) and Pediatric Complement Receptor Deficiency What to Read Next ...
activates plasminogen activator; destroys C3B; C5A (i.e., complement factors). pYV (70.3 kb). Yops (proteins). interferes with ...
In most conditions, there were more C3d-containing immune complexes than C3b/iC3b. Although CR1 (C3b receptors) rapidly ... Monoclonal antibodies against complement 3 neoantigens for detection of immune complexes and complement activation. ... Monoclonal antibodies against complement 3 neoantigens for detection of immune complexes and complement activation. ... Relationship between immune complex levels, state of C3, and numbers of receptors for C3b.. ...
Lane 5 is a 4-fold longer exposure of lane 3. C3, 30 ng; C3b, 30 ng; B cells, 7.4 × 104 cell equivalents; Farage, 6.3 × 105 ... An intracellular complement system (ICS) has recently been described in immune and nonimmune human cells. This system can be ... One difference between native cells and cell lines was the time absent from a fluid-phase complement source; therefore, we ... A C3(H20) recycling pathway is a component of the intracellular complement system. ...
Complement C[bdi2] inhibitor (inactivator) immunological test system.. II. 866.5260. Complement C3b inactivator immunological ... Complement components immunological test system.. II. 866.5250. ...
Indeed, it now seems clear that complement first evolved as part of the innate immune system, where it still plays an important ... Although first discovered as an effector arm of the antibody response, complement can also be activated early in infection in ... This activity was said to complement the antibacterial activity of antibody, hence the name. ... Complement was discovered many years ago as a heat-labile component of normal plasma that augments the opsonization of bacteria ...
Complement receptors CR1 and CR2 are active in the immune response and autoimmune diseases. The susceptibility and severity of ... A method and a package for identifying single nucleotide polymorphisms in complement receptor is useful in identifying ... autoimmune disease is determined by genotyping or phenotyping an individual for complement receptor. ... The primary opsonins of the complement system are C3b and C4b which are activated by cleavage of fragments C3 and C4. C3b and ...
Home » Lateral distribution and diffusion of the C3b receptor of complement, HLA antigens, and lipid probes in peripheral blood ... Lateral distribution and diffusion of the C3b receptor of complement, HLA antigens, and lipid probes in peripheral blood ... Lateral distribution and diffusion of the C3b receptor of complement, HLA antigens, and lipid probes in peripheral blood ...
Investigation of Interaction of Vaccinia Virus Complement Control Protein and Curcumin with Complement Components C3 and C3b ... C3b-VCPps, C3b-VCP, C3b-tVCPps, and C3b-tVCPg indicate adsorption of C3b on VCPps, VCPg, tVCPps, and tVCPg. ... The dD/dF values for the binding of AMs to C3b were found to be of the following order: C3b vs tVCP ≤ C3b vs VCP , Cur vs C3bps ... Investigation of Interaction of Vaccinia Virus Complement Control Protein and Curcumin with Complement Components C3 and C3b ...
complement (C3b). Genes Expressed immunoglobulin. Cellular Products immunoglobulin. Tumorigenic Yes Effects Yes, in nude mice ...
  • In addition, surface-bound C3b has opsonic and immune adherence activities which are mediated via binding to CR1 (CD35) complement receptors. (emdmillipore.com)
  • Complement receptors on white blood cells are able to bind iC3b, so iC3b functions as an opsonin. (wikipedia.org)
  • This gene is a member of the receptors of complement activation (RCA) family and is located in the 'cluster RCA' region of chromosome 1. (nih.gov)
  • The complement system as understood today is a multimolecular system composed of more than 32 proteins and consisting of serum proteins, serosal proteins, and cell membrane receptors that bind to complement fragments. (medscape.com)
  • The complement system consists of 7 serum and 9 membrane regulatory proteins, 1 serosal regulatory protein, and 8 cell membrane receptors that bind complement fragments. (medscape.com)
  • Human complement (c3b) receptors defined by a mouse monoclonal antibod" by J Gerdes, M Naiem et al. (jax.org)
  • Human complement (c3b) receptors defined by a mouse monoclonal antibody. (jax.org)
  • and Stein, H, "Human complement (c3b) receptors defined by a mouse monoclonal antibody. (jax.org)
  • Expression of the complement anaphylatoxin C3a and C5a receptors on bronchial epithelial and smooth muscle cells in models of sepsis and asthma. (medscape.com)
  • Structure, function and cellular expression of complement anaphylatoxin receptors. (medscape.com)
  • Relationship between immune complex levels, state of C3, and numbers of receptors for C3b. (jci.org)
  • Although CR1 (C3b receptors) rapidly converted immune complex-bound iC3b to C3dg/C3d and lupus patients had reduced CR1, no correlation between the state of C3 on circulating immune complexes or levels of immune complexes and CR1 numbers was seen. (jci.org)
  • First, it generates large numbers of activated complement proteins that bind covalently to pathogens, opsonizing them for engulfment by phagocytes bearing receptors for complement. (nih.gov)
  • Complement receptors CR1 and CR2 are active in the immune response and autoimmune diseases. (google.com)
  • The attachment of complement proteins, C3b/C4b to microbial membranes or immune complexes, a process commonly known as opsonization, facilitates the binding of opsonized material to cell receptors. (google.com)
  • Over 30 proteins and protein fragments make up the complement system, including serum proteins , and cell membrane receptors . (wikipedia.org)
  • The complement system (CS) is composed of receptors and regulators bound to the cell membrane and different plasma proteins that interact with cells and mediators of the immune system ( Figure 1 ). (scielo.br)
  • The role of membrane receptors for C3b and C3d in phagocytosis. (rupress.org)
  • We conclude that two fragments of the C3 molecule, that is, C3b and C3d, can function as opsonins if the phagocyte has the appropriate membrane receptors. (rupress.org)
  • On the other hand, C3 primarily mediates the binding of the particle via complement receptors. (rupress.org)
  • Complement receptors C5aR1 and C5aR2 act differentially during the early immune response after bone fracture but are similarly involved in bone repair. (upenn.edu)
  • Complement-activation fragment C4a mediates effector functions by binding as untethered agonist to protease-activated receptors 1 and 4. (upenn.edu)
  • During PMN activation the surface expression of receptors (R) for C3b and C3bi increases rapidly. (osti.gov)
  • C3 is split into activation fragments, among which C3b binds to T cells via CD46 receptors. (news-medical.net)
  • The complement system is a complex cascade involving proteolytic cleavage of serum glycoproteins often activated by cell receptors. (sigmaaldrich.com)
  • The staphylococcal proteins surface immunoglobulin-binding protein (Sbi) and extracellular fibrinogen-binding protein (Efb) bind C3/C3b simultaneously with plasminogen. (nih.gov)
  • Various proteins of the complement system interact specifically with platelets, which, in turn, activates them and promotes thrombosis. (rupress.org)
  • We identified P-selectin as a C3b-binding protein, and confirmed by surface plasmon resonance binding that these two proteins interact specifically with a dissociation constant of 1 μM. (rupress.org)
  • Complement is a multi-component system that involves several plasma and cell-expressed proteins, and has been conserved throughout evolution. (rupress.org)
  • Also, C3b on the cell surface participates in the serial activation of complement proteins (C5-C9) that polymerize and form the C5b-9 complex, also known as the membrane attack complex. (rupress.org)
  • Several negative regulatory proteins exist to prevent uncontrolled activation of the complement system and widespread tissue damage. (rupress.org)
  • Several proteins of the complement system, including C3 and C5-C9, were shown to potentiate thrombin-induced platelet secretion and aggregation ( 4 ). (rupress.org)
  • Also, treatment of platelets with sublytic concentrations of C5b-9 caused transient membrane depolarization ( 6 ), granule secretion ( 7 ), generation of procoagulant platelet microparticles ( 8 ), and translocation of phosphatidylserine to the outer membrane leaflet ( 9 , 10 ) Collectively, these studies make the case that the complement system may serve as a link between inflammation and thrombosis, and reveal specific interactions between complement proteins and platelets. (rupress.org)
  • The complement system is a group of proteins that work together to destroy foreign invaders (such as bacteria and viruses), trigger inflammation, and remove debris from cells and tissues. (medlineplus.gov)
  • One of these pieces, called C3b, interacts with several other proteins on the surface of cells to trigger the complement system's response. (medlineplus.gov)
  • The classical complement pathway can also be activated by apoptotic cells, necrotic cells, and acute phase proteins. (wikipedia.org)
  • The complement system is made up of a large number of distinct plasma proteins that react with one another to opsonize pathogens and induce a series of inflammatory responses that help to fight infection. (nih.gov)
  • A number of complement proteins are proteases that are themselves activated by proteolytic cleavage. (nih.gov)
  • In this way, the activation of a small number of complement proteins at the start of the pathway is hugely amplified by each successive enzymatic reaction, resulting in the rapid generation of a disproportionately large complement response. (nih.gov)
  • Second, the small fragments of some complement proteins act as chemoattractants to recruit more phagocytes to the site of complement activation, and also to activate these phagocytes. (nih.gov)
  • The complement system involves a group of proteins that play a role in host defense against infection. (google.com)
  • The inflammatory response is triggered by way of the cascade, in which low molecular weight peptides are cleaved from complement proteins. (google.com)
  • This convertase, the alternative pathway C3-convertase, although only produced in small amounts, can cleave multiple C3 proteins into C3a and C3b. (wikipedia.org)
  • Complement is composed of a network of more than 50 proteins including inactive precursor molecules, fluid-phase, and membrane-bound regulators as well as distinct inhibitors ( 6 - 10 ). (frontiersin.org)
  • The complement system consists of a number of small proteins found in the blood, in general synthesized by the liver , and normally circulating as inactive precursors ( pro-proteins ). (wikipedia.org)
  • Most of the proteins and glycoproteins that constitute the complement system are synthesized by hepatocytes . (wikipedia.org)
  • The decreased expression of complement regulatory proteins (CRP) seems to play an important role in RA activity, and is associated with worsening of the clinical symptoms. (scielo.br)
  • rheumatoid arthritis, complement system proteins, complement activation. (scielo.br)
  • C3 and C4, mainly produced by the liver, are the major plasma proteins of the immune system complement pathways. (thermofisher.com)
  • The Classical pathway of activation of the complement system is a group of blood proteins that mediate the specific antibody response. (wikipathways.org)
  • We show that these hybrid proteins are able to deplete complement, both in vitro and in vivo. (springer.com)
  • Human C3/CVF hybrid proteins represent a novel class of biologicals as potential therapeutic agents in many diseases where complement is involved in the pathogenesis. (springer.com)
  • Human C3/cobra venom factor hybrid proteins for therapeutic complement depletion: in vivo activity and fine mapping of important domains. (springer.com)
  • Furthermore, the structure and functions of several complement proteins as well as the protein-protein interactions that underlie these functions are now being investigated with the aid of cross-disciplinary approaches ranging from mathematics and biophysics to comparative phylogenesis, in silico studies, mimetics and proteomics. (upenn.edu)
  • Our laboratory, extending its research beyond the scope of traditional complement pathobiology, has embraced this global and combinatorial approach to biomedical research and has been actively engaged in defining the function of complement proteins in several biological contexts and pathophysiological states. (upenn.edu)
  • In the classical complement cascade, binding of complement protein C1q to a pathogen or antigen-bound antibody triggers a series of protein cleavages that activate several other complement proteins, including C3. (jneurosci.org)
  • The regulators of complement activation gene cluster encodes a group of proteins that have evolved to control the amplification of complement at the critical step of C3 activation. (sigmaaldrich.com)
  • Both FH and FHL-1 (which is a truncated version of FH that results from an alternative splice site in the FH transcript [ 71 ]) are serum proteins that negatively regulate the alternative pathway of complement. (asm.org)
  • 4 Under normal pregnancy conditions, the fetus is protected from maternal immune responses through an array of mechanisms, including trophoblast expression of complement regulatory proteins that inhibit complement at different steps of the activation cascade. (ahajournals.org)
  • 1. Which of the following complement proteins is responsible for opsonizing bacteria? (coursehero.com)
  • Dr. Koury looks at a study that demonstrates that C3b-mediated erythrocyte clearance of damaged plasma proteins can improve treatment of diseases characterized by tissue accumulation of misfolded or denatured proteins. (hematology.org)
  • VCP contains 4 short consensus repeat domains (SCR) that are also present in eukaryotic complement regulatory proteins ( 9 ). (asm.org)
  • Thus, the poxvirus complement control proteins might be attractive therapeutic targets to treat poxvirus infections. (asm.org)
  • Binds complement components C3B and C4B with cofactor activity for the I-dependent cleavage of these proteins. (biolegend.com)
  • The complement system is part of the innate immune system and is composed of a diverse array of structural proteins and enzymes that promote or inhibit complement activation, which, in turn, leads to target cell chemotaxis, cellular activation, lysis, or apoptosis. (arvojournals.org)
  • X-ray and neutron-scattering techniques characterize proteins in solution and complement high-resolution structural studies. (royalsocietypublishing.org)
  • We also discuss the applications to the large multi-domain proteins of the complement system, most notably its major regulator factor H, which is important in age-related macular degeneration and renal diseases. (royalsocietypublishing.org)
  • In recent years, a greater range of proteins have been successfully studied by scattering, including antibodies of adaptive immunity and the complement proteins of innate immunity. (royalsocietypublishing.org)
  • After enzymatic C3b coupling or standard amine C3b coupling, we analyzed and compared the binding of four C3b ligands to the surface: factor B, factor H, C5 and the soluble complement receptor 1 (sCR1, CD35). (diva-portal.org)
  • Mouse monoclonal to CD35.CT11 reacts with CR1, the receptor for the complement component C3b /C4, composed of four different allotypes (160, 190, 220 and 150 kDa). (healthweblognews.info)
  • In summary, we have found that platelets are capable of activating the complement system, and have identified P-selectin as a receptor for C3b capable of initiating complement activation. (rupress.org)
  • We have also identified P-selectin expressed on activated platelets as a receptor for C3b, thus linking thrombosis and local activation of the complement system on platelets. (rupress.org)
  • The role of cell membrane-associated human factor H for the binding of cell-bound C3b to complement receptor-carrying (CR+) cells was investigated. (nih.gov)
  • While the anaphylatoxin C3a interacts with its C3a receptor (C3aR) to recruit leukocytes, C3b contributes to further downstream complement activation. (wikipedia.org)
  • Membrane immune adherence receptor that plays a critical role in the capture and clearance of complement-opsonized pathogens by erythrocytes and monocytes/macrophages (PubMed:2963069). (nih.gov)
  • Difference in the clustering of complement receptor type 1 (CR1) on polymorphonuclear leukocytes and erythrocytes: effect on immune adherence. (medscape.com)
  • Wakabayashi M, Ohi H, Tamano M, Onda K, Fujita T, Tomino Y. Acquired loss of erythrocyte complement receptor type 1 in patients with diabetic nephropathy undergoing hemodialysis. (medscape.com)
  • A method and a package for identifying single nucleotide polymorphisms in complement receptor is useful in identifying individual susceptibility to a disease. (google.com)
  • The susceptibility and severity of autoimmune disease is determined by genotyping or phenotyping an individual for complement receptor. (google.com)
  • 2. The method of claim 1 wherein said identity of nucleotide 5932 affects C3b binding by a CR1 receptor. (google.com)
  • 5. The method of claim 4 wherein said complement receptor is CR1. (google.com)
  • No. 60/106,643 filed Nov. 2, 1998 entitled "Genetic Polymorphism in a Complement Receptor. (google.com)
  • The present invention relates generally to compounds and methods for identifying polymorphism in a cellular receptor, and more particularly, to compounds and methods for identifying and typing single nucleotide polymorphisms that code for a complement receptor and applying these polymorphisms to delineation of disease susceptibility and severity. (google.com)
  • Complement receptor type 1 (CR1 or CD35) is a peripheral glycosylated membrane protein that regulates the complement activation in the control of immune responses. (intechopen.com)
  • It is identical with CR-3, the receptor for the iC3b fragment of the third complement component. (rcsb.org)
  • Complement receptor 1 (CR1) is the most versatile of these inhibitors with both receptor and regulatory functions. (sigmaaldrich.com)
  • Our studies underscore the potential importance of CR1 on an epithelial cell population as both an intrinsic complement regulator and an immune adherence receptor. (sigmaaldrich.com)
  • COVID-19 patients have CD4 T cells in their lungs bearing CD46, and when this is bound by C3b, an autocrine loop is set up, which results in a coordinated increase in Th1 differentiation and then a suppression of T cell activity, in synchrony with T cell receptor stimulation. (news-medical.net)
  • complement receptor a membrane receptor that can bind activated complement components. (thefreedictionary.com)
  • a cell-surface receptor capable of binding activated complement components. (thefreedictionary.com)
  • A Familial C3GN Secondary to Defective C3 Regulation by Complement Receptor 1 and Complement Factor H. (semanticscholar.org)
  • CD46 is a transmembrane protein that is known as a complement membrane cofactor protein, MCP, and measles virus receptor. (biolegend.com)
  • Factor H binds to C3b via three interaction sites. (diva-portal.org)
  • Herein we report that the only known naturally occurring positive regulator of complement, properdin, binds predominantly to late apoptotic and necrotic cells, but not to early apoptotic cells. (jimmunol.org)
  • This binding occurs independently of C3b, which is additional to the standard model wherein properdin binds to preexisting clusters of C3b on targets and stabilizes the convertase C3bBb. (jimmunol.org)
  • It was originally shown that properdin binds to C3b and increases the stability of the alternative pathway convertases at least 10-fold on target surfaces and immune complexes ( 20 ). (jimmunol.org)
  • We found that properdin binds predominantly to late apoptotic and necrotic cells independently of C3b, but not to early apoptotic cells, leading to alternative pathway-mediated complement activation. (jimmunol.org)
  • It binds complement components C3b and C4b, mediating phagocytosis by granulocytes and monocytes. (healthweblognews.info)
  • The C3b component of the cleaved C3 binds to C3 convertase (C4b2b) to generate C5 convertase (C4b2b3b), which cleaves the C5 protein. (wikipedia.org)
  • C3b binds to the C3 convertase (C4b2b), to form C5 convertase (C4b2b3b). (wikipedia.org)
  • Here, C3b binds to factor B that is cleaved by factor D to Bb. (medscape.com)
  • Finally, the alternative pathway can be initiated when a spontaneously activated complement component binds to the surface of a pathogen. (nih.gov)
  • The pathway is triggered when the C3b protein directly binds a microbe . (wikipedia.org)
  • [3] Complement factor H preferentially binds to vertebrate cells (because of affinity for sialic acid residues), allowing preferential protection of host (as opposed to bacterial) cells from complement-mediated damage. (wikipedia.org)
  • When an IgG1 anti-fHbp MAb binds to sparsely exposed fHbp on the bacterial surface, there appears to be insufficient complement activation for bacteriolysis unless fH binding also is inhibited. (asm.org)
  • It has been suggested by several labs, including our own, that B. burgdorferi binds FH/FHL-1 on its surface to inhibit the activation of the alternative pathway of complement and prevent its destruction during the earliest stages of mammalian infection ( 4 , 10 , 40 , 48 , 71 ). (asm.org)
  • VCP inhibits activation of complement, binds C4b and C3b, acts as a cofactor in the enzymatic inactivation of C4b and C3b by factor I, prevents the formation of the classical and alternative pathway C3 convertases, and accelerates their decay ( 6 , 12 , 15 , 18 ). (asm.org)
  • CD46 binds complement components C3b and C4b and has been reported to play a role in T cell regulation. (biolegend.com)
  • The C3 gene provides instructions for making a protein called complement component 3 (or C3). (medlineplus.gov)
  • This protein plays a key role in a part of the body's immune response known as the complement system. (medlineplus.gov)
  • The C3 protein is essential for turning on (activating) the complement system. (medlineplus.gov)
  • This genetic change is described as a "gain-of-function" mutation because it leads to an altered version of the protein that overactivates the complement system. (medlineplus.gov)
  • These mutations are described as "loss-of-function" because the abnormal or missing C3 protein prevents normal activation of the complement system. (medlineplus.gov)
  • iC3b is a protein fragment that is part of the complement system, a component of the vertebrate immune system. (wikipedia.org)
  • Complement factor I can further cleave iC3b into a protein fragment known as C3d. (wikipedia.org)
  • The classical complement pathway can be initiated by the binding of antigen-antibody complexes to the C1q protein. (wikipedia.org)
  • The protein mediates cellular binding to particles and immune complexes that have activated complement. (nih.gov)
  • The classical pathway can be initiated by the binding of C1q, the first protein in the complement cascade, directly to the pathogen surface. (nih.gov)
  • Vaccinia virus complement control protein (VCP) and curcumin (Cur) are natural compounds with different biological origins reported to regulate complement activation. (openbiochemistryjournal.com)
  • VCP is known to be structurally similar to C4B binding protein (C4Bbp), but functionally to CR1, a human complement regulatory molecule known to bind C3b. (openbiochemistryjournal.com)
  • CFHR5 (Complement Factor H-Related protein 5) is able to bind to act as a cofactor for factor I, has decay accelerating activity and is able to bind preferentially to C3b at host surfaces. (wikipedia.org)
  • CFI (Complement Factor I) is a Protein Coding gene. (genecards.org)
  • Responsible for cleaving the alpha-chains of C4b and C3b in the presence of the cofactors C4-binding protein and factor H respectively. (genecards.org)
  • One hybrid protein, HC3-1496, is shown to be effective in reducing complement-mediated damage in two disease models in mice, collagen-induced arthritis and myocardial ischemia/reperfusion injury. (springer.com)
  • Depletion of plasma complement in vivo by a protein of cobra venom: its effect on various immunologic reactions. (springer.com)
  • Binding of the complement-downregulating protein factor H (fH) to the surface of the meningococcus is important for survival of the organism in human serum. (asm.org)
  • We report here the discovery and characterization of Ehp, a new secreted Staphylococcus aureus protein that potently inhibits the alternative complement activation pathway. (rcsb.org)
  • The mature Ehp polypeptide is composed of 80 residues and is 44% identical to the complement inhibitory domain of S. aureus Efb (extracellular fibrinogen-binding protein). (rcsb.org)
  • Our current research efforts focus on the structural-functional aspects of protein-protein interactions and the rational design of small-size complement inhibitors. (upenn.edu)
  • The antibody targets a regulatory protein known as complement factor H (CFH), which normally protects healthy cells in the body from attack and destruction by the immune system. (cancer.gov)
  • CFH normally protects healthy cells by binding to the cell surface and preventing an immune system protein known as complement C3b from being deposited there. (cancer.gov)
  • It is well recognized that B. burgdorferi expresses multiple lipoproteins on its surface that bind the human complement inhibitors factor H and factor H-like protein 1 (FH/FHL-1). (asm.org)
  • Many human pathogens, including serum-resistant B. burgdorferi , evade complement destruction by binding complement factor H (FH) and FH-like protein 1 (FHL-1) ( 4 , 29 , 32 , 40 , 55 ). (asm.org)
  • C3 is the most abundant protein of the complement system with serum protein levels of about 1.3 mg/ml. (acris-antibodies.com)
  • The vaccinia virus complement control protein (VCP) is secreted by infected cells and has been shown to inhibit complement activation through interactions with C3b/C4b. (asm.org)
  • The vaccinia virus complement control protein (VCP) is a 35-kDa protein that is encoded by the C3L gene and secreted by cells infected with vaccinia virus ( 7 , 8 ). (asm.org)
  • Dissection of CR1, factor H, membrane cofactor protein, and factor B binding and functional sites in the third complement component. (semanticscholar.org)
  • Complement protein C3 plasma levels [ Time Frame: Up to 14 days after treatment. (clinicaltrials.gov)
  • A polyclonal antibody specific for human complement C3b has been pre-coated onto a 96-well microplate with removable strips. (innov-research.com)
  • Complement C3b in standards and samples is sandwiched by the immobilized antibody and biotinylated polyclonal antibody specific for complement C3b, which is recognized by a streptavidin-peroxidase conjugate. (innov-research.com)
  • The classical complement pathway is initiated by antigen-antibody complexes with the antibody isotypes IgG and IgM. (wikipedia.org)
  • Certain variants of the IgM antibody were found to bind the Methicillin-resistant Staphylococcus aureus these IgM were found to be critical in complement activation through the classical pathway and subsequent destruction of the bacteria. (wikipedia.org)
  • This activity was said to ' complement ' the antibacterial activity of antibody , hence the name. (nih.gov)
  • Although first discovered as an effector arm of the antibody response, complement can also be activated early in infection in the absence of antibodies. (nih.gov)
  • Complement is active in immune defenses, especially antibody mediated events by way of the "classical pathway. (google.com)
  • Complement response to an invasion by a foreign particle can also embody an antibody independent mechanism which is known as the "alternative pathway. (google.com)
  • The classical complement pathway typically requires antigen-antibody complexes for activation (specific immune response), whereas the alternative pathway can be activated by spontaneous C3 hydrolysis, foreign material, pathogens, or damaged cells. (wikipedia.org)
  • The following product was used in this experiment: Complement Polyclonal Antibody from Thermo Fisher Scientific, catalog # RAHU-C. (thermofisher.com)
  • 9. A chimeric antibody characterized in that it comprises at least one of the sequences corresponding to SEQ ID NO: 2, 4, 6, 8, or 12, wherein the antibody recognizes a region corresponding to sequence 727-744 (SEQ ID NO:15) of the C5 component of human complement or a region having at least 80% homology thereto. (google.com)
  • Complement, a phylogenetically conserved arm of innate immunity, functions together with the adaptive immune response by serving as an important inflammatory mediator of antigen-antibody interactions. (upenn.edu)
  • Formalin-Fixed, Paraffin-Embedded Human Placenta tissue stained with Complement C3c Antibody Cat. (acris-antibodies.com)
  • VCP inhibits the antibody-dependent, complement-enhanced neutralization of vaccinia virus virions ( 3 ). (asm.org)
  • Complement C3b may be an opsonin for antigen-antibody complexes which helps prevent damage from the formation of large, insoluble immune aggregates. (sigmaaldrich.com)
  • Subsequent binding of the antibody to complement C1q subunits of C1 result in catalytically active C1s subunits. (sigmaaldrich.com)
  • We conclude that constrained scattering modelling makes useful contributions to our understanding of antibody and complement structure and function. (royalsocietypublishing.org)
  • The SPR technique is particularly suitable for analysis of the alternative complement pathway (AP) because the inherent nature of the latter is to amplify deposition of C3b on various surfaces. (diva-portal.org)
  • The pivotal role of the complement system in the handling of dying cells has been demonstrated for the classical pathway (via C1q) and lectin pathway (via mannose-binding lectin and ficolin). (jimmunol.org)
  • By binding to late apoptotic or necrotic cells, properdin serves as a focal point for local amplification of alternative pathway complement activation. (jimmunol.org)
  • Our data indicate that direct recognition of dying cells by properdin is essential to drive alternative pathway complement activation. (jimmunol.org)
  • In humans, homozygous deficiency of any of the early components of the classical pathway of complement activation (C1q, C1r, C1s, C4, and C2) predisposes to the development of SLE ( 9 ), suggesting that complement is involved in removal of dying cells and the immune regulation associated with this process. (jimmunol.org)
  • Nevertheless, the role of the complement system in the handling of dying cells has been mostly linked to the classical pathway (via C1q) and lectin pathway (via mannose-binding lectin (MBL) and ficolin) ( 10 , 11 , 12 , 13 , 14 ). (jimmunol.org)
  • The alternative pathway of complement is thought to be activated following hydrolysis of C3, generation of C3b, and formation of a positive feedback loop to mount a rapid local response ( 17 ). (jimmunol.org)
  • The alternative pathway was initially recognized to amplify complement activation triggered by the classical pathway. (jimmunol.org)
  • Once bound to target surfaces C3b becomes an essential subunit of both the classical and alternative pathway C5 cleaving enzymes. (emdmillipore.com)
  • Once activated by one of the three main pathways (i.e., the classical, lectin, or alternative pathway), C3, the central component of the complement system, is cleaved by C3 convertases to release C3a and to deposit C3b on the surface of the complement activation site. (jimmunol.org)
  • Unlike intact C3b, iC3b cannot associate with factor B, thus preventing amplification of the complement cascade through the alternative pathway. (wikipedia.org)
  • The classical complement pathway is one of three pathways which activate the complement system, which is part of the immune system. (wikipedia.org)
  • The classical pathway is distinct from the other complement pathways in its unique activation triggers and cascade sequence. (wikipedia.org)
  • Activation of the complement pathway through the classical, lectin or alternative complement pathway is followed by a cascade of reactions eventually leading to the membrane attack complex. (wikipedia.org)
  • Obesity in turn results in an abnormally high level of complement activation via production of the C1 component of the classical pathway, which can lead to tissue inflammation and eventually insulin resistance, however the exact mechanisms that causes this is yet unknown. (wikipedia.org)
  • This is important for targeting the virus in its intracellular phase because the antibodies specific to the synthetic peptides can trigger the classical complement pathway and induce the death of HIV infected cells. (wikipedia.org)
  • Lack of regulation of the classical complement pathway through the deficiency in C1-inhibitor results in episodic angioedema. (wikipedia.org)
  • Acts also in the inhibition of spontaneous complement activation by impairing the formation and function of the alternative and classical pathway C3/C5 convertases, and by serving as a cofactor for the cleavage by factor I of C3b to iC3b, C3c and C3d,g, and of C4b to C4c and C4d (PubMed:2972794, PubMed:8175757). (nih.gov)
  • Depending on the nature of complement activators, the classic pathway, the alternative pathway, or the more recently discovered lectin pathway is activated predominantly to produce C3 convertase. (medscape.com)
  • Binding of factor H to C3b increases its inactivation by factor I. Properdin stabilizes it, preventing its inactivation by factors H and I. The alternate pathway does not result in a truly nonspecific activation of complement because it requires specific types of compounds for activation. (medscape.com)
  • This in turn cleaves and activates the next zymogen in the complement pathway. (nih.gov)
  • The alternative pathway of the complement system is an innate component of the immune system 's natural defense against infections. (wikipedia.org)
  • The alternative pathway is one of three complement pathways that opsonize and kill pathogens. (wikipedia.org)
  • The addition of properdin forms the complex C3bBbP, a stable compound which can bind an additional C3b to form alternative pathway C5-convertase. (wikipedia.org)
  • The C5-convertase of the alternative pathway consists of (C3b) 2 BbP (sometimes referred to as C3b 2 Bb). (wikipedia.org)
  • After the creation of C5 convertase (either as (C3b) 2 BbP or C4b2a3b from the classical pathway), the complement system follows the same path regardless of the means of activation (alternative, classical, or lectin). (wikipedia.org)
  • Three biochemical pathways activate the complement system: the classical complement pathway , the alternative complement pathway , and the lectin pathway . (wikipedia.org)
  • While all three MAbs elicited similar C1q-dependent C4b deposition on live bacteria (classical complement pathway), only those antibodies that inhibited binding of fH to fHbp (JAR 3 and JAR 5) had bactericidal activity with human complement. (asm.org)
  • Ehp potently inhibited C3b deposition onto sensitized surfaces by the alternative complement activation pathway. (rcsb.org)
  • equivalent in action to C3B, which means that it can activate the alternative complement pathway. (drugs.com)
  • however, it was an even more potent regulator (>95% reduction in C3b deposition) of the alternative pathway. (sigmaaldrich.com)
  • The binding of FH/FHL-1 on the cell surface can also inhibit alternative pathway activation by promoting factor I-mediated cleavage of surface-bound C3b to iC3b ( 51 , 71 ). (asm.org)
  • Component C2 which is part of the classical pathway of the complement system is cleaved by activated factor C1 into two fragments: C2b and C2a. (uniprot.org)
  • In the alternate pathway complement C3 undergoes spontaneous cleavage resulting in complement B binding to C3b. (sigmaaldrich.com)
  • Recently, properdin, a positive regulator of the alternative pathway of complement, has been shown to bind to surfaces and promote complement activation. (pubmedcentralcanada.ca)
  • Moreover, the mechanisms involved in alternative pathway-mediated complement activation or its consequences on infection in C. pneumoniae remain unknown. (pubmedcentralcanada.ca)
  • Activation of the classical complement pathway [ Time Frame: Up to 14 days after treatment. (clinicaltrials.gov)
  • Cleavage of the C3-α chain at peptide bond 77 by either of the complement C3 convertase enzymes results in production of C3a (M.W. 9083) and C3b (M.W. 180,000) fragments. (emdmillipore.com)
  • For these functions to be executed, the complement system requires activation that is marked by the formation of the C3 convertase complex on the surface of target cells. (rupress.org)
  • This convertase cleaves large quantities of C3 into C3b, the main effector of complement, and C3a, a potent mediator of inflammation released into the medium. (rupress.org)
  • The deposited C3b facilitates phagocytosis (opsonization) of the target cells and the formation of C5 convertase, which activates C5 into C5a and C5b. (jimmunol.org)
  • In addition, the C5 convertase initiates the terminal phase of the complement system, leading to the assembly of the membrane attack complex (MAC). (wikipedia.org)
  • C3 convertase then cleaves C3 into C3a and C3b. (wikipedia.org)
  • In the first phase, a series of specific interactions leads to formation of intrinsic complement proteinase, termed C3 convertase. (medscape.com)
  • C3bBb complex then acts as the C3 convertase and generates more C3b through an amplification loop. (medscape.com)
  • This system can be activated in a convertase-independent manner from intracellular stores of the complement component C3. (jci.org)
  • It may inhibit stabilization of C3 convertase by properdin or it may have more than one site of action on the complement components. (openbiochemistryjournal.com)
  • Properdin can bind to C3 (H 2 O) and C3b for the assembly of the C3 convertase. (openbiochemistryjournal.com)
  • By doing so, it may prevent binding of properdin or Bb to C3 and C3b, and thereby inhibit the formation of the AP convertase. (openbiochemistryjournal.com)
  • An inhibitory activity for an erythrocyte in termediate bearing the properdin (P)-stabilized amplification C3 convertase, PC3bBb, was recognized in whole normal human serum and separated from C3b inactivator by its distinct physicochemical and functional characteristics. (pnas.org)
  • beta1H restores control of the system by decay-dissociation of the bimolecular complex, therby exposing C3b to C3b inactivator whose irreversible action prevents regeneration of the convertase at that site. (pnas.org)
  • The formation of a C3 convertase can also be prevented when a plasma protease called complement factor I cleaves C3b into its inactive form, iC3b. (wikipedia.org)
  • This heterodimer can cleave and inactivate the complement components C4b and C3b, and it prevents the assembly of the C3 and C5 convertase enzymes. (genecards.org)
  • The cleavage product C3B joins the complex to form C5 convertase, which cleaves C5. (wikipathways.org)
  • Additional copies of the cleavage product C3B are recruited to the complex, resulting in an alternative C5 convertase, which cleaves C5 and contributes C5B to the formation of the Membrane Attack Complex. (wikipathways.org)
  • A novel bifunctional chimeric complement inhibitor that regulates C3 convertase and formation of the membrane attack complex. (springer.com)
  • C2a, a serine protease, then combines with complement factor C4b to generate the C3 or C5 convertase. (uniprot.org)
  • The two activated C1s subunits are then able to catalyze the assembly of the C3 convertase (complement C4b2a) from complements C2 and C4. (sigmaaldrich.com)
  • Pretreatment of CR+ cells with antibodies to factor H inhibited the adherence of C3b-coated red cells to human tonsil lymphocytes (TL) and peripheral blood monocytes (M phi). (nih.gov)
  • The adherence of C3b-coated erythrocytes to PMN remained unaffected by anti-H antibodies in the presence of DFP. (nih.gov)
  • Polyclonal as well as monoclonal antibodies directed against human factor I inhibited the binding of C3b cells to Raji cells but not to TL. (nih.gov)
  • Monoclonal antibodies against complement 3 neoantigens for detection of immune complexes and complement activation. (jci.org)
  • Complement was discovered many years ago as a heat-labile component of normal plasma that augments the opsonization of bacteria by antibodies and allows antibodies to kill some bacteria. (nih.gov)
  • The complement system is a part of the immune system that enhances (complements) the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promotes inflammation, and attacks the pathogen's cell membrane . (wikipedia.org)
  • The complement system can be recruited and brought into action by antibodies generated by the adaptive immune system . (wikipedia.org)
  • In the early 20th century, this controversy was resolved when it became understood that complement can act in combination with specific antibodies, or on its own in a non-specific way. (wikipedia.org)
  • The complement system is a biochemical cascade that helps, or complements, the ability of antibodies to clear pathogens from an organism. (wikipathways.org)
  • While some fHbp-specific monoclonal antibodies (MAbs) block binding of fH to fHbp, the stoichiometry of blocking in the presence of high serum concentrations of fH and its effect on complement-mediated bactericidal activity are unknown. (asm.org)
  • In preclinical studies with mice, antibodies elicited by fHbp vaccines bound to the bacterial surface, activated complement-mediated bactericidal activity directly ( 8 , 16 , 17 , 33 , 47 ), and inhibited binding of fH to fHbp ( 8 , 30 , 47 ). (asm.org)
  • The present invention refers to recombinant antibodies of human origin specific for the C5 component of the activated complement and characterised by the ability to inhibit the conversion of the C5 alpha chain to C5a and C5b. (google.com)
  • Moreover the present invention refers to the nucleotide sequences coding for such antibodies and to the therapeutic use of both polypeptide and nucleotide sequences, in particular for the therapy of diseases involving tissue damage deriving from uncontrolled activation of the complement system. (google.com)
  • In renal transplant, the allograft is responsible for triggering many innate and adaptive immune mechanisms, either mediated by cells, such as macrophages and lymphocytes, or by soluble components, such as antibodies and the complement system, which can ultimately lead to graft rejection [ 1 ]. (hindawi.com)
  • Monoclonal antibodies detecting neo-epitopes have been used for direct quantification of activation at different steps in the complement cascade. (acris-antibodies.com)
  • Monoclonal antibodies to complement componenets without the need of their prior purification. (acris-antibodies.com)
  • 2004 . Novel monoclonal antibodies against C3 interfering with complement activation: description of fine specificity and applications to various immunoassays. (acris-antibodies.com)
  • To elucidate which SCR domains are involved in abolishing complement-enhanced neutralization of vaccinia virus virions, we generated and characterized a panel of mouse monoclonal antibodies (MAbs) raised against VCP. (asm.org)
  • It has been suggested that the main product of complement activation, iC3b, facilitates the removal of dead material and mediates peripheral tolerance ( 10 , 15 , 16 ). (jimmunol.org)
  • iC3b is produced when complement factor I cleaves C3b. (wikipedia.org)
  • Accordingly, we found that the C3 split products inactivated C3b (iC3b) and C3a were elevated in serum, overlying ARPE-19 cells that had accumulated A2E and were irradiated to induce A2E photooxidation. (pnas.org)
  • Patients with autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis, and Sjogren's syndrome, and paracoccidioidomycosis were found to contain immune complexes bearing C3b/iC3b or C3d. (jci.org)
  • In most conditions, there were more C3d-containing immune complexes than C3b/iC3b. (jci.org)
  • Ultimately, it is thought that the inactivation of C3b to iC3b inhibits the deposition of terminal complement components, which then prevents the formation of the bactericidal membrane attack complex. (asm.org)
  • Using heterologous cells expressing P-selectin, we found that P-selectin alone is sufficient to activate the complement system, marked by increases in C3b deposition, C3a generation, and C5b-9 formation. (rupress.org)
  • Those resembling erythema nodosum (EN) show small vessel vasculitis and perivascular lymphocytic and mononuclear cell infiltration and fibrin deposition in the vessel wall, while the punched out ulcers are characterized by a leucocytoclastic vasculitis (neutrophil infiltrate) with fibrinoid necrosis. (angelfire.com)
  • Additionally, the deposition of complement components C3, C6, and C5b-9 was enhanced on the surface of the CspA mutant compared to that of the wild-type strain. (asm.org)
  • The combined data lead us to conclude that the CspA-mediated binding of human FH confers serum resistance by directly inhibiting complement deposition on the surface of B. burgdorferi . (asm.org)
  • The binding of these physiological forms accelerates complement activation on the Chlamydia pneumoniae surface, as measured by C3b and C9 deposition. (pubmedcentralcanada.ca)
  • This then acts similarly to C1 esterase and cleaves C2 and C4 to form C2aC4b, which is the C3 esterase that cleaves C3 to form C3b. (medscape.com)
  • In such a cascade, an active complement enzyme generated by cleavage of its zymogen precursor then cleaves its substrate, another complement zymogen, to its active enzymatic form. (nih.gov)
  • The Human Complement C3b ELISA (Enzyme-Linked Immunosorbent Assay) kit is designed for detection of human complement C3b in plasma, serum, urine, milk, saliva, CSF, and cell culture supernatant samples. (innov-research.com)
  • An earlier study ( 10 ) reported that Cremophor EL, the commonly used solvent for paclitaxel, but not the paclitaxel itself, activates complement in vitro after incubation with serum. (jimmunol.org)
  • To this end, we established an in vitro assay by using human serum as a source of complement, and we measured products of C3 activation by enzyme immunoassay. (pnas.org)
  • Precoating of microtiter plates with two species of oxidized A2E, peroxy-A2E, and furano-A2E, followed by incubation with serum, also activated complement. (pnas.org)
  • Measurements of serum complement components C3 and C4 are useful in the diagnosis and monitoring of immune complex disease. (thermofisher.com)
  • Borrelia burgdorferi has developed efficient mechanisms for evading the innate immune response during mammalian infection and has been shown to be resistant to the complement-mediated bactericidal activity of human serum. (asm.org)
  • In fact, with regard to the major borrelial genospecies that cause Lyme disease, B. burgdorferi and Borrelia afzelii are resistant to the complement-mediated bactericidal activity of serum, while most strains of Borrelia garinii are killed by human serum ( 4 , 7 , 10 , 48 ). (asm.org)
  • Consistent with this notion, the terminal complement components (C5b, C6, C7, C8, and C9) are deposited more efficiently and abundantly on the surface of serum-sensitive strains of Borrelia spp. (asm.org)
  • Third, the terminal complement components damage certain bacteria by creating pores in the bacterial membrane. (nih.gov)
  • Which complement is part of the Membrane Attack Complex? (brainscape.com)
  • The end result of this complement activation or complement fixation cascade is stimulation of phagocytes to clear foreign and damaged material, inflammation to attract additional phagocytes, and activation of the cell-killing membrane attack complex . (wikipedia.org)
  • Complement C3b initiates the breakdown of the cell membrane, which causes the cell to die. (cancer.gov)
  • However, in older lesions, 2-5 days old, IgG and complement (C3) were found in the basement membrane in almost all of the sixteen biopsies from patients with minor aphthous ulcers. (angelfire.com)
  • A complex of complements C5b,C6, C7, and C8 mediates the polymerization of up to eighteen C9 molecules into a tube-like membrane attack complex that is inserted into the plasma membrane of an unwanted organism such as of gram-negative bacteria and viral infected cells. (sigmaaldrich.com)
  • Which complement is an anaphylatoxin (induces inflammation)? (brainscape.com)
  • Proteolysis by certain enzymes results in the cleavage of C3 releasing C3a anaphylatoxin and C3b. (acris-antibodies.com)
  • Complement C5a, like C3a is an anaphylatoxin, and is a chemotactic attractant for induction of neutrophilic release of antimicrobial proteases and oxygen radicals. (sigmaaldrich.com)
  • The complement system, a component of the innate immune system, helps macrophages find and clear pathogens and cellular debris by increasing vascular permeability, directing chemotaxis, and tagging targets to promote phagocytosis. (jneurosci.org)
  • The complement system is a central component of the innate immune response and is involved in many functions, including recognition, opsonization, phagocytosis, and destruction of foreign cells, as well as generation of chemotactic fragments (C3a and C5a) and activation of adaptive immunity ( 30 , 32 , 51 ) Three pathways of complement activation are known: the classical, lectin, and alternative pathways. (pubmedcentralcanada.ca)
  • Upon host infection, the human pathogenic microbe Staphylococcus aureus (S. aureus) immediately faces innate immune reactions such as the activated complement system. (nih.gov)
  • Soluble factors from the innate immune system such as complement or pentraxins can opsonize apoptotic cells, thereby promoting their removal by phagocytes ( 6 , 7 , 8 ). (jimmunol.org)
  • C3b and factor H: key components of the complement system. (mysciencework.com)
  • Inflammation and thrombosis are two responses that are linked through a number of mechanisms, one of them being the complement system. (rupress.org)
  • In this paper, we show that the converse is also true: activated platelets can activate the complement system. (rupress.org)
  • Activation of the complement system proceeded to its final stages, which was marked by the increased generation of the anaphylotoxin C3a and the C5b-9 complex. (rupress.org)
  • The complement system mediates cell-cell interactions in many physiological processes, such as hematopoiesis, organogenesis, and in reproduction ( 1 ). (rupress.org)
  • Here, we show that upon activation, platelets activate the complement system, which proceeds to its final stages marked by the formation of the C5b-9 complex. (rupress.org)
  • This process must be carefully regulated so the complement system targets only unwanted materials and does not damage the body's healthy cells. (medlineplus.gov)
  • Complement, a key component of the innate immune system, has been associated with neuroinflammation, a potentially important trigger of some types of neuropathic pain. (jimmunol.org)
  • Complement is an important part of the innate immune system, which plays a primary role in protecting the host from infections ( 6 ). (jimmunol.org)
  • Because of its role in the innate immune system classical complement has been implicated in a number of pathogen related disorders. (wikipedia.org)
  • In an investigation of a potential trigger for complement activation in AMD, we explored the notion that the complex mixture of products resulting from photooxidation of A2E might include a range of fragments that could be recognized by the complement system as "foreign" and that could serve to activate the complement system, leading to low-grade inflammation. (pnas.org)
  • We suggest that products of the photooxidation of bis-retinoid lipofuscin pigments in RPE cells could serve as a trigger for the complement system, a trigger than would predispose the macula to disease and that, over time, could contribute to chronic inflammation. (pnas.org)
  • The complement system functions as an interactive sequence, with one reaction leading to another in the form of a cascade. (medscape.com)
  • An intracellular complement system (ICS) has recently been described in immune and nonimmune human cells. (jci.org)
  • Complement components immunological test system. (fda.gov)
  • Complement C[bdi2] inhibitor (inactivator) immunological test system. (fda.gov)
  • Indeed, it now seems clear that complement first evolved as part of the innate immune system , where it still plays an important role. (nih.gov)
  • In the case of the complement system, the precursor zymogens are widely distributed throughout body fluids and tissues without adverse effect. (nih.gov)
  • The complement system activates through a triggered-enzyme cascade. (nih.gov)
  • There are three ways in which the complement system protects against infection. (nih.gov)
  • As part of the body's natural defenses, the complement system operates as a biological cascade in which one component activates successive components. (google.com)
  • The complement system functions to promote the inflammatory response, to modify the membranes of infectious organisms, and also to identify pathogenic material for removal. (google.com)
  • Complement regulatory molecules might prove beneficial in the prevention of damage to the central nervous system (CNS) from up-regulated complement components in chronic as well as acute neurodegenerative disorders. (openbiochemistryjournal.com)
  • In the past two decades, VCP has been thoroughly investigated for its effect on components of the complement system. (openbiochemistryjournal.com)
  • Dysregulation of the complement system has been implicated in several diseases and pathologies. (wikipedia.org)
  • Complement component C3 plays a central role in the activation of complement system. (senescence.info)
  • Ehrlich introduced the term "complement" as part of his larger theory of the immune system. (wikipedia.org)
  • Ehrlich, therefore, named this heat-labile component "complement," because it is something in the blood that "complements" the cells of the immune system. (wikipedia.org)
  • In several models of autoimmune diseases, the overactivation of the complement system (CS) is the cause of disease exacerbation. (scielo.br)
  • The complement system in B cell regulation. (springer.com)
  • Using complement as a model system we apply ideas and methods embodied in engineering, computer science, physics, chemistry, and other fields to address today's challenges in biomedical research. (upenn.edu)
  • The complement system has been long appreciated as a major effector arm of the innate immune response. (upenn.edu)
  • In an era that nurtures the integrated study of biological systems as the prevalent concept in contemporary scientific thinking, complement research is being revisited and our current knowledge of this innate immune system is enriched by findings that point to novel functions that do not strictly correlate with immunological defense and surveillance, immune modulation or inflammation. (upenn.edu)
  • Besides its immunological role, the complement system contributes to normal CNS development by promoting synaptic pruning. (jneurosci.org)
  • Through similar mechanisms, the complement system may contribute to synaptic loss and thus to cognitive decline during aging. (jneurosci.org)
  • Tumor cells have been found to produce CFH and take advantage of the protection it confers to evade destruction by the complement system, which is a component of the body's immune response. (cancer.gov)
  • The complement system is an important part of the humoral response in innate immunity, consisting of three different pathways. (acris-antibodies.com)
  • The complement system plays a crucial role in the progression of age-related macular degeneration (AMD). (arvojournals.org)
  • During this journey, from circulating cells to endothelial cells, C. pneumoniae encounters the innate immune system, in which the complement system may play a fundamental role in controlling Chlamydia infection. (pubmedcentralcanada.ca)
  • The third complement component, C3, is central to the classical, alternative and lectin pathways of complement activation. (acris-antibodies.com)
  • The role of the CD19/CD21 complex in B cell processing and presentation of complement-tagged antigens. (medscape.com)
  • CD35 is caTagorized as a regulator of complement avtivation. (healthweblognews.info)
  • CD35) on epithelial cells: A model for understanding complement-mediated damage in the kidney. (sigmaaldrich.com)
  • The target sites are exposed on the C3b, C3c and C3d fragments of C3, respectively. (diva-portal.org)
  • The second phase for each involves cleavage of C3b, generating multiple biologically important fragments and large, potentially cytolytic complexes. (medscape.com)
  • [2] and act as a cofactor for Factor I -mediated cleavage of C3b. (wikipedia.org)
  • The deposited C4b and C3b were progressively cleaved with a t½ of ∼ 30 min to C4d and C3d, respectively, by CR1-dependent cofactor activity. (sigmaaldrich.com)
  • C3b is also essential for propagation of the complement cascade to the stage of the lytic terminal complement complexes. (mysciencework.com)
  • Schematic overview of the complement cascade. (nih.gov)
  • In the early phases of an infection, the complement cascade can be activated on the surface of a pathogen through any one, or more, of the three pathways shown in Fig. 2.8 . (nih.gov)
  • This gene encodes a serine proteinase that is essential for regulating the complement cascade. (genecards.org)
  • The complement cascade can also be activated by spontaneous cleavage of C3. (jneurosci.org)
  • The Classical Complement Cascade Mediates CNS Synapse Elimination. (freepatentsonline.com)
  • Activation products of the complement cascade contain neo-epitopes that are not present in the individual native components. (acris-antibodies.com)
  • The complement cascade is activated in normal pregnancy, and excessive complement activation propagates the systemic inflammatory response in severe preeclampsia. (ahajournals.org)
  • Ischaemic infarction may also cause initiation of the complement cascade. (sigmaaldrich.com)
  • Complement C3b inactivator immunological. (fda.gov)
  • The complement components that Cur might bind could be the one central to the activation of CP and AP. (openbiochemistryjournal.com)
  • Based on our previous results [ 1 ] it can be proposed that Cur may bind to C3 (H 2 O) and/or C3b. (openbiochemistryjournal.com)
  • Since C3b is free and abundant in the plasma, it can bind to either a host cell or a pathogen surface. (wikipedia.org)
  • Monocytes, that bind both C3b and C3d, respond to both as opsonins. (rupress.org)
  • PMN, which do not bind C3d, respond only to particles opsonized with C3b. (rupress.org)
  • and inactivation of exposed C3b by C3b inactivator. (pnas.org)
  • In order to prevent damage to self cells and tissues and restrict overconsumption of the complement components, C3b molecules need to be controlled by factor H. Defect in C3 functions leads to compromised microbial defence and increased susceptibility to certain autoimmune diseases. (mysciencework.com)
  • Deficiency of factor H, or a functional defect in its N terminus, often leads to membranoproliferative glomerulonephritis and complement depletion, owing to continuous overconsumption of C3. (mysciencework.com)
  • In future, analysis of patient samples for defects in these key complement components may prove useful in diagnosis of these diseases and new therapeutic targets will certainly be the aim for use in the recently recognized factor H-related diseases. (mysciencework.com)
  • Ehrlich and Morgan termed this factor complement. (medscape.com)
  • Association with and adaption to various hosts most likely correlates with the spirochetes' ability to acquire complement regulator factor H (FH) to overcome the host's innate immune response. (frontiersin.org)
  • Defects in this gene cause complement factor I deficiency, an autosomal recessive disease associated with a susceptibility to pyogenic infections. (genecards.org)
  • Diseases associated with CFI include Complement Factor I Deficiency and Hemolytic Uremic Syndrome, Atypical 3 . (genecards.org)
  • Complement factor I, which is responsible for cleaving the alpha-chains of C4b and C3b. (ebi.ac.uk)
  • Prior research by the same team has shown that complement is among the most active pathways in CD4 T cells infiltrating the lung tissue, and that it is powerfully stimulated by SARS-CoV-2, especially the complement factor 3 (C3) in the lung epithelium. (news-medical.net)
  • Molecular interactions between complement factor H and its heparin and heparan sulphate ligands. (ucl.ac.uk)
  • Bound plasminogen is converted by bacterial activator staphylokinase or by host-specific urokinase-type plasminogen activator to plasmin, which in turn leads to degradation of complement C3 and C3b. (nih.gov)
  • Cur as well as VCP showed binding to both C3 and to C3b, Cur however bound to C3b to a lesser extent. (openbiochemistryjournal.com)
  • Moreover, CR1 efficiently and stably bound but didn't internalize C4b/C3b opsonized immune complexes. (sigmaaldrich.com)
  • For example, component C3b is bound to neutrophils, B lymphocytes and macrophages. (thefreedictionary.com)
  • The seven remaining MAbs did not alter VCP function in the complement neutralization assay and recognized VCP bound to C3b/C4b. (asm.org)
  • In all three complement pathways, the central molecule is C3, which, upon activation cleavage, forms the major opsonin C3b - the key component of complement. (mysciencework.com)
  • Agnello, V., Winchester, R. J. and Kunkel, H. G., 1970, Precipitin reactions of the Clq component of complement with aggregated 'Y-globulin and immune complexes in gel diffusion, Immunology 19:909. (indigo.ca)
  • Immunofluorescence studies on the subcomponents of the first component of complement (C1): detection of C1q and C1s in different cells of biopsy material and on human as well as on guinea pig peritoneal macrophages. (freepatentsonline.com)
  • Human complement component C3: cDNA coding sequence and derived primary structure. (springer.com)
  • Specifically, the C3 cleavage product C3b tags synapses to be engulfed and eliminated by microglia. (jneurosci.org)
  • Inhibition of binding of fH to the bacterial surface would be expected to increase susceptibility of the bacteria to complement-mediated bacteriolysis. (asm.org)
  • Complement inhibition is an intriguing treatment option for patients with severe preeclampsia. (ahajournals.org)
  • Efb creates a fibrinogen shield surrounding the bacteria by simultaneously binding complement C3b and fibrinogen at the bacterial surface. (imperial.ac.uk)
  • In this study, we have used this technique to study interactions between the central complement component C3b and its multiple ligands by using the Biacore equipment. (diva-portal.org)
  • Binding of each ligand to C3b was detected when C3b had been coupled either enzymatically or using the amine coupling, but the half-lives of the interactions were found to vary depending on the coupling procedure. (diva-portal.org)
  • In conclusion, this study shows that SPR is a powerful tool in analyzing and mapping the interactions of C3b with its multiple ligands. (diva-portal.org)
  • These two compounds have also not been compared to each other with respect to their interactions with C3 and C3b. (openbiochemistryjournal.com)
  • This technology was applied to characterize the interactions of VCP, Cur and appropriate controls with the key complement components. (openbiochemistryjournal.com)
  • Integrin alpha-M/beta-2 is implicated in various adhesive interactions of monocytes, macrophages and granulocytes as well as in mediating the uptake of complement-coated particles. (rcsb.org)
  • Mapping interactions between complement C3 and regulators using mutations in atypical hemolytic uremic syndrome. (semanticscholar.org)
  • We determined whether a reciprocal interaction also exists, whereby platelets can activate complement. (rupress.org)
  • The classical and alternative complement pathways. (wikipedia.org)
  • C1-inhibitor plays the role of inactivating C1r and C1s to prevent further downstream classical complement activity. (wikipedia.org)
  • Safety and Efficacy of the Complement Inhibitor AMY-101 in a Natural Model of Periodontitis in Non-human Primates. (upenn.edu)
  • Safety, tolerability, pharmacokinetics (PK) and pharmacodynamics (PD) of a Single Ascending Dose (SAD) and a Multiple Dose (MD) of the complement inhibitor AMY-101. (clinicaltrials.gov)
  • Properdin, discovered in 1954 ( 18 ), is the only known naturally occurring positive regulator of complement activation ( 19 ). (jimmunol.org)
  • The stabilization of C3bBb by activated properdin minimizes intrinsic decay and protects C3b in the bimolecular complex from C3b inactivator. (pnas.org)
  • Here we studied whether properdin-mediated complement activation occurs on the surface of Chlamydia pneumoniae , an obligate intracellular Gram-negative bacterium that causes 10 to 20% of community-acquired pneumonia. (pubmedcentralcanada.ca)
  • As might be expected, there are many regulatory mechanisms to prevent uncontrolled complement activation. (nih.gov)
  • We also study the viral molecular mimicry and immune evasion strategies, as well as the evolution of complement biology. (upenn.edu)
  • A revised mechanism for the activation of complement C3 to C3b: a molecular explanation of a disease-associated polymorphism. (ucl.ac.uk)
  • Also, mice deficient in the negative regulator of complement, CD59b, exhibit platelet hyperreactivity ( 3 ). (rupress.org)
  • Amplification of C3 cleavage by C3bBb may well determine whether initial complement activation by the classical or alternative activating sequence is beneficial or detrimental to the host. (pnas.org)
  • Its expression by this cell population has aroused considerable speculation as to its biologic function in view of many complement-mediated renal diseases. (sigmaaldrich.com)
  • Complement inhibitors are being studied as potential therapeutics for immune diseases and Alzheimer's. (sigmaaldrich.com)
  • Soluble opsonins such as complement can opsonize dying cells, thereby promoting their removal by phagocytes and modulating the immune response. (jimmunol.org)
  • C3b and its degradation products fixed on target cells functions as opsonins, thereby marking the cell for destruction by phagocytes attracted by anaphylotoxins (C3a and C5a). (rupress.org)
  • Complements C3a and C4b are opsonins that bridge phagocytes to microorganisms. (sigmaaldrich.com)
  • Thus, S. aureus Sbi and Efb comprise platforms to recruit plasmin(ogen) together with C3 and its activation product C3b for efficient degradation of these complement components in the local microbial environment and to protect S. aureus from host innate immune reactions. (nih.gov)
  • C3 and C3b, the components central to the complement activation, also play a damaging role in several inflammatory disorders. (openbiochemistryjournal.com)
  • This is accomplished mainly by inhibiting the activation or uptake of complement components, especially C3b. (medscape.com)
  • Complement components C6, C7, C8 and C9. (ebi.ac.uk)
  • In this respect, recent evidence produced by our laboratory (and others) suggests that complement components can modulate diverse biological processes by closely interacting with other intra- and intercellular networks. (upenn.edu)
  • In addition we study the involvement of various complement components with developmental pathways and the role of complement in tissue regeneration, early hematopoietic development and cancer. (upenn.edu)
  • In addition to the complement components, CD46 has been shown to interact with moesin, c-Src, tetraspanin 4, c-Yes, and integrin β1. (biolegend.com)
  • In this study, the authors sought to evaluate the pathophysiologic roles of complement components C3a and C5a in the human choroid in AMD. (arvojournals.org)