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.

Chimeric receptors of the human C3a receptor and C5a receptor (CD88). (1/332)

Chimeras were generated between the human anaphylatoxin C3a and C5a receptors (C3aR and C5aR, respectively) to define the structural requirements for ligand binding and discrimination. Chimeric receptors were generated by systematically exchanging between the two receptors four receptor modules (the N terminus, transmembrane regions 1 to 4, the second extracellular loop, and transmembrane region 5 to the C terminus). The mutants were transiently expressed in HEK-293 cells (with or without Galpha-16) and analyzed for cell surface expression, binding of C3a and C5a, and functional responsiveness (calcium mobilization) toward C3a, C5a, and a C3a as well as a C5a analogue peptide. The data indicate that in both anaphylatoxin receptors the transmembrane regions and the second extracellular loop act as a functional unit that is disrupted by any reciprocal exchange. N-terminal substitution confirmed the two-binding site model for the human C5aR, in which the receptor N terminus is required for high affinity binding of the native ligand but not a C5a analogue peptide. In contrast, the human C3a receptor did not require the original N terminus for high affinity binding of and activation by C3a, a result that was confirmed by N-terminal deletion mutants. This indicates a completely different binding mode of the anaphylatoxins to their corresponding receptors. The C5a analogue peptide, but not C5a, was an agonist of the C3aR. Replacement of the C3aR N terminus by the C5aR sequence, however, lead to the generation of a true hybrid C3a/C5a receptor, which bound and functionally responded to both ligands, C3a and C5a.  (+info)

Regional specificity of ASP binding in human adipose tissue. (2/332)

Obesity, in particular omental (OM) adiposity, is associated with diabetes and cardiovascular disease. Thus site-specific regulation of fat storage is important to understand. Acylation-stimulating protein (ASP) is a potent stimulator of glucose transport and triglyceride synthesis in adipocytes. In the present study, we characterized receptor binding of 125I-labeled ASP to human adipocyte plasma membranes from paired OM and subcutaneous (SC) sites in normal (N) and obese (O) male (M) and female (F) subjects (n = 24). Overall, specific binding of 125I-ASP was in the order of SC > OM and O > N (in SC tissue, particularly in F). Receptor affinity of 125I-ASP was higher [lower dissociation constant (Kd)] in SC than in OM (63.6 +/- 16.2 vs. 160.7 +/- 38.6 nM, P < 0.02), especially in F (37.0 +/- 11.1 F-N and 26.3 +/- 6.7 nM F-O) and lower (higher Kd) in male OM (291.8 +/- 116.8 M-N and 149.4 +/- 56.4 M-O). The greater binding and higher affinity of 125I-ASP binding to SC suggests that ASP may be an important factor in maintaining regional adipose tissue mass. Conversely, lower binding and receptor affinity in male OM adipose tissue may contribute to the fatty acid imbalance and metabolic complications associated with this syndrome, by reducing the efficiency of adipose fatty acid trapping by the ASP pathway.  (+info)

Effect of permeability on indices of haemodialysis membrane biocompatibility. (3/332)

BACKGROUND: Increases in plasma anaphylatoxins frequently are used as an index of haemodialysis membrane biocompatibility; however, their plasma levels may be influenced by the loss of anaphylatoxins into the dialysate compartment. METHODS: We compared the generation and compartmental distribution of anaphylatoxins, C3a and C5a, in a high flux and a low flux polysulfone membrane dialyser when whole human blood was recirculated through an in vitro haemodialysis circuit. RESULTS: Plasma C3a levels in high flux polysulfone (2.31 +/- 0.81 microg/ml) and low flux polysulfone (3.02 +/- 0.98 microg/ml) dialysers were comparable after 120 min (P = NS). In contrast, dialysate C3a in high flux polysulfone (0.65 +/- 0.31 microg/ml) accounted for 37.5 +/- 7.0% of the total detected (plasma + dialysate) C3a mass in the dialysers, while dialysate C3a in low flux polysulfone dialysers (0.01 +/- 0.01 microg/ml) accounted for only 0.3 +/- 0.3% of the total mass (P < 0.05; high flux vs low flux). Anaphylatoxin C5a was undetectable in the dialysate compartment of either dialyser examined. CONCLUSIONS: Our results indicate that anaphylatoxins readily traverse certain high flux dialysis membranes; consequently, plasma C3a levels may not accurately reflect the C3-activating potential of these membranes.  (+info)

Modulation of C3a activity: internalization of the human C3a receptor and its inhibition by C5a. (4/332)

The C3a receptor (C3aR) is expressed on most human peripheral blood leukocytes with the exception of resting lymphocytes, implying a much higher pathophysiological relevance of the anaphylatoxin C3a as a proinflammatory mediator than previously thought. The response to this complement split product must be tightly regulated in situations with sustained complement activation to avoid deleterious effects caused by overactivated inflammatory cells. Receptor internalization, an important control mechanism described for G protein-coupled receptors, was investigated. Using rabbit polyclonal anti-serum directed against the C3aR second extracellular loop, a flow cytometry-based receptor internalization assay was developed. Within minutes of C3a addition to human granulocytes, C3aR almost completely disappeared from the cell surface. C3aR internalization could also be induced by PMA, an activator of protein kinase C. Similarly, monocytes, the human mast cell line HMC-1, and differentiated monocyte/macrophage-like U937-cells exhibited rapid agonist-dependent receptor internalization. Neither C5a nor FMLP stimulated any cross-internalization of the C3aR. On the contrary, costimulation of granulocytes with C5a, but not FMLP, drastically decreased C3aR internalization. This effect could be blocked by a C5aR-neutralizing mAb. HEK293-cells transfected with the C3aR, with or without Galpha16, a pertussis toxin-resistant G protein alpha subunit required for C3aR signal transduction in these cells, did not exhibit agonist-dependent C3aR internalization. Additionally, preincubation with pertussis toxin had no effect on C3a-induced internalization on PMNs. C3aR internalization is a rapid negative control mechanism and is influenced by the C5aR pathway.  (+info)

Mechanisms involved in the regulation of free fatty acid release from isolated human fat cells by acylation-stimulating protein and insulin. (5/332)

The effects of acylation-stimulating protein (ASP) and insulin on free fatty acid (FFA) release from isolated human fat cells and the signal transduction pathways to induce these effects were studied. ASP and insulin inhibited basal and norepinephrine-induced FFA release by stimulating fractional FFA re-esterification (both to the same extent) and by inhibiting FFA produced during lipolysis (ASP to a lesser extent than insulin). Protein kinase C inhibition influenced none of the effects of ASP or insulin. Phosphatidylinositol 3-kinase inhibition counteracted the effects of insulin but not of ASP. Phosphodiesterase 3 (PDE3) activity was stimulated by ASP and insulin, whereas PDE4 activity was slightly increased by ASP only. Selective PDE3 inhibition reversed the effects of both ASP and insulin on fractional FFA re-esterification and lipolysis. Selective PDE4 inhibition slightly counteracted the ASP but not the effect of insulin on fractional FFA re-esterification and did not prevent the action of ASP or insulin on lipolysis. Thus, ASP and insulin play a major role in regulating FFA release from fat cells as follows: insulin by stimulating fractional FFA re-esterification and inhibiting lipolysis and ASP mainly by stimulating fractional FFA re-esterification. For both ASP and insulin these effects on FFA release are mediated by PDE3, and for ASP PDE4 might also be involved. The signaling pathway preceding PDE is not known for ASP but involves phosphatidylinositol 3-kinase for insulin.  (+info)

Genetic deficiency of acylation stimulating protein (ASP(C3ades-Arg)) does not cause hyperapobetalipoproteinemia in mice. (6/332)

The acylation stimulating protein (ASP) is a 76-amino acid peptide that has been proposed as a potent mediator of triglyceride synthesis and, when functionally impaired, as a major cause of hyperapobetalipoproteinemia (HyperapoB). Purification and sequence analysis of ASP from human sera have revealed that ASP is identical to the complement C3-derived activation peptide C3ades-Arg. Because C3 is the precursor for C3ades-Arg and therefore ASP, a deficiency in C3 would be predicted to result in a phenotype characteristic of HyperapoB. To test this hypothesis in vivo, the current study was undertaken in which ASP(C3ades-Arg)-deficient mice were used as a model system. No significant differences were found in the triglyceride, cholesterol, or free fatty acid concentrations in the plasma of fasted normal and ASP(C3ades-Arg)-deficient animals. In addition, plasma lipoprotein analyses indicated that the very low density lipoprotein, low density lipoprotein, and high density lipoprotein cholesterol and triglyceride concentrations as well as the apolipoprotein B-48 and B-100 levels were not significantly different in the plasma of ASP(C3ades-Arg)-deficient and wild type mice. Furthermore, when challenged with an oral fat load, the ASP(C3ades-Arg)-deficient mice showed no impaired ability to clear triglycerides and free fatty acids from their circulation when compared with their wild-type littermates. Collectively, these results indicate that ASP(C3ades-Arg) deficiency does not cause HyperapoB in mice and that the physiological importance of impaired ASP(C3ades-Arg) function as a cause of hyperapobetalipoproteinemia needs to be reevaluated.  (+info)

Role of C3 cleavage in monocyte activation during extracorporeal circulation. (7/332)

BACKGROUND: We previously demonstrated that inhibiting formation of terminal complement components (C5a and C5b-9) prevents platelet and neutrophil (PMN) but not monocyte activation during simulated extracorporeal circulation (SECC). This study examined whether earlier complement inhibition during SECC, blocking C3a formation, would additionally prevent monocyte activation. METHODS AND RESULTS: SECC was established by recirculating heparinized whole blood from human volunteers on a membrane oxygenator. CAB-2, a chimeric protein constructed from genes encoding the complement regulatory proteins CD46 and CD55, inactivates the C3/C5 convertases and blocks in vitro generation of C3a, C5a, and C5b-9. CAB-2 was used in 4 experiments at a final concentration of 300 micrograms/mL and 4 experiments at 30 micrograms/mL; 4 control runs used vehicle alone. Samples were assayed for C3a and C5b-9, monocyte activation (CD11b upregulation), PMN activation (CD11b upregulation and elastase release), and platelet activation (P-selectin expression and monocyte-platelet conjugate formation). CAB-2 at both doses significantly inhibited formation of C3a and C5b-9 during SECC. High-dose CAB-2 significantly blocked monocyte and PMN CD11b upregulation and PMN elastase release. CAB-2 also inhibited formation of platelet activation-dependent monocyte-platelet conjugates. CONCLUSIONS: Blockade of complement activation early in the common pathway inhibited monocyte CD11b upregulation during SECC, suggesting that early complement components contribute most to monocyte activation during SECC. As expected, PMN and platelet activation were blocked by terminal complement inhibition. This investigation further elucidates the relation between complement and blood cell activation during simulated cardiopulmonary bypass.  (+info)

Possible mechanism for in vitro complement activation in blood and plasma samples: futhan/EDTA controls in vitro complement activation. (8/332)

BACKGROUND: Ongoing in vitro complement (C) activation in citrate or EDTA plasma has prevented an accurate analysis of C-activation products generated in vivo. The aim of this study was to characterize handling and storage conditions required to prevent in vitro C activation in blood and plasma samples collected with Futhan/EDTA. METHODS: Biotrak(TM) RIAs were used to quantitatively measure C3a and C4a in blood and/or plasma samples from healthy individuals (controls) and from liver transplant patients. Blood samples were routinely drawn into either EDTA (1 g/L) tubes or into tubes containing both EDTA (1 g/L) and Futhan (0.1 g/L) and immediately centrifuged at 2000g for 15 min at 4 degrees C. RESULTS: In controls, C4a, but not C3a, in fresh samples (time 0) was higher in EDTA plasma than in Futhan/EDTA plasma (n = 20; P = 0.002). Futhan/EDTA prevented C3a and C4a generation in blood and plasma samples held at room temperature (22-23 degrees C) for 1 h and in plasma held for 24 h at 4 degrees C or -70 degrees C. The mean C3a concentration (1.76 mg/L; n = 19) at time 0 in EDTA plasma samples from liver transplant patients was significantly higher than for controls (0.34 mg/L; n = 11). In these patients, the mean C3a in EDTA samples increased to 13.8 mg/L after 60 min at room temperature, but there was no change in the C3a concentration of an EDTA plasma from a control. In the patients, C3a concentrations were lower in Futhan/EDTA plasma than in EDTA at time 0 and after 60 min at room temperature (1.40 and 2.02 mg/L, respectively). The mean patient C4a was 4.02 mg/L in EDTA plasma at time 0 vs 0.24 mg/L for controls; it increased to 16.9 mg/L after 60 min at room temperature compared with 0.76 mg/L for controls. The mean patient C4a was 0.83 mg/L in Futhan/EDTA plasma at time 0 vs 0.1 mg/L for controls. Neither patient nor control C4a concentrations increased vs time in Futhan/EDTA. CONCLUSION: The combination of Futhan (0.1 g/L) and EDTA (1 g/L) eliminates in vitro C activation.  (+info)

Postprandial lipemia and fatty acid fluxes occur several times daily, resulting in very efficient absorption of dietary fat and redistribution to various tissues. Absorbed dietary lipids are incorporated into chylomicrons to distribute triglycerides either for storage in adipose tissue or for immediate use in muscle. Commonly, the dietary sources of fat exceed the actual needs and the tissues are faced with dealing with the excess. Under these circumstances, the removal process of dietary triglycerides and fatty acids becomes overloaded, resulting in excessive postprandial lipemia and accumulation of chylomicrons, remnant particles and non-esterified fatty acids. These particles are associated with disruptions in lipoprotein metabolism and changes in inflammatory factors, thus their association with cardiovascular disease, metabolic syndrome and diabetes is not surprising. Dietary factors, not just fat, influence postprandial fluxes. This leads to the question: do we need a standardized fat ...
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Metabolic Surgery Symposium: Current Status GBP & the reversal of diabetes-6 sec https://www.ncbi.nlm.nih.gov/pubmed/?term=17715408 https://www.ncbi.nlm.nih.gov/pubmed/24018646 Keyword(s): acylation-stimulating protein, adiponectin, anti-diabetic GI procedures, Asian Indians, bariatric surgery, BMI, Caucasians, COSMID trial, Cushings syndrome, CV risk, diabetes remission, diet-induced weight loss, DJ exclusion, DJB, endoluminal DJ sleeve, fasting glucose, fundus, ghrelin, GI Dynamics, GI surgery, glucose homeostasis, glycemia, […]. ...
The structure of the human C5aR antagonist, C5a-A8, reveals a three-helix bundle conformation similar to that observed for human C5a-desArg, whereas murine C5a and C5a-desArg both form the canonical four-helix bundle. These conformational differences are discussed in light of the differential C5aR activation properties observed for the human and murine complement anaphylatoxins across species. Complement is an ancient part of the innate immune system that plays a pivotal role in protection against invading pathogens and helps to clear apoptotic and necrotic cells. Upon complement activation, a cascade of proteolytic events generates the complement effectors, including the anaphylatoxins C3a and C5a. Signalling through their cognate G-protein coupled receptors, C3aR and C5aR, leads to a wide range of biological events promoting inflammation at the site of complement activation. The function of anaphylatoxins is regulated by circulating carboxypeptidases that remove their C-terminal arginine ...
Activation of complement C5 generates the potent anaphylatoxin C5a and leads to pathogen lysis, inflammation and cell damage. The therapeutic potential of C5 inhibition has been demonstrated by eculizumab, one of the worlds most expensive drugs. However, the mechanism of C5 activation by C5 convertases remains elusive, thus limiting development of therapeutics. Here we identify and characterize a new protein family of tick-derived C5 inhibitors. Structures of C5 in complex with the new inhibitors, the phase I and phase II inhibitor OmCI, or an eculizumab Fab reveal three distinct binding sites on C5 that all prevent activation of C5. The positions of the inhibitor-binding sites and the ability of all three C5-inhibitor complexes to competitively inhibit the C5 convertase conflict with earlier steric-inhibition models, thus suggesting that a priming event is needed for activation.
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The objectives are to define the complete structure of the human receptor for complement fragments C3b/C4b and its functional role in immune and inflammatory re...
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TY - JOUR. T1 - An anti-inflammatory function for the complement anaphylatoxin C5a-binding protein, C5L2. AU - Gerard, Norma P.. AU - Lu, Bao. AU - Liu, Pixu. AU - Craig, Stewart. AU - Fujiwara, Yuko. AU - Okinaga, Shoji. AU - Gerard, Craig. PY - 2005/12/2. Y1 - 2005/12/2. N2 - C5L2 is an enigmatic serpentine receptor that is co-expressed with the C5a receptor on many cells including polymorphonuclear neutrophils. The apparent absence of coupling of C5L2 with G proteins suggests that this receptor may modulate the biological activity of C5a, perhaps by acting as a decoy receptor. Alternatively, C5L2 may affect C5a function through formation of a heteromeric complex with the C5aR, or it may utilize a G protein-independent signaling pathway. Here we show that in mice bearing a targeted deletion of C5L2, the biological activity of C5a/C5adesArg is enhanced both in vivo and in vitro. The biological role of C5L2 thus appears to be limiting to the pro-inflammatory response to the anaphylatoxin. ...
Background: Elevated interleukin-6 (IL-6) and complement activation are associated with detrimental effects of inflammation in coronary artery disease (CAD). The complement anaphylatoxins C5a and C3a interact with their receptors; the highly inflammatory C5aR1, and the C5aR2 and C3aR. We evaluated the effect of the IL-6 receptor (IL-6R)-antagonist tocilizumab on the expression of the anaphylatoxin receptors in whole blood from non-ST-elevation myocardial infarction (NSTEMI) patients. Separately, anaphylatoxin receptor expression in peripheral blood mononuclear cells (PBMC) from patients with different entities of CAD was investigated. Materials and Methods: NSTEMI patients were randomized to one dose of tocilizumab (n = 28) or placebo (n = 32) and observed for 6 months. Whole blood samples drawn at inclusion, at day 2, 3 and after 6 months were used for mRNA isolation. Plasma was prepared for analysis of complement activation measured as sC5b-9 by ELISA. Furthermore, patients with different CAD ...
Now, they may soon add a new risk factor to the list: activation of the complement system. The complement system is usually implicated in immune responses, but now theres a role for it in cardiovascular disease. In a new research report appearing in the January 2011 print issue of the FASEB Journal (http://www.fasebj.org), scientists from Europe and the United States show that anaphylatoxin C5a, a protein released when complement is activated, contributes to atherosclerotic disease. C5a causes plaques to break free from where they would be anchored to ultimately cause blockages elsewhere in the body. This new discovery not only shows that C5a is a new marker for identifying risk for heart attack and stroke, but it also establishes C5a as a new therapeutic target for preventing these problems.. Given the huge impact of cardiovascular disease in general, and atherosclerosis in particular, on public health, we feel that unraveling mechanisms involved in the development and progression of the ...
Patzelt, J.; Mueller, K. A. L.; Breuning, S.; Karathanos, A.; Schleicher, R.; Seizer, P.; Gawaz, M.; Langer, H. F.; Geisler, T. ...
gi,119370332,sp,P01024.2,CO3_HUMAN RecName: Full=Complement C3; AltName: Full=C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1; Contains: RecName: Full=Complement C3 beta chain; Contains: RecName: Full=Complement C3 alpha chain; Contains: RecName: Full=C3a anaphylatoxin; Contains: RecName: Full=Acylation stimulating protein; Short=ASP; AltName: Full=C3adesArg; Contains: RecName: Full=Complement C3b alpha chain; Contains: RecName: Full=Complement C3c alpha chain fragment 1; Contains: RecName: Full=Complement C3dg fragment; Contains: RecName: Full=Complement C3g fragment; Contains: RecName: Full=Complement C3d fragment; Contains: RecName: Full=Complement C3f fragment; Contains: RecName: Full=Complement C3c alpha chain fragment 2; Flags: ...
Background and Purpose: Inflammation seems to be a key player in the pathophysiology of stroke. In this study, we compared plasma C3 and C3a levels in cryptogenic and large-vessel disease (LVD) subtypes of ischemic stroke and control subjects and evaluated their association to outcome at 3 months and 2 years. Methods: C3 and C3a levels in plasma of 79 cryptogenic stroke and 73 LVD stroke patients, sampled within 10 days and at 3 months after stroke, and age- and sex-matched control subjects from the Sahlgrenska Academy Study on Ischemic Stroke were measured by ELISA. Functional outcome was assessed with the modified Rankin Scale. Results: Plasma C3 was increased in both stroke groups at both time points. Systemic elevation of C3a was limited to the acute phase in the cryptogenic stroke group, whereas plasma C3a levels in the LVD group were also elevated at the 3-month follow-up. In the LVD group, plasma C3 levels in the upper third at the 3-month follow-up were associated with an unfavorable ...
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Results : CNV resulted in an increase in splenic IL-17-producing γδT- and Th17-cells; yet in the CNV eye, only elevated levels of γδT-cells could be observed. Administration of anti-C5 or anti-C5a-blocking antibodies to reduce levels of C5a production in the eye, blunted the CNV-induced production of splenic Th17- and γδT-cells, reduced CNV size (anti-C5: 3666 ± 359.9 pixels; anti-C5a: 3453 ± 253.8) when compared to control (12B4: 5572 ± 630.6; p ≤ 0.01) and eliminated ocular γδT-cell infiltration. In ARPE-19 cell monolayers, IL-17 triggered a pro-inflammatory state; and T-cell proliferation was elevated in response to ocular proteins Conclusions : Taken together, we demonstrated that CNV lesions trigger a systemic immune response, augmenting local ocular inflammation via the infiltration of IL-17-producing γδT-cells, which are presumably recruited to the eye in a C5a-dependent manner. Finally, understanding complement-mediated pathological mechanisms will aid in the development ...
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This test measures the amount of C3 proteins in your blood. C3 proteins are part of your immune system. This test can help diagnose lupus.
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Esophageal carcinoma is a common malignancy worldwide, with a low 5‑year survival rate. As the majority of cases are diagnosed at an advanced stage, there is an urgent need for an effective biomarker for early diagnosis of esophageal cancer patients. Surface‑enhanced laser desorption ionization time‑of‑flight mass spectrometry (SELDI‑TOF‑MS) was applied to detect the serum protein expression in esophageal cancer patients using ProteinChip software, and the results were analyzed and screened using Biomarker Patterns and SPSS16.0 software. The ELISA method was conducted to determine the concentration of anaphylatoxin C3a, which is one of the complement proteins, in the serum of esophageal cancer patients and non‑esophageal cancer participants. A total of 144 effective differential expression protein peaks in the window of 1‑10 kDa were obtained ( ...
In addition to being a component of innate immunity and an ancient defense mechanism against invading pathogens, complement activation also participates in the adaptive immune response, inflammation, hemostasis, embryogenesis, and organ repair and development. Activation of the complement system via classical, lectin, or alternative pathways generates anaphylatoxins (C3a and C5a) and membrane attack complex (C5b-9) and opsonizes targeted cells. Complement activation end products and their receptors mediate cell-cell interactions that regulate several biological functions in the extravascular tissue. Signaling of anaphylatoxin receptors or assembly of membrane attack complex promotes cell dedifferentiation, proliferation, and migration in addition to reducing apoptosis. As a result, complement activation in the tumor microenvironment enhances tumor growth and increases metastasis. In this Review, I discuss immune and nonimmune functions of complement proteins and the tumor-promoting effect of ...
In addition to being a component of innate immunity and an ancient defense mechanism against invading pathogens, complement activation also participates in the adaptive immune response, inflammation, hemostasis, embryogenesis, and organ repair and development. Activation of the complement system via classical, lectin, or alternative pathways generates anaphylatoxins (C3a and C5a) and membrane attack complex (C5b-9) and opsonizes targeted cells. Complement activation end products and their receptors mediate cell-cell interactions that regulate several biological functions in the extravascular tissue. Signaling of anaphylatoxin receptors or assembly of membrane attack complex promotes cell dedifferentiation, proliferation, and migration in addition to reducing apoptosis. As a result, complement activation in the tumor microenvironment enhances tumor growth and increases metastasis. In this Review, I discuss immune and nonimmune functions of complement proteins and the tumor-promoting effect of ...
Complement C3-C5 Convertases: Serine proteases that cleave COMPLEMENT C3 into COMPLEMENT C3A and COMPLEMENT C3B, or cleave COMPLEMENT C5 into COMPLEMENT C5A and COMPLEMENT C5B. These include the different forms of C3/C5 convertases in the classical and the alternative pathways of COMPLEMENT ACTIVATION. Both cleavages take place at the C-terminal of an ARGININE residue.
Effect of Fructose on Postprandial Triglycerides: A Systematic Review and Meta-Analysis of Controlled Feeding Trials Academic Article ...
This gene encodes a G-protein coupled receptor 1 family member involved in the complement system of the innate immune response. Unlike classical G-protein coupled receptors, the encoded protein does not associate with intracellular G-proteins. It may instead modulate signal transduction through the beta-arrestin pathway, and may alternatively act as a decoy receptor. This gene may be involved in coronary artery disease and in the pathogenesis of sepsis. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Nov 2012 ...
Complement C5 (C3 And PZP Like Alpha 2 Macroglobulin Domain Containing Protein 4 or C5) - Pipeline Review, H2 2017 Download the full report: https://www.
https://luminusdiagnostics.com/wp-content/uploads/2016/09/Luminus-Full-color-header-1.png 0 0 Daniel Battaglia https://luminusdiagnostics.com/wp-content/uploads/2016/09/Luminus-Full-color-header-1.png Daniel Battaglia2018-10-01 20:08:262018-12-11 20:21:53COMPLEMENT C3 ...
C3a is an anaphylatoxin that triggers a response by stimulating inflammatory cells to release histamine, enzymes, cytokines and other mediators.
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Glomerular mesangial cells (MCs) are central to the pathogenesis of progressive glomeruli-associated renal diseases. However, molecular mechanisms underlying changes in MC functions still remain poorly understood. Here, we show that in MCs, the urokinase-type plasminogen activator (uPA) induces, via its specific receptor (uPAR, CD87), upregulated expression of the complement anaphylatoxin C5a receptor (C5aR, CD88), and modulates C5a-dependent functional responses. This effect is mediated via the interaction of the uPA-specific receptor (uPAR, CD87) and gp130, a signal transducing subunit of the receptor complexes for the IL-6 cytokine family. The Janus kinase Tyk2 and the transcription factor Stat3 serve as downstream components in the signaling cascade resulting in upregulation of C5aR expression. In vivo, expression of C5aR and uPAR was increased in the mesangium of wild-type mice in a lipopolysaccharide (LPS)-induced model of inflammation, whereas in uPAR -/- animals C5aR expression remained ...
C3a and C5a anaphylatoxins are two proinflammatory peptides generated during complement activation that act through distinct G$_i$ protein-coupled receptors named C3aR and C5aR, respectively. We have demonstrated previously that human astrocytes expressed C3aR and C5aR constitutively and were able to produce a functional complement. In this study, we examined the effect of an anaphylatoxin stimulation on cytokine expression by human astrocyte cell lines. Interleukin (IL)-1$\beta$, IL-6, tumor necrosis factor-\alpha$, and transforming growth factor-$\beta$ mRNA expression was studied by quantitative RT-PCR. Whereas IL-1$\beta$, tumor necrosis factor-$\alpha$, and transforming growth factor-$\beta$ mRNA levels remained unchanged, stimulation of astrocytoma cells (T98G, CB193, U118MG) by C3a, C5a, and peptidic C3aR and C5aR agonists induced an increase in the IL-6 mRNA level. The amount of IL-6 was markedly increased at 3 and 6 h and returned to the basal level at 9 h of stimulation. This response was
Genome-wide association studies have identified GALNT2 as a candidate gene in lipid metabolism, but it is not known how the encoded enzyme ppGalNAc-T2, which contributes to the initiation of mucin-type O-linked glycosylation, mediates this effect. In two probands with elevated plasma high-density lipoprotein cholesterol and reduced triglycerides, we identified a mutation in GALNT2. It is shown that carriers have improved postprandial triglyceride clearance, which is likely attributable to attenuated glycosylation of apolipoprotein (apo) C-III, as observed in their plasma. This protein inhibits lipoprotein lipase (LPL), which hydrolyses plasma triglycerides. We show that an apoC-III-based peptide is a substrate for ppGalNAc-T2 while its glycosylation by the mutant enzyme is impaired. In addition, neuraminidase treatment of apoC-III which removes the sialic acids from its glycan chain decreases its potential to inhibit LPL. Combined, these data suggest that ppGalNAc-T2 can affect lipid metabolism ...
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Walk-In Labs complement C3 serum test helps determine causes of recurrent infections, autoimmune disorders & more. A cheap, convenient online blood test.
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Content - SummaryComplement C5 (C3 And PZP Like Alpha 2 Macroglobulin Domain Containing Protein 4 or C5) pipeline Target constitutes close to 33 molec
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GPCRs play important roles in cell signaling pathways. Their dysfunction causes many human developmental and metabolic disorders, as well as certain cancers. However, being a membrane protein, it is difficult to obtain the 3D crystal structures of GPCRs for virtual screening of ligands by molecular docking. We evaluated the virtual screening performance of homology models of 19 human GPCRs with respect to the corresponding crystal structures, suggesting that ligand candidates predicted with consensus scores from multiple models can be the optimal option in practical applications where the performance of each model cannot be estimated. Meanwhile, in collaboration with Dr. Cheng Zhang from the University of Pittsburgh, we contributed to the determination of crystal structures of GPCRs including a lipid GPCR CRTH2 as the receptor for prostaglandin D2, the C5a receptor (C5aR) that can induce strong inflammatory events in response to the anaphylatoxin C5a peptide, and N-formyl peptide receptor 2 ...
The Candida antigen CR3-RP (complement receptor 3-related protein) is supposed to be a mimicry protein because of its ability to bind antibody directed against the α subunit of the mammalian CR3 (CD11b/CD18). This study aimed to (i) investigate the specific humoral isotypic response to immunization with CR3-RP in vivo in a rabbit animal model, and (ii) determine the role of CR3-RP in the adherence of Candida albicans in vitro using the model systems of buccal epithelial cells (BECs) and biofilm formation. The synthetic C. albicans peptide DINGGGATLPQ corresponding to 11 amino-acids of the CR3-RP sequence DINGGGATLPQALXQITGVIT, determined by N-terminal sequencing, was used for immunization of rabbits to obtain polyclonal anti-CR3-PR serum and for subsequent characterization of the humoral isotypic response of rabbits. A significant increase of IgG, IgA and IgM anti-CR3-RP specific antibodies was observed after the third (P<0.01) and the fourth (P<0.001) immunization doses. The elevation of IgA
Cleavage of C5 requires complement fragment C3b which binds C5 and renders it susceptible to cleavage by the C4b,2a complex. Includes former EC 3.4.21.44. Complement component C2a is in peptidase family S1 (trypsin family). Links to other databases: BRENDA, EXPASY, KEGG, MEROPS, Metacyc, PDB, CAS registry number: 56626-15-4. References 1. Kerr, M.A. The second component of human complement. Methods Enzymol. 80 (1980) 54-64. [PMID: 7043188]. 2. Müller-Eberhard, H.J. Molecular organization and function of the complement system. Annu. Rev. Biochem. 57 (1988) 321-347. [PMID: 3052276]. ...
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Protects the body from potent vasoactive and inflammatory peptides containing C-terminal Arg or Lys (such as kinins or anaphylatoxins) which are released into the circulation.
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Complement C6 Polyclonal Antibody from Invitrogen for Western Blot and Immunohistochemistry (Frozen) applications. This antibody reacts with Mouse samples. Supplied as 100 µg purified antibody (0.1 mg/ml) in PBS with 0.1% BSA and 0.02% sodium azide.
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The complement system is an important part of the humoral response in innate immunity, consisting of three different pathways. The third complement…
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Complement peptide C5a, C4a, and C3a receptors". Pharmacological Reviews. 65 (1): 500-43. doi:10.1124/pr.111.005223. PMID ... The C5a receptor also known as complement component 5a receptor 1 (C5AR1) or CD88 (Cluster of Differentiation 88) is a G ... Complement component 5a for binding mechanism GRCh38: Ensembl release 89: ENSG00000197405 - Ensembl, May 2017 GRCm38: Ensembl ... Brennan FH, Gordon R, Lao HW, Biggins PJ, Taylor SM, Franklin RJ, Woodruff TM, Ruitenberg MJ (April 2015). "The Complement ...
The anaphylatoxins C3a, C4a, and C5a are cationic fragments generated during the complement cascade that participate in host ... Complement peptide C5a, C4a, and C3a receptors". Pharmacol. Rev. 65 (1): 500-43. doi:10.1124/pr.111.005223. PMID 23383423. Ohno ... "Complement Peptide Receptors: C5a2". IUPHAR Database of Receptors and Ion Channels. International Union of Basic and Clinical ... Cain SA, Monk PN (2002). "The orphan receptor C5L2 has high affinity binding sites for complement fragments C5a and C5a des-Arg ...
... bacteria-induced complement activation also causes the formation of complement component 3a (C3a) by cleavage from complement ... Complement peptide C5a, C4a, and C3a receptors". Pharmacological Reviews. 65 (1): 500-43. doi:10.1124/pr.111.005223. PMID ... the C3a receptor, whose gene is located at chromosome 12p13; C3a also acts through C5L2. Mouse formyl peptide receptor genes ... Paral D, Sohns B, Crass T, Grove M, Köhl J, Klos A, Bautsch W (Aug 1998). "Genomic organization of the human C3a receptor". ...
C3a and C5a, proteins produced from the complement system, attract neutrophils to the vessels. Once activated, neutrophils then ... immune complexes deposit in vessel walls leading to activation of the complement system. ...
"Complement fragment C3a controls mutual cell attraction during collective cell migration". Developmental Cell. 21 (6): 1026-37 ... C3a in neural crest cells), that stimulates other cells in the group that have the receptors to that chemo-attractant. Cells ...
C3a - the other fragment C3 is cleaved into along with C3b Liszewski, M. Kathryn; Atkinson, John P. (2015-06-10). "Complement ... The C1 complement complex binds to these antibodies resulting in its activation via cross proteolysis. This activated C1 ... C3b is the larger of two elements formed by the cleavage of complement component 3, and is considered an important part of the ... In the alternative pathway, C3, present in the blood stream, spontaneously cleaves at low rates into C3b and C3a. If a microbe ...
Complement 3 (C3) through its interaction with factors B and D (adipsin) generates C3a. In the human body, C3a is rapidly ... Complement peptide C5a, C4a, and C3a receptors". Pharmacol. Rev. 65 (1): 500-43. doi:10.1124/pr.111.005223. PMID 23383423. ... The view of C3a/C3adesArg as an acylation stimulating activity is not universally accepted. The evidence is discussed in a ... Thus, most of plasmatic C3a is present in C3adesArg form. C3adesArg is more commonly named ASP or acylation-stimulating-protein ...
"Europium-Labeled Synthetic C3a Protein as a Novel Fluorescent Probe for Human Complement C3a Receptor" (PDF). Bioconjugate ... β2-adrenergic receptor and C3a receptor. The emitted photons from excited lanthanides are detected by highly sensitive devices ...
Isohemagglutinins also activate the complement cascade via C3a and C5a, which then promote inflammatory cytokine release from ...
C3a, C5a, IL-8 are all chemotactic factors of the activated complement system. Part of their role is to recruit ... or complement mediated. They then looked at the complement factors and immunoglobulin deposits to identify the underlying cause ... Inactive and active complement proteins that split fragments are found in the glomeruli. There are currently drugs available ... There are no current clinical trials for DPGN happening.[citation needed] Activating complement pathways plays a large role in ...
C3a, C4a and C5a) that are produced as part of the activation of the complement system. Complement components C3, C4 and C5 are ... C3a works with C5a to activate mast cells, recruit antibody, complement and phagocytic cells and increase fluid in the tissue, ... coded for by a single exon within the complement protein gene. The C3a, C4a and C5a components are referred to as ... This term is reserved only for fragments of the complement system. C3, C4A, C4B, C4B-1, C5, FBLN1, FBLN2 Allergy Anaphylatoxin ...
His work also confirmed that an anaphylatoxin molecule of complement activation "C3a" enhances intestinal stem cell expansion, ... Tsokos established the role of complement activation in tissue injury and regeneration. His findings demonstrated for the first ... deposition of C4d and C5b-9 in human subjects of trauma and patients with severe trauma maintain high deposition of complement ...
Cleavage of complement C3 by a free floating convertase, thrombin, plasmin or even a bacterial enzyme leads to formation of C3a ... DAF protects host cells from damage by autologous complement. DAF acts on C2b and Bb and dissociates them rapidly from C4b and ... Hourcade D (2006). "The Role of Properdin in the Assembly of the Alternative Pathway C3 Convertases of Complement". J Biol Chem ... Hourcade D, Holers VM, Atkinson JP (1989). "The regulators of complement activation (RCA) gene cluster". Adv Immunol. Advances ...
... can cleave multiple C3 proteins into C3a and C3b. The complex is believed to be unstable until it binds properdin, a serum ... there are several different kinds of regulatory proteins that disrupt the complement activation process: *Complement Receptor 1 ... Complement Factor H can inhibit the formation of the C3 convertase by competing with factor B for binding to C3b;[1] accelerate ... "Inhibition of the alternative complement pathway by antisense oligonucleotides targeting complement factor B improves lupus ...
... complement components C5a and C3a which are chemotactic factors formed during the activation of the host's blood complement ...
... s have a variety of specific receptors, including ones for complement, cytokines like interleukins and IFN-γ, ... C3a, C5a, and Leukotriene B4, which these cells use to direct the path of their migration. ...
Antibodies are produced against the RBCs, which leads to complement activation. Complement fragments, such as C3a, C4a and C5a ... Cases may also arise with complement alone or with IgA, IgM or a combination of these three antibody classes and complement. ... IgM is a potent activator of the classical complement pathway, thus, AIHA involving IgM is characterized by complement mediated ... When these RBCs return to central regions, they are damaged by complement. Patients may present with one or both types of ...
... 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 c3a MeSH D12.776.124.486.274.024.260 - complement c4a MeSH D12.776.124.486.274.024.270 - complement c5a MeSH D12.776 ... 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. ...
The structure of an AT module was determined for the complement-derived anaphylatoxin C3a, and was found to be a compact alpha- ...
... histamine-inducers Complement proteins C3a, C4a, and C5a work by triggering histamine release from mast cells and basophil ...
The cause of damage is as a result of the action of cleaved complement anaphylotoxins C3a and C5a, which, respectively, mediate ... are far more capable of interacting with complement; these medium-sized complexes, formed in the slight excess of antigen, are ... leading to small immune complexes being formed that fix complement and are not cleared from the circulation. It involves ...
The aureolysin derived C3a and C3b are further degraded by host complement inhibitor factor H and I. In the lectin pathway, ... Of all the proteases, aureolysin is the most effective against the complement cascade. In all three pathways of complement ... The active site has a high affinity for C3 and will cleave it into C3a and C3b however, the protein is cleaved two amino acid ... Further immune evasion outside of the complement system occurs in various ways. Aureolysin cleaves and inactivates protease ...
Activation of complement primarily results in cleavage of soluble complement proteins forming C5a and C3a, which activate ... An Arthus reaction is a local vasculitis associated with deposition of immune complexes and activation of complement. Immune ...
C3a / C3b / iC3b C5 - C5a C3-convertase C5-convertase Late stage Membrane attack complex (MAC) C6 C7 C8 C9 Complement pathway ... system Complement system Classical complement pathway Mannan-binding lectin pathway Alternate complement pathway Complement ... Complement receptor of the immunoglobulin family) Anaphylatoxin receptors C3a receptor C5a receptor (CD88) C5AR2 Fc receptor Fc ... see complement proteins section) Collectins Mannan-binding lectin (MBL) Surfactant protein A (SP-A) Surfactant protein D (SP-D ...
Complement Peptide C5a, C4a, and C3a Receptors". Pharmacological Reviews. 65 (1): 500-43. doi:10.1124/pr.111.005223. PMID ... 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 ... Three biochemical pathways activate the complement system: the classical complement pathway, the alternative complement pathway ...
... may refer to: C3a (complement) C3a receptor 3 CaO • Al2O3, Tricalcium aluminate in cement chemist notation This ...
"Characterization of synthetic C3a analog peptides on human eosinophils in comparison to the native complement component C3a". ... is a G protein-coupled receptor protein involved in the complement system. The receptor binds to complement component C3a, ... Complement peptide C5a, C4a, and C3a receptors". Pharmacological Reviews. 65 (1): 500-43. doi:10.1124/pr.111.005223. PMID ... The C3a receptor also known as complement component 3a receptor 1 (C3AR1) ...
Complement peptide C5a, C4a, and C3a receptors". Pharmacological Reviews. 65 (1): 500-43. doi:10.1124/pr.111.005223. PMID ... Polymorphisms of complement component 3, complement factor B, and complement factor I, as well as deletion of complement factor ... The complement system, also known as complement cascade, is a part of the immune system that enhances (complements) the ability ... Three biochemical pathways activate the complement system: the classical complement pathway, the alternative complement pathway ...
C3a is one of the proteins formed by the cleavage of complement component 3; the other is C3b. C3a is a 77 residue ... C3a molecules induce responses through the GPCR C3a receptor. Like other anaphylatoxins, C3a is regulated by cleavage of its ... C3a has a regulatory process and a structure homologous to complement component C5a, with which it shares 36% of its sequence ... C3a formation occurs through activation and cleavage of complement component 3 in a reaction catalyzed by C3-convertase. There ...
Zipfel, P. F., Hallström, T., & Riesbeck, K. (2013). Human complement control and complement evasion by pathogenic microbes- ... C3 laguneb produktideks C3a ja C3b, mis käivitavad edasiste reaktsioonide kaskaadi. Komplemendisüsteemi osade hulka kuulub ka ... 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. ...
... (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 ...
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 ...
... s have a variety of specific receptors, including ones for complement, cytokines like interleukins and IFN-γ, ... C3a, C5a, and Leukotriene B4, which these cells use to direct the path of their migration. ...
4,0 4,1 Rosa PA, Ogata RT, Zepf NE (1989). "Sequence of the gene for murine complement component C4". J. Biol. Chem. 264 (28): ... C3a, C4a i C5a komponente se nazivaju anafilatoksinima.[4][5] Oni izazivaju kontrakcije glatkih mišića, otpuštanje histamina iz ... Anafilatoksini, ili anafilotoksini, su fragmenti (C3a, C4a i C5a) koji se formiraju tokom aktivacije sistema komplementa[2]. ... Hugli TE (1986). "Biochemistry and biology of anaphylatoxins". Complement 3 (3): 111-27. PMID 3542363. ...
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. ...
Complement component 1r. *Complement component 1s. *Cyclin D2. *Cystic fibrosis transmembrane conductance regulator ...
Anafilatoksin (C3a, C5a) • Angiotenzin (1, 2) • Apelin • Bombezin (BRS3, GRPR, NMBR) • Bradikinin (B1, B2) • Hemokin • ... Sengeløv H (1996). "Complement receptors in neutrophils.". Crit. Rev. Immunol. 15 (2): 107-31. PMID 8573284. ... 1996). "Molecular cloning and characterization of the human anaphylatoxin C3a receptor.". J. Biol. Chem. 271 (34): 20231-4. ... "Function, structure and therapeutic potential of complement C5a receptors". British Journal of Pharmacology 152 (4): 429-48. ...
a b https://www.britannica.com/science/complement-immune-system-component *↑ a b c d e f g h i OpenStax, Microbiology, openstax ... 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 ... Sîstema temamker an jî sîstema tewawker (bi îngilîzî: complement system)[1] beşek ji sîstema bergiriya giştî ye. Sîstema ...
Complement receptors. *CR1. *CR2. *CR3. *CR4. *CD11b/CD11c/CD18. *Anaphylatoxin *C3a. *C5a ...
Decay accelerating factor (DAF/CD55), a regulatory protein of the complement cascade, interacts with the first and second EGF- ...
C3a is an anaphylotoxin and the precursor of some cytokines such as ASP, and C3b serves as an opsonizing agent. Factor I can ... Complement component 3, often simply called C3, is a protein of the immune system. It plays a central role in the complement ... "Entrez Gene: C3 complement component 3". Sahu A, Lambris JD (Apr 2001). "Structure and biology of complement protein C3, a ... In the alternative complement pathway, C3 is cleaved by C3bBb, another form of C3-convertase composed of activated forms of C3 ...
Complement peptide C5a, C4a, and C3a receptors". Pharmacological Reviews. 65 (1): 500-43. doi:10.1124/pr.111.005223. PMID ... Complement peptide C5a, C4a, and C3a receptors". Pharmacological Reviews. 65 (1): 500-43. doi:10.1124/pr.111.005223. PMID ... C5a is a protein fragment released from cleavage of complement component C5 by protease C5-convertase into C5a and C5b ... September 2002). "Complement-induced impairment of innate immunity during sepsis". Journal of Immunology. 169 (6): 3223-31. doi ...
1996). "Molecular cloning and characterization of the human anaphylatoxin C3a receptor". J. Biol. Chem. 271 (34): 20231-4. doi: ... Complement component 5 is involved in the complement system. It is cleaved into C5a and C5b: C5a plays an important role in ... Complement component 5 is the fifth component of complement, which plays an important role in inflammatory and cell killing ... 2008). "Structure of and influence of a tick complement inhibitor on human complement component 5". Nat Immunol. 9 (7): 753-60 ...
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 peptide C5a, C4a, and C3a receptors". Pharmacological Reviews. 65 (1): 500-43. doi:10.1124/pr.111.005223. PMID ... Complement component 4 (C4), in humans, is a protein involved in the intricate complement system, originating from the human ...
C3a is an anaphylatoxin that triggers a response by stimulating inflammatory cells to release histamine, enzymes, cytokines and ... C3a. C3a is a one of the peptides (complement split products) formed by the cleavage of complement component 3. C3a is an ... The ELISA method is sensitive and specific for C3a, using monoclonal anti-C3a antibodies to capture C3a on the 96-well ELISA ... Through these mediators C3a can induce changes in the vascular permeability and local blood flow. It has been shown to be a ...
C3a is one of the proteins formed by the cleavage of complement component 3; the other is C3b. C3a is a 77 residue ... C3a molecules induce responses through the GPCR C3a receptor. Like other anaphylatoxins, C3a is regulated by cleavage of its ... C3a has a regulatory process and a structure homologous to complement component C5a, with which it shares 36% of its sequence ... C3a formation occurs through activation and cleavage of complement component 3 in a reaction catalyzed by C3-convertase. There ...
complement components 3/5;. C3a/5a,. bioactive fragments of C3/5;. C3aR/5aR,. Cea/5a receptors;. RPE,. retinal pigmented ... Drusen complement components C3a and C5a promote choroidal neovascularization. Miho Nozaki, Brian J. Raisler, Eiji Sakurai, J. ... Drusen complement components C3a and C5a promote choroidal neovascularization. Miho Nozaki, Brian J. Raisler, Eiji Sakurai, J. ... Drusen complement components C3a and C5a promote choroidal neovascularization. Miho Nozaki, Brian J. Raisler, Eiji Sakurai, J. ...
Since there is complement activation in all areas of tissue injury, and both C3a and C5a activate MSC, it was asked whether ... when supernatants from C3a-stimulated MSC were used, while C3a itself had no direct angiogenic effect on HUVECs. The signaling ... C3a caused significant up-regulation of various angiogenic factors, including VEGF, CXCL8/IL-8 and IL-6. In contrast there was ... Furthermore the production of angiogenic factors induced by C3a was of physiological relevance: Supernatants of MSCs cultured ...
... single chain C3a complement component. It has many biological activities, such as smooth muscle contraction, platelet ... More,, Complement C3a, Human, is a native, single chain C3a complement component. It has many biological activities, such as ... Complement C3a, Human, is a native, single chain C3a complement component. It has many biological activities, such as smooth ... Native, human C3a complement component. Single chain, 77 amino acid peptide. Activation of either complement pathway can result ...
C3a without the COOH-terminal arginine at the 77-position; also known as the acylation-stimulating protein or ASP; a paracrine ... complement C3a, des-Arg-(77); C3a des-Arg; C3a des-Arg(77); C3a des-Arg77; complement 3a, des-Arg-; complement 3a, des-arginine ... Complement System Proteins: 21537*Complement C3: 812*Complement C3a: 43*des-Arg-(77) complement C3a: 14 ... des-Arg-(77) complement C3a. Subscribe to New Research on des-Arg-(77) complement C3a ...
Complement activation leads to the concomitant generation of C3a and C5a in vivo, and concentrations of C3a exceed ... Complement fragment C3a stimulates Ca2+ influx in neutrophils via a pertussis toxin sensitive G protein. Eur. J. Biochem. 217: ... Complement C3a and C5a Induce Different Signal Transduction Cascades in Endothelial Cells. Ingrid U. Schraufstatter, Khanh ... Complement activation leads to the production of the anaphylatoxins C3a and C5a, which are basic polypeptides of 74-77 aa ...
Mouse Monoclonal Anti-Complement C3a Antibody (K13/16-5.7) [Alexa Fluor® 405]. Validated: WB, ELISA, ICC/IF, IHC, IHC-P. Tested ... Home » Complement C3a » Complement C3a Antibodies » Complement C3a Antibody (K13/16-5.7) [Alexa Fluor® 405] ... Blogs on Complement C3a. There are no specific blogs for Complement C3a, but you can read our latest blog posts. ... PTMs for Complement C3a Antibody (NBP1-05122AF405). Learn more about PTMs related to Complement C3a Antibody (NBP1-05122AF405). ...
... Pasupuleti, Mukesh LU ; ... Human C3a and C4a (but not C5a) were antimicrobial, in... (More). The human anaphylatoxin peptide C3a, generated during ... article{9d06ba00-5f88-4746-895e-2c5bbf9fe49b, abstract = {The human anaphylatoxin peptide C3a, generated during complement ... The human anaphylatoxin peptide C3a, generated during complement activation, exerts antimicrobial effects. Phylogenetic ...
Regulation by complement C3a and C5a anaphylatoxins of cytokine production in human umbilical vein endothelial cells. FASEB J. ... Complement c3a and c5a induce different signal transduction cascades in endothelial cells. J. Immunol. 169: 2102-2110. ... C3a powerfully increased P-selectin expression and reduced TM on the HMEC-1 surface, indicating a major role for C3a as a ... These results identify Stx-induced complement activation, via P-selectin, as a key mechanism of C3a-dependent microvascular ...
Complement activation via a C3a receptor pathway alters CD4+ T lymphocytes and mediates lung cancer progression. Jeff W Kwak, ... Complement activation via a C3a receptor pathway alters CD4+ T lymphocytes and mediates lung cancer progression ... Complement activation via a C3a receptor pathway alters CD4+ T lymphocytes and mediates lung cancer progression ... Complement activation via a C3a receptor pathway alters CD4+ T lymphocytes and mediates lung cancer progression ...
The "C" in C3a and C4a stands for complement. Complement proteins work with antibodies to destroy pathogens. They activate ... Role of C3a and C4a Complement Proteins in Chronic Lyme Disease​ August 12, 2014 in Science/Research by Ginger Savely, DNP ... The C3a complement protein level was normal in the AIDS patients, the healthy patients and the chronic Lyme patients. So, ... Patients often ask if there are other medical conditions that may lower or raise the C3a and/or C4a. Both of these complement ...
As of September 2016, FDA Guidance release recommends the use of the SC5b9 Complement Activation Assay ... The effects evaluated include adverse reactions such as thrombosis, hemolysis, platelet, leukocyte, and complement activation, ...
Objective To investigate expression of terminal complement components C3a and C5a on circulating myeloperoxidase (MPO)-positive ... Microparticles expressing myeloperoxidase and complement C3a and C5a as markers of renal involvement in antineutrophil ... Microparticles expressing myeloperoxidase and complement C3a and C5a as markers of renal involvement in antineutrophil ... Microparticles expressing myeloperoxidase and complement C3a and C5a as markers of renal involvement in antineutrophil ...
C3a des-Arg Antibody (clone 2991) for WB/Western LS-C140007 ... Human C3a des-Arg. Specificity:. Human Complement C3a/C3a des- ... Most Popular Complement C3a / C3a des-Arg Antibodies. Anti-Complement C3a / C3a des-Arg Antibody (clone 2991) LS-C140007 ... About Complement C3a / C3a des-Arg. Description:. C3a is one of the proteins formed by the cleavage of complement component 3; ... Mouse Monoclonal [clone 2991] (IgG1) to Human Complement C3a / C3a des-Arg. ...
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). ... Expression of the complement anaphylatoxin C3a and C5a receptors on bronchial epithelial and smooth muscle cells in models of ... C3a, C4a, and C5a (CD88) receptors. Receptors for C3a and C5a have been identified; whether a distinct receptor for C4a is ...
C3a). No significant cross-reactivity or interference between Complement Component 3a (C3a) and analogues was observed. ... Intra-assay Precision (Precision within an assay): 3 samples with low, middle and high level Complement Component 3a (C3a) were ... Inter-assay Precision (Precision between assays): 3 samples with low, middle and high level Complement Component 3a (C3a) were ... This assay has high sensitivity and excellent specificity for detection of Complement Component 3a ( ...
... is an octapeptide corresponding to the COOH terminus of C3a, exhibits the specificity and 1 to 2% biologic activities of C3a ... C3a (70-77) selectively desensitizes ileal smooth muscle to C3a but not to human C5a, a related anaphylatoxin. Conversely, C3a ... C3a 70-77 (Synonyms: Complement 3a (70-77)). Cat. No.: HY-P1505 Data Sheet Handling Instructions ... C3a or C3a(70-77) is introduced into some suspensions at the same time as the stimulus or buffer. After 3 d for the mitogen- ...
Complement C3a Receptor 1, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human ... complement component C3a receptor activity. IEA,IDA. 10571060. GO:0004930. G protein-coupled receptor activity. IEA,IPI. ... C3a is an anaphylatoxin released during activation of the complement system. The protein encoded by this gene is an orphan G ... C3a is an anaphylatoxin released during activation of the complement system. The protein encoded by this gene is an orphan G ...
Mechanical injury to the skin results in activation of the complement component C3 and release of the anaphylatoxin C3a. C3a ... Production of the complement cleavage product, C3a, by activated macrophages and its tumorolytic effects. Clin. Exp. Immunol. ... Absence of the complement anaphylatoxin C3a receptor suppresses Th2 effector functions in a murine model of pulmonary allergy. ... C3a inhibition of IL-4 production is mediated by IL-12. (A) C3a induces IL-12 p70 secretion by BALB/c splenic DCs. (B) ...
Measurements of C3a. Formation of C3a was quantitated by BD OptEIA ELISA for human C3a (BD PharMingen). 1 ml PRP (platelet ... Activation of complement on activated platelets. (A) Generation of C3a by activated platelets. 1 ml PRP was stimulated with ... C3a generation in activated platelets. As an additional test of whether platelets activate complement, we examined generation ... P-Selectin activates the complement system. C3a generation.. The data described before identified P-selectin as a C3b-binding ...
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). ... This protein plays a key role in a part of the bodys immune response known as the complement system. The complement system is ... One of these pieces, called C3b, interacts with several other proteins on the surface of cells to trigger the complement ...
We recently demonstrated the roles of complement C3a and extracellular matrix (ECM) turnover in an in vitro model for deposit ... Rosario Fernandez-Godino, Donita Garland, Eric A Pierce; Complement C3a causes human RPE cells to make basal deposits in vitro ... Complement C3a causes human RPE cells to make basal deposits in vitro ... Complement C3a causes human RPE cells to make basal deposits in vitro ...
Similarly, application of complement fragments C5a (0.1-10.0 nM) or C3a (100 nM) generates biphasic [Ca2+]i transients composed ... Mechanisms of C5a and C3a complement fragment-induced [Ca2+]i signaling in mouse microglia ... Mechanisms of C5a and C3a complement fragment-induced [Ca2+]i signaling in mouse microglia. ... i signals in response to subsequent complement fragment application. Our data suggest that complement factors induce [Ca2+]i ...
... previous studies indicated that C3a causes mast cell degranulation, at least in part, via a C3a receptor-independent mechanism ... Although human mast cells express G protein coupled receptors for the anaphylatoxin C3a, ... Complement C3a Grant support * R01 HL085774/HL/NHLBI NIH HHS/United States ... We found that C3a, a C3a receptor "superagonist" (E7) and compound 48/80 induced Ca(2+) mobilization and degranulation in a ...
7. Complement System and Toll-Like Receptors. The complement system effectively identifies and clears hazardous agents as well ... J. M. Thurman, A. M. Lenderink, P. A. Royer et al., "C3a is required for the production of CXC chemokines by tubular epithelial ... The complement inhibitor, complement receptor 1-related protein y (Crry), is expressed by proximal renal tubules on the ... "Altered renal tubular expression of the complement inhibitor Crry permits complement activation after ischemia/reperfusion," ...
The gas emulsion was assayed for complement activation using an in-vitro C3a diagnostic kit supplied by Quidel Corp. (San Diego ... indicating that the gas emulsion does not activate complement. It is well known that naked microbubbles activate complement. ... In addition, bubbles created in vivo in this way will be "naked", and consequently will have the complement activation problem ... In addition, "naked" microbubbles have been shown to produce adverse responses such as the activation of complement (See, for ...
The gas emulsion was assayed for complement activation using an in-vitro C3a diagnostic kit supplied by Quidel Corp. (San Diego ... indicating that the gas emulsion does not activate complement. It is well known that naked microbubbles activate complement. ... In addition, bubbles created in vivo in this way will be "naked", and consequently will have the complement activation problem ... In addition, "naked" microbubbles have been shown to produce adverse responses such as the activation of complement (See, for ...
When C3a or C5a is injected into the skin, it elicits an immediate wheal and flare response, similar to that found with ... 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 ... Table 1. Proteins of the Human Complement (C) System, Classical Pathway* *Table 2. Proteins of the Human Complement (C) System ...
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  • Both in patients with AMD and in a recently described mouse model of AMD, early subretinal pigmented epithelium deposition of complement components C3 and C5 occurs, suggesting a contributing role for these inflammatory proteins in the development of AMD. (pnas.org)
  • Complement activation leads to the production of the anaphylatoxins C3a and C5a, which are basic polypeptides of 74-77 aa derived from the α-chains of their parent proteins. (jimmunol.org)
  • Human C3a and C5a were produced after cleavage of their parent proteins, C3 and C5, respectively, using a fluid phase C3/C5 convertase, CVF, and Bb ( 28 ). (jimmunol.org)
  • Complement proteins work with antibodies to destroy pathogens. (publichealthalert.org)
  • There are about 30 of these complement proteins that circulate in the bloodstream making up complement "cascades", so called because activation of one protein initiates activation of the next, etc. (publichealthalert.org)
  • Various proteins of the complement system interact specifically with platelets, which, in turn, activates them and promotes thrombosis. (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 presence of complement components, ECM proteins and other proinflammatory molecules was quantified by inmunofluorescence and ELISA. (arvojournals.org)
  • The accumulation of ECM proteins under the RPE plus the diminished MMP-2 activity in culture media demonstrates that C3a can regulate the ECM formation and turnover by the RPE in vitro . (arvojournals.org)
  • 1 microgram/ml) inhibited both C5a- and C3a-triggered [Ca2+]i responses, suggesting the involvement of PTX-sensitive G-proteins in the signal transduction chain. (mdc-berlin.de)
  • 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)
  • The complement system is one of the major contributors to innate immunity and contains a series of soluble and cell surface proteins, including plasma components, specific receptors and diverse regulators. (nature.com)
  • 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)
  • 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)
  • 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)
  • C3a and C5a, proteins produced from the complement system, attract neutrophils to the vessels. (wikipedia.org)
  • Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case-letter suffixes, e.g. (thefreedictionary.com)
  • C3 and C4, mainly produced by the liver, are the major plasma proteins of the immune system complement pathways. (thermofisher.com)
  • Results of studies published since 2002 reveal that T cells and antigen-presenting cells (APCs) produce complement proteins. (springer.com)
  • 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)
  • Over 30 proteins and protein fragments make up the complement system, including serum proteins , and cell membrane receptors . (wikipedia.org)
  • Most of the proteins and glycoproteins that constitute the complement system are synthesized by hepatocytes . (wikipedia.org)
  • The contribution of the complement cascade to acute inflammation is well established, as is the continuous activation and consumption of complement proteins in chronic inflammatory states ( 7 , 8 ). (aacrjournals.org)
  • Thus, the recent finding that complement proteins C3, C4, and C5a may aid tumor growth through immunosuppression ( 11 ) is unexpected and suggests an insidious and previously unrecognized relationship between the complement system and cancer. (aacrjournals.org)
  • The latter fragment is the critical first protein that combines with C6, C7, C8, and multiple C9 proteins to form the MAC, the terminal, pore-forming complement protein complex responsible for lysis of cells and pathogens. (aacrjournals.org)
  • Additionally, C3b generated by alternative pathway C3 convertase can attach to target surfaces and bind Bb, forming a C3 convertase that amplifies downstream complement proteins locally at the target surface. (aacrjournals.org)
  • The complement system is a network of more than 50 plasma proteins and receptors, which have the role of mediating innate and adaptive host defence mechanisms, whereas they also participate in various (patho)physiological processes. (els.net)
  • The primary functions mediated by complement proteins include phagocytosis of foreign elements (bacteria, viruses, particles etc .), cell lysis, inflammation, solubilisation of immune complexes, apoptotic cell clearance and enhancement of humoral immune responses. (els.net)
  • Complement is a multiprotein network of plasma proteins and cell surface receptors. (els.net)
  • Jun 10, 2002 (CIDRAP News) The smallpox virus has a protein that inhibits the human complement system far more effectively than does its counterpart protein in the closely related vaccinia virus, used in smallpox vaccine, according to researchers who compared the two proteins. (umn.edu)
  • Human complement components C3b and C4b then were incubated with SPICE, VCP, and other complement regulatory proteins. (umn.edu)
  • Because erythrocytes are lysed in the presence of an increasing amount of complement, the test was done by individually placing the two proteins, along with sheep or rabbit erythrocytes, in blood serum samples from the four species and then measuring the extent of hemolysis. (umn.edu)
  • This convertase, the alternative pathway C3-convertase, although only produced in small amounts, can cleave multiple C3 proteins into C3a and C3b. (wikipedia.org)
  • C3a is a 77 residue anaphylatoxin that binds to the C3a receptor (C3aR), a class A G protein-coupled receptor. (wikipedia.org)
  • C3a molecules induce responses through the GPCR C3a receptor. (wikipedia.org)
  • C3a induces an immunological response through a 482 residue G-protein-coupled receptor called C3aR. (wikipedia.org)
  • The C3a receptor binds C3a and C4a. (medscape.com)
  • The protein encoded by this gene is an orphan G protein-coupled receptor for C3a. (genecards.org)
  • Binding of C3a by the encoded receptor activates chemotaxis, granule enzyme release, superoxide anion production, and bacterial opsonization. (genecards.org)
  • C3AR1 (Complement C3a Receptor 1) is a Protein Coding gene. (genecards.org)
  • Gene Ontology (GO) annotations related to this gene include G protein-coupled receptor activity and complement component C3a receptor activity . (genecards.org)
  • Receptor for the chemotactic and inflammatory peptide anaphylatoxin C3a. (genecards.org)
  • 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)
  • Although human mast cells express G protein coupled receptors for the anaphylatoxin C3a, previous studies indicated that C3a causes mast cell degranulation, at least in part, via a C3a receptor-independent mechanism similar to that proposed for polycationic molecules such as compound 48/80. (nih.gov)
  • The purpose of the present study was to delineate the receptor specificity of C3a-induced degranulation in human mast cells. (nih.gov)
  • We found that C3a, a C3a receptor "superagonist" (E7) and compound 48/80 induced Ca(2+) mobilization and degranulation in a differentiated human mast cell line, LAD2. (nih.gov)
  • To delineate the receptor specificity for C3a and compound 48/80 further, we generated stable transfectants expressing MrgX1 and MrgX2 in a rodent mast cell line, RBL-2H3 cells. (nih.gov)
  • one involving the C3a receptor and the other MrgX2. (nih.gov)
  • C3a is a anaphylatoxin that binds to the C3aR receptor. (quidel.com)
  • Cyclic AMP plays a critical role in C3a-receptor-mediated regulation of dendritic cells in antigen uptake and T-cell stimulation. (springer.com)
  • The C5a receptor also known as complement component 5a receptor 1 (C5AR1) or CD88 (Cluster of Differentiation 88) is a G protein-coupled receptor for C5a. (wikipedia.org)
  • It functions as a complement receptor. (wikipedia.org)
  • The C3a receptor (C3aR) has been reported to be involved in various physiological and pathological processes, including the regulation of cellular structure development. (spandidos-publications.com)
  • C3a was initially reported to be involved in the chemotaxis, recruitment and activation of inflammatory cells by binding to the C3a receptor (C3aR) on immune cells ( 3 - 5 ). (spandidos-publications.com)
  • The antibody detects endogenous levels of total C3a Receptor protein. (fishersci.com)
  • This polyclonal antibody was raised in Rabbit against C3AR / C3a Receptor. (fishersci.com)
  • This antibody is useful for testing in the following assays: IHC-P. The specificity of this antibody has been described as follows: Human C3a Receptor. (fishersci.com)
  • We assessed the effect of anaphylatoxin C3a receptor (C3aR) and C5a receptor (C5aR) knockout (KO) on light damage-induced migration of microglia/macrophages into the mouse outer retina via immunofluorescence and real-time quantitative PCR. (molvis.org)
  • Interestingly, S. suis invasion of inner organs was also detectable in C5aR −/− mice, suggesting that chemotaxis and activation of immune cells via the anaphylatoxin receptor C5aR is, in addition to opsonization, a further important function of the complement system in defense against mucosal S. suis infection. (asm.org)
  • Potent cyclic antagonists of the complement C5a receptor on human polymorphonuclear leukocytes. (semanticscholar.org)
  • Complement Receptor C5aR1 Plays an Evolutionarily Conserved Role in Successful Cardiac Regeneration. (semanticscholar.org)
  • Pharmacological inhibition of complement C5a-C5a1 receptor signalling ameliorates disease pathology in the hSOD1G93A mouse model of amyotrophic lateral sclerosis. (semanticscholar.org)
  • The ELISA method is sensitive and specific for C3a, using monoclonal anti-C3a antibodies to capture C3a on the 96-well ELISA plate, and a second enzyme-linked anti-C3a antibody for detection. (nationaljewish.org)
  • We also show that genetic ablation of receptors for C3a or C5a reduces VEGF expression, leukocyte recruitment, and CNV formation after laser injury, and that antibody-mediated neutralization of C3a or C5a or pharmacological blockade of their receptors also reduces CNV. (pnas.org)
  • There are currently no images for Complement C3a Antibody (NBP1-05122AF405). (novusbio.com)
  • 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 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)
  • This antibody reacts with the C-terminus of C3a. (genetex.com)
  • complement fixation the combining of complement with the antigen-antibody complex , rendering the complement inactive, or fixed. (thefreedictionary.com)
  • Ehrlich's term for the thermolabile substance, normally present in serum, that is destructive to certain bacteria and other cells sensitized by a specific complement-fixing antibody. (thefreedictionary.com)
  • The following product was used in this experiment: Complement Polyclonal Antibody from Thermo Fisher Scientific, catalog # RAHU-C. (thermofisher.com)
  • The alternative complement pathway provides innate protection against microbial agents in the absence of specific antibody. (quidel.com)
  • Antibody and complement in transplant vasculopathy. (springer.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)
  • Since its discovery, the complement system has been primarily considered an effector of innate immunity with the ability to "complement" antibody-mediated clearance of foreign pathogens, dispose of dead cells, and cause inflammatory states ( 12 ). (aacrjournals.org)
  • Formalin-Fixed, Paraffin-Embedded Human Placenta tissue stained with Complement C3c Antibody Cat. (acris-antibodies.com)
  • The components of complement system can be organised into three major pathways: The classical pathway is mainly initiated by the binding of C1q to antigen-antibody complexes, whereas the lectin pathway is triggered by binding of mannose‐binding lectin ( MBL ) or ficolins to glycosylated surfaces on microbial cell walls. (els.net)
  • The RIA technique is a sensitive and specific competitive inhibition in vitro assay that utilizes 125-iodine labeled C3a and anti-C3a antibodies. (nationaljewish.org)
  • The classical pathway of complement activation is initiated when the C1 complex, made up of C1r and C1s serine proteases, recognizes the Fc region of IgM or IgG antibodies bound to a pathogen. (wikipedia.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)
  • 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)
  • Like other anaphylatoxins, C3a is regulated by cleavage of its carboxy-terminal arginine, which results in a molecule with lowered inflammatory function (C3a desarginine). (wikipedia.org)
  • Anaphylatoxins are small complement peptides that induce proinflammatory responses in tissues. (wikipedia.org)
  • C3a, one of the three complement-derived anaphylatoxins, expresses a wide variety of biological activities which include smooth muscle contraction, platelet and neutrophil activation and aggregation, skin wheal and flare, and immunoregulatory reactions. (emdmillipore.com)
  • Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. (thefreedictionary.com)
  • As a fundamental component of innate immunity, the complement cascade ( Fig. 1 ) contains some of the most powerful proinflammatory molecules in the body, including most notably the anaphylatoxins C3a and C5a. (aacrjournals.org)
  • The anaphylatoxins C3a and C5a mediate the inflammatory responses of complement. (els.net)
  • These divergent properties of complement anaphylatoxins in the light damage model provide a rationale for testing the differential effects of these receptors in additional retinal and neurodegeneration models. (molvis.org)
  • Identifying mechanisms through which complement anaphylatoxins modulate inflammation in the retina may provide a rationale for targeted drug design. (molvis.org)
  • Here, we seek to elucidate the relationship between complement anaphylatoxins and microglia in the light damage model using C3aR and C5aR KO mice. (molvis.org)
  • These conformational differences are discussed in light of the differential C5aR activation properties observed for the human and murine complement anaphylatoxins across species. (osti.gov)
  • Upon complement activation, a cascade of proteolytic events generates the complement effectors, including the anaphylatoxins C3a and C5a. (osti.gov)
  • The function of anaphylatoxins is regulated by circulating carboxypeptidases that remove their C-terminal arginine residue, yielding C3a-desArg and C5a-desArg. (osti.gov)
  • Activation of the complement cascade generates anaphylatoxins including C5a and C3a. (ovid.com)
  • Specific binding sites for interactions between C3a and C3aR are unknown, but it has been shown that sulfation of tyrosine 174, one of the amino acids in the extracellular domain, is required for C3a binding. (wikipedia.org)
  • The functional role of C3a was documented by data showing that glomerular fibrin(ogen), platelet clumps, and TM loss were markedly decreased in HUS mice receiving C3aR antagonist. (jimmunol.org)
  • Also, these drugs will not affect the C3a-C3aR axis. (nature.com)
  • Since chronic complement activation has been reported in renal diseases, which indicate sustained C3aR activation in renal cells, including podocytes and podocyte progenitors, the possible role of C3aR in the dysregulation of podocyte architecture and podocyte regeneration requires further research. (spandidos-publications.com)
  • We found that the mRNA levels of C3, C5, C3aR, C5aR, and two activators of the complement alternative pathway, Cfb and Cfd, were all upregulated after light exposure. (molvis.org)
  • Note that cells keep being attracted to one another by co‐attraction (C3a/C3aR pathway) and repelled upon contact via contact inhibition of locomotion (N‐cadherin‐Wnt/PCP‐RhoA‐ROCK pathway). (els.net)
  • Signalling through their cognate G-protein coupled receptors, C3aR and C5aR, leads to a wide range of biological events promoting inflammation at the site of complement activation. (osti.gov)
  • C3a is an anaphylatoxin that triggers a response by stimulating inflammatory cells to release histamine, enzymes, cytokines and other mediators. (nationaljewish.org)
  • The human anaphylatoxin peptide C3a, generated during complement activation, exerts antimicrobial effects. (lu.se)
  • article{9d06ba00-5f88-4746-895e-2c5bbf9fe49b, abstract = {The human anaphylatoxin peptide C3a, generated during complement activation, exerts antimicrobial effects. (lu.se)
  • Other than the alternative pathway, which is constantly active, C3a formation is triggered by pathogenic infection. (wikipedia.org)
  • The alternative pathway of complement activation is typically always active at low levels in blood plasma through a process called tick-over, in which C3 spontaneously hydrolyzes into its active form, C3(H2O). (wikipedia.org)
  • Factor B-deficient mice after Stx2/LPS exhibited less thrombocytopenia and were protected against glomerular abnormalities and renal function impairment, indicating the involvement of complement activation via the alternative pathway in the glomerular thrombotic process in HUS mice. (jimmunol.org)
  • 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)
  • Three pathways of complement activation: the classic pathway, lectin pathway, and alternative pathway, which of them converge at the level of complement component 3 (C3) convertase, from which functional products are generated in a sequential manner 5 . (nature.com)
  • Finally, the alternative pathway can be initiated when a spontaneously activated complement component binds to the surface of a pathogen. (nih.gov)
  • The immune cell-derived, alternative pathway complement components activate spontaneously, yielding local, but not systemic, production of C3a and C5a. (springer.com)
  • 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)
  • Through these mediators C3a can induce changes in the vascular permeability and local blood flow. (nationaljewish.org)
  • Here we provide evidence that bioactive fragments of these complement components (C3a and C5a) are present in drusen of patients with AMD, and that C3a and C5a induce VEGF expression in vitro and in vivo . (pnas.org)
  • The anaphylotoxin C3a was found to induce platelet activation and aggregation ( 5 ). (rupress.org)
  • Our data suggest that complement factors induce [Ca2+]i responses by Ca2+ release from internal pools and subsequent activation of Ca2+ entry controlled by the filling state of the intracellular Ca2+ depots. (mdc-berlin.de)
  • Complement factors C3a, C5a and C4 can induce vasodilatation, increased capillary permeability, and expression of leukocyte adhesion molecules. (sigmaaldrich.com)
  • 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)
  • C1-inh irreversibly binds to and inactivates C1r and C1s proteinases in the C1 complex of classical pathway of complement. (bionity.com)
  • 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)
  • 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)
  • C3a formation occurs through activation and cleavage of complement component 3 in a reaction catalyzed by C3-convertase. (wikipedia.org)
  • The C3 convertase enzymes of either complement activation pathway will cleave the C3 α-chain at peptide bond 77 resulting in the production and release of the C3a peptide. (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)
  • In the first phase, a series of specific interactions leads to formation of intrinsic complement proteinase, termed C3 convertase. (medscape.com)
  • 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)
  • The formation of C2a4b creates C3 convertase, which cleaves C3 into C3a and C3b. (aacrjournals.org)
  • MBL or ficolin activation of mannose-associated serine proteases (MASP) results in cleavage of C2 and C4 similar to the C1 complex, with subsequent production of C3 convertase and complement cascade activation resembling the classic pathway. (aacrjournals.org)
  • The hydrolysis induces a conformational change that allows factor B to bind and form the alternative complement activation pathway C3 convertase (amplification loop is represented by the bold dotted arrow). (els.net)
  • Cleavage of native C3 by the C3 convertase results in the release of the C3a anaphylatoxin. (els.net)
  • C2a, a serine protease, then combines with complement factor C4b to generate the C3 or C5 convertase. (uniprot.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 assay has high sensitivity and excellent specificity for detection of Complement Component 3a (C3a). (biotecnika.org)
  • C3a (70-77) is an octapeptide corresponding to the COOH terminus of C3a, exhibits the specificity and 1 to 2% biologic activities of C3a. (medchemexpress.com)
  • The complement system exerts many of its effects through complement receptors (CRs). (medscape.com)
  • Of the 8 plasma membrane receptors for complement, only deficiencies of CR3 and CR4 due to CD18 deficiency have been described, known as leukocyte adhesion deficiency (LAD) type 1 . (medscape.com)
  • [ 6 ] These receptors play a role in C3a-mediated and C5a-mediated anaphylactic reactions. (medscape.com)
  • C3 inhibition could simultaneously block C3a and C5a generation, as well as intrapulmonary C3 activation and IL-6 release from alveolar macrophages, or other cells that express C3a receptors (C3aRs) and/or C5a receptors (C5aRs), thereby ameliorating lung injury. (nature.com)
  • The data support the need for further efficacy testing of targeting complement and/or its receptors to improve kidney transplant outcome in humans. (jci.org)
  • The complement system is a complex cascade involving proteolytic cleavage of serum glycoproteins often activated by cell receptors. (sigmaaldrich.com)
  • Because activated microglia are also associated with AMD, we studied the relationship between complement anaphylatoxin receptors and microglial recruitment. (molvis.org)
  • Retinal Iba1-positive microglia/macrophages express receptors for C3a and C5a. (molvis.org)
  • To test the common view that Ca 2+ bursts mediate rearrangement of the actin cytoskeleton in response to the activation of G protein-coupled receptors, we combined single-cell manipulation with fluorescence imaging and monitored the Ca 2+ concentration in individual human neutrophils during complement-mediated chemotaxis. (sciencemag.org)
  • It has been shown to be a chemoattractant for eosinophils, and the form C3a desArg is also known as ASP (Acylation Stimulating Protein), a peptide that participates in fatty acid metabolism. (nationaljewish.org)
  • Preservation of antimicrobial properties of complement peptide C3a - from invertebrates to humans. (lu.se)
  • The C3a peptide, also known as the C3a anaphylatoxin, modulates inflammation and possesses antimicrobial activity. (senescence.info)
  • 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)
  • A recent study of SARS-CoV, which is closely related to SARS-CoV-2, found that activation of complement component C3 exacerbates disease in SARS-CoV-associated ARDS 4 . (nature.com)
  • These data suggest that, in addition to the biomaterial surface, the blood-gas interface seems to play an important role in the activation of complement and that this activation is inhibitable by high concentrations of soluble glucose aminoglycans. (nih.gov)
  • Complement component C3 plays a central role in the activation of complement system. (senescence.info)
  • C3a is an effector of the complement system with a range of functions including T cell activation and survival, angiogenesis stimulation, chemotaxis, mast cell degranulation, and macrophage activation. (wikipedia.org)
  • C3a is also able to play a role in chemotaxis for mast cells and eosinophils, but C5a is a more potent chemoattractant. (wikipedia.org)
  • In leukocytes, C3a and C5a cause chemotaxis in a G i -dependent, pertussis toxin (PT)-sensitive fashion. (jimmunol.org)
  • C3a and C5a are known for their stimulatory effect on leukocytes including chemotaxis of neutrophils, eosinophils, and monocytes ( 1 , 2 , 3 , 4 , 5 ). (jimmunol.org)
  • Complements C3a and C4a promote phagocyte chemotaxis. (sigmaaldrich.com)
  • To investigate the physiological role of intracellular calcium (Ca 2+ ) bursts in this complex behavior, Francis and Heinrich presented nonadherent human neutrophils with various targets that induced complement-mediated chemotaxis. (sciencemag.org)
  • Inflammation and thrombosis are two responses that are linked through a number of mechanisms, one of them being the complement system. (rupress.org)
  • The complement system plays an important role in innate immunity inducing liver diseases as well as signaling immune cell activation in local inflammation regulating immunomodulatory effects such as liver damage and/or liver regeneration. (hindawi.com)
  • It is well established that activation of the complement cascade alters functional responses of neutrophils (PMN) in the course of systemic inflammation and contributes to the development of organ failure [ 15 , 23 ]. (hindawi.com)
  • This article is sought to provide insights into the pathogenesis of multiorgan failure associated with systemic inflammation with particular focus on the role of the complement system. (hindawi.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)
  • Nevertheless, emerging literature examining the mechanistic relationship between inflammation and cancer ( 4 , 9 , 10 ) has almost completely omitted the role of the complement cascade. (aacrjournals.org)
  • The signaling cascade responsible for the production of angiogenic factors by C3a or C5a could be defined as activation of the rho cascade which was necessary for nuclear translocation of NF κ B p65 and of phospho-ERK1/2. (scirp.org)
  • The complement system functions as an interactive sequence, with one reaction leading to another in the form of a cascade. (medscape.com)
  • The complement system activates through a triggered-enzyme cascade. (nih.gov)
  • 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)
  • 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)
  • Emerging evidence over the last decade unexpectedly identified the complement cascade as a common thread in this process. (jci.org)
  • Emerging evidence over the past 15 years supports the concept that the complement cascade, traditionally considered a component of innate immunity, unexpectedly regulates kidney IR injury, T cell and humoral alloimmunity that underlie transplant rejection, and progressive kidney injury that results in late graft failure. (jci.org)
  • Following the complement cascade, C5b with C6-C9 forms the "membrane attack complex" (MAC), capable of lysing infected cells and pathogens [ 17 , 18 ]. (hindawi.com)
  • Ischaemic infarction may also cause initiation of the complement cascade. (sigmaaldrich.com)
  • Furthermore, potential therapeutic strategies targeting the complement cascade to prevent the development of MOF as well as possible future research directions are addressed. (hindawi.com)
  • The complement cascade comprises the classic, alternative, and MBL pathways. (aacrjournals.org)
  • Activation products of the complement cascade contain neo-epitopes that are not present in the individual native components. (acris-antibodies.com)
  • The importance of complement activation on phagocytosis, and on the release of cytokines and chemokines, was investigated using inhibitors acting at different levels of the complement cascade. (diva-portal.org)
  • The activation of the complement cascade can cause damage to cells, therefore the inhibition of the complement cascade can work as a medicine in certain conditions [1] . (bionity.com)
  • Similarly, application of complement fragments C5a (0.1-10.0 nM) or C3a (100 nM) generates biphasic [Ca2+]i transients composed of an initial peak followed by a plateau in cultured microglia. (mdc-berlin.de)
  • Locally produced complement fragments C5a and C3a provide both costimulatory and survival signals to naive CD4+ T cells. (springer.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)
  • These complement components form the final membrane attack complex (MAC). (thefreedictionary.com)
  • Using fluo-3 microfluorimetry, we have found that external application of the complement fragment C5a (4-10 nM) induced [Ca2+]i elevation in microglial cells in situ in corpus callosum slices. (mdc-berlin.de)
  • The restoration of the extracellular Ca2+ concentration within 30-60 sec after the beginning of the complement fragment-induced [Ca2+]i elevation led to the recovery of the plateau phase. (mdc-berlin.de)
  • Inhibition of the endoplasmic reticulum Ca2+ pumps with 500 nM thapsigargin transiently increased the [Ca2+]i and blocked the [Ca2+]i signals in response to subsequent complement fragment application. (mdc-berlin.de)
  • A recent preprint study reported that lung biopsy samples from patients with severe COVID-19 showed widespread complement activation, characterized by C3a generation and C3-fragment deposition 6 . (nature.com)
  • Human C3a anaphylatoxin (C3a), a C3 split fragment produced during the activation of the complement system, is one of the complement molecules that have been reported to serve non-immune roles. (spandidos-publications.com)
  • Complement fragment C3a controls mutual cell attraction during collective cell migration. (nyu.edu)
  • C3a is primarily regarded for its role in the innate and adaptive immune responses as an anaphylatoxin, moderating and activating multiple inflammatory pathways. (wikipedia.org)
  • C3a is able to regulate B cell and monocyte production of IL-6 and TNF-α, and human C3a has been shown to dampen the polyclonal immune response through dose-dependent regulation of B cell molecule production. (wikipedia.org)
  • This protein plays a key role in a part of the body's immune response known as the complement system. (medlineplus.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)
  • This body of literature, to be reviewed herein, suggests that complement components produced by the liver as well as by kidney cells and immune cells play crucial roles as pathogenic mediators of transplant rejection in animals and humans. (jci.org)
  • In ALF, extensive liver injury can be caused by a variety of molecules of the innate immune system, and the complement system plays an important role in this process [ 9 , 10 ]. (hindawi.com)
  • Complement inhibitors are being studied as potential therapeutics for immune diseases and Alzheimer's. (sigmaaldrich.com)
  • The underlying immune response is highly complex and involves activation of the complement system as a crucial entity of innate immunity. (hindawi.com)
  • In general, immune complexes deposit in vessel walls leading to activation of the complement system. (wikipedia.org)
  • Measurements of serum complement components C3 and C4 are useful in the diagnosis and monitoring of immune complex disease. (thermofisher.com)
  • Complement: a key system for immune surveillance and homeostasis. (springer.com)
  • 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)
  • As a part of the immune system, the complement system is initially involved in host defense against pathogens. (spandidos-publications.com)
  • Variola virus immune evasion design: expression of a highly efficient inhibitor of human complement. (umn.edu)
  • The complement system is involved in innate and adaptive immune responses. (asm.org)
  • Complement is an ancient part of the innate immune system that plays a pivotal role in protection against invading pathogens and helps to clear apoptotic and necrotic cells. (osti.gov)
  • Immune cells migrate toward pathogens using chemotactic cues that are either pathogen-derived or generated by the host, such as components of the complement system. (sciencemag.org)
  • C5a, but not C3a, was chemotactic for human immortalized dermal microvascular endothelial cells. (jimmunol.org)
  • Human C3a and C4a (but not C5a) were antimicrobial, in concert with the separate evolutionary development of the chemotactic C5a. (lu.se)
  • 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)
  • Although rho was only transiently activated, inhibition of the rho or "downstream of it" of the NF κ B pathway, prevented C3a-and C5a-induced up-regulation of angiogenic factors. (scirp.org)
  • The direct interaction of C3a(70-77) with human mononuclear leukocytes in culture results in a concentrationdependent inhibition of the generation of LIF evoked by mitogens and by the antigen SK-SD. (medchemexpress.com)
  • However, C5 inhibition by these agents can be partial, allowing residual terminal pathway activity to skew efficacy in cases of excessive complement activation, which is often seen in infections. (nature.com)
  • Terminal complement inhibition decreases early acute humoral rejection in sensitized renal transplant recipients. (springer.com)
  • Medof ME, Kinoshita T, Nussenzweig V. Inhibition of complement activation on the surface of cells after incorporation of decay-accelerating factor (DAF) into their membranes. (springer.com)
  • 3) Both Borrelia strains were efficiently phagocytized by granulocytes and monocytes, with substantial inhibition by complement blockade at the levels of C3 and C5. (diva-portal.org)
  • C1-inhibitor ( C1-inh , C1 esterase inhibitor ) is a serine protease inhibitor (serpin) protein, the main function of which is the inhibition of the complement system to prevent spontaneous activation. (bionity.com)
  • The third complement component, C3, is central to the classical, alternative and lectin pathways of complement activation. (acris-antibodies.com)
  • The MicroVue C3a Plus EIA measures the amount of C3a-desArg present in human plasma and serum. (quidel.com)
  • C3 is the most abundant protein of the complement system with serum protein levels of about 1.3 mg/ml. (acris-antibodies.com)
  • Mouse monoclonal [2991] to C3a / C3a des Arg ( Abpromise for all tested applications). (bio-medicine.org)
  • The complement system mediates cell-cell interactions in many physiological processes, such as hematopoiesis, organogenesis, and in reproduction ( 1 ). (rupress.org)
  • C3a mediates epithelial-to-mesenchymal transition in proteinuric nephropathy. (springer.com)
  • This complex has the ability to catalyze the formation of C3a and C3b after it binds properdin, a globulin protein, and is stabilized. (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)
  • This model provides a valuable tool to study the pathogenesis of the RPE in early stages of AMD as well as the role of the complement system in the formation of BD. (arvojournals.org)
  • Aim: Here we investigated the role of complement activation in phagocytosis and the release of cytokines and chemokines in response to two clinical isolates: Borrelia afzelii K78, which is resistant to complement-mediated lysis, and Borrelia garinii LU59, which is complement-sensitive. (diva-portal.org)
  • 5) Both strains induced a similar release of cytokines and chemokines, which in contrast to the phagocytosis, was almost totally unaffected by complement blockade. (diva-portal.org)
  • Conclusions: Our results show that complement activation plays an important role in the process of phagocytosis but not in the subsequent cytokine release in response to live Borrelia spirochetes. (diva-portal.org)
  • C5b subsequently takes the lead in formation of the terminal C5b-9 complement complex ( TCC ), ultimately resulting into cell lysis. (els.net)
  • C3a also plays an important role in adaptive immunity, moderating leukocyte production and proliferation. (wikipedia.org)
  • In this study, we explored whether Stx triggers complement-dependent microvascular thrombosis in in vitro and in vivo experimental settings of HUS. (jimmunol.org)
  • We recently demonstrated the roles of complement C3a and extracellular matrix (ECM) turnover in an in vitro model for deposit formation in inherited macular degeneration using primary mouse RPE cells. (arvojournals.org)
  • For this study we tested the hypothesis that C3a can cause the formation of BD in vitro by human RPE cells. (arvojournals.org)
  • Electron micrographs showed that RPE treated with C3a in vitro accumulate collagen fibers and wide-spaced collagen under the basal membrane. (arvojournals.org)
  • Specific for human C3, C3a and C3a (desArg) and does not cross-react with C4a or C5a. (novusbio.com)
  • Thus, regions of the ancient C3a from Carcinoscorpius rotundicauda as well as corresponding parts of human C3a exhibited helical structures upon binding to bacterial lipopolysaccharide permeabilized liposomes and were antimicrobial against Gram-negative and Gram-positive bacteria. (lu.se)
  • Human C3a and C4a (but not C5a) were antimicrobial, in. (lu.se)
  • Although lacking 69 residues at the NH2 terminus, it maintains 1 to 2% of the activity of natural human C3a. (medchemexpress.com)
  • C3a (70-77), Ala-Ser-HisLeu-Gly-Leu-Ala-Arg, induces histamine release and degranulation of rat mast cells, promotes contraction of guinea pig ileal tissue, and enhances vascular permeability in human skin. (medchemexpress.com)
  • C3a (70-77) selectively desensitizes ileal smooth muscle to C3a but not to human C5a, a related anaphylatoxin. (medchemexpress.com)
  • Modulation of human lymphocyte function by C3a and C3a(70-77). (medchemexpress.com)
  • RPE cultures were treated with different doses of recombinant human C3a protein every 72 hours for 1, 2 or 4 weeks. (arvojournals.org)
  • Human fetal RPE cells produce BD in response to stimulation with C3a, further suggesting a key role for C3a in the formation of sub-RPE deposits. (arvojournals.org)
  • Our aim is to evaluate the role of complement components in acute liver failure (ALF) caused by viral hepatitis, involving virus-induced ALF in human subjects using peripheral blood, samples of liver tissues, and ex vivo assays. (hindawi.com)
  • A rabbit antiserum raised against human complement C3a protein. (quidel.com)
  • An immortal human podocyte line (HPC) was transfected with a C3a expression lentivirus vector or recombinant C3a. (spandidos-publications.com)
  • Lane 1 : Complement C3 isolated from Human plasma. (acris-antibodies.com)
  • 2009) Complement in human diseases: Lessons from complement deficiencies. (els.net)
  • 2011) Structure of human complement C8, a precursor to membrane attack. (els.net)
  • Because SPICE efficiently inhibits the stability of human C3b and C4b, it essentially inactivates the convertases and, therefore, both the classical and alternative pathways of complement," the report says. (umn.edu)
  • To study whether the effect of SPICE is specific to human complement, the experimenters also compared the ability of SPICE and VCP to inhibit complement from humans, dogs, guinea pigs, and baboons. (umn.edu)
  • The results showed that SPICE and VCP both inhibited complement, but SPICE preferentially inhibited human and baboon complement, whereas VCP preferentially inhibited dog and guinea pig complement. (umn.edu)
  • The fact that SPICE functions better against human complement quantitatively and qualitatively demonstrates that variola exhibits human preference at the protein level, a concept previously suggested, but not shown," the report states. (umn.edu)
  • Whereas human C3a and C3a-desArg adopt a canonical four-helix bundle fold, the conformation of human C5a-desArg has recently been described as a three-helix bundle. (osti.gov)
  • Proximal complement inhibitors (which target C3 or its upstream activators) could be more effective, but these are still in clinical development, and none has yet been approved, although limited data from phase II clinical trials are available. (nature.com)
  • The findings support the need for design and testing of complement inhibitors in humans. (springer.com)
  • Inhibitors of the complement system have long been of interest as potential drugs for the treatment of diseases such as sepsis, rheumatoid arthritis, Crohn's disease and ischaemia-reperfusion injuries1. (ovid.com)
  • Therefore, measurement of C3a-desArg allows reliable conclusions about the level of complement activation in the test samples. (acris-antibodies.com)
  • In addition, migration and degranulation of neutrophils can be suppressed in the presence of C3a. (wikipedia.org)
  • Other deleterious effects of complement activation include, degranulation of neutrophils, basophils and mast cells, unwanted release of the neutrophil products elastase and oxygen radicals, and extracorporeal blood circulation. (sigmaaldrich.com)
  • Diseases associated with C3AR1 include Hemolytic Uremic Syndrome, Atypical 1 and Complement Component 3 Deficiency . (genecards.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)
  • Intra-assay Precision (Precision within an assay): 3 samples with low, middle and high level Complement Component 3a (C3a) were tested 20 times on one plate, respectively. (biotecnika.org)
  • Inter-assay Precision (Precision between assays): 3 samples with low, middle and high level Complement Component 3a (C3a) were tested on 3 different plates, 8 replicates in each plate. (biotecnika.org)
  • We used a custom-made single nucleotide polymorphism (SNP) genotyping assay consisting of 98 SNPs in 18 genes that encode components of the complement system. (frontiersin.org)
  • Dr. Ritchie Shoemaker and his colleagues published a study in 2008 reporting elevated C3a and C4a levels in acute Lyme disease. (publichealthalert.org)
  • suggested that elevated C3a and C4a levels can serve as early markers in the diagnosis of acute Lyme disease. (publichealthalert.org)
  • So, although C3a was shown to be elevated in a cohort of early, acute Lyme disease patients, it appears to be normal in chronic Lyme patients. (publichealthalert.org)
  • In summary, our data suggest that the complement system may be involved in liver dysfunction in viral-induced acute liver failure cases using ex vivo assays. (hindawi.com)
  • Here, we assessed the toxicological effects of the complement system in the peripheral blood of patients during acute liver failure. (hindawi.com)
  • Details of possible complement activation in acute myocardial infarction (AMI) and the in vivo effects of fibrinolytic agents on this activation are not yet known. (biomedsearch.com)
  • Complement activation in acute humoral renal allograft rejection: diagnostic significance of C4d deposits in peritubular capillaries. (springer.com)
  • Local synthesis of complement component C3 regulates acute renal transplant rejection. (springer.com)
  • Despite uncontrolled auto-activation, it is important to note that levels of key complement components are low during an acute attack, because they are being consumed - indeed, low levels of C4 are a key diagnostic test for hereditary angioedema. (bionity.com)
  • Although the activation and amplification of the three pathways differ initially, they commonly cleave C3 into C3a and C3b, resulting in terminal formation of the MAC. (aacrjournals.org)
  • C3 convertases generated by all pathways are able to cleave C3 into C3a and C3b, latter of which forms additional convertases, thereby rapidly amplifying complement response. (els.net)
  • In the case of the complement system, the precursor zymogens are widely distributed throughout body fluids and tissues without adverse effect. (nih.gov)
  • Three biochemical pathways activate the complement system: the classical complement pathway , the alternative complement pathway , and the lectin pathway . (wikipedia.org)
  • In humans, the plasma levels of complement activation products rise early, are persistently elevated in patients after thermal injury, trauma, and sepsis, and correlate with the severity of injury and inversely with the outcome [ 16 - 22 ]. (hindawi.com)
  • The report concludes, "Assuming that complement is as critical to orthopoxvirus containment in humans as it is in rodents, SPICE seems to be a virulence factor for variola virus. (umn.edu)
  • As a central entity of innate immunity, the complement system is immediately activated after trauma or infection in order to control the replication of intruding pathogens. (hindawi.com)
  • For example, the complement system participates in inflammatory reactions and facilitates removal of invading pathogens. (mddionline.com)
  • 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)
  • Our findings displayed low levels of C3a in plasma samples with high frequency of C3a, C5a, and C5b/9 deposition in liver parenchyma. (hindawi.com)
  • 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)
  • Quidel's polyclonal antiserum to C3a can been used in a variety of immunochemical techniques including RID, EIA, Ouchterlony. (quidel.com)
  • This way, C1-inh prevents the proteolytic cleavage of later complement components C4 and C2 by C1 and MBL. (bionity.com)
  • C3a is a one of the peptides (complement split products) formed by the cleavage of complement component 3. (nationaljewish.org)
  • In the search for mechanisms linking complement activation and thrombosis, we found that exuberant complement activation in response to Stx generated an increased amount of C3a that caused further endothelial P-selectin expression, thrombomodulin (TM) loss, and thrombus formation. (jimmunol.org)
  • Studies suggest that the mechanisms of thrombosis in PNH and familial HUS are related to platelet activation induced by complement activation. (rupress.org)
  • As might be expected, there are many regulatory mechanisms to prevent uncontrolled complement activation. (nih.gov)
  • Dysregulation of the complement system has been implicated, but molecular mechanisms are incompletely understood. (frontiersin.org)
  • In the present review, mechanisms of the inflammatory response in the development of MOF in sepsis and SIRS with particular focus on the complement system are discussed. (hindawi.com)
  • Phylogenetic analysis, sequence analyses, and structural modeling studies paired with antimicrobial assays of peptides from known C3a sequences showed that, in particular in vertebrate C3a, crucial structural determinants governing antimicrobial activity have been conserved during the evolution of C3a. (lu.se)
  • No reaction is seen with a synthetic octapeptide representing the C3a C-terminal. (novusbio.com)
  • Third, the terminal complement components damage certain bacteria by creating pores in the bacterial membrane. (nih.gov)
  • Complement participates in innate and adaptive immunity. (els.net)
  • In experimental sepsis, the blockade of complement anaphylatoxin C5a virtually prevented the appearance of MOF and improved the outcome [ 24 - 26 ]. (hindawi.com)
  • Complement deficiency or blockade attenuates T cell-mediated autoimmunity and delays allograft rejection in mice. (springer.com)
  • Since there is complement activation in all areas of tissue injury, and both C3a and C5a activate MSC, it was asked whether stimulation with C3a or C5a would upregulate the production of trophic factors by MSC. (scirp.org)
  • In this paper, we show that the converse is also true: activated platelets can activate the complement system. (rupress.org)
  • We determined whether a reciprocal interaction also exists, whereby platelets can activate complement. (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)
  • A deficiency in the negative regulators of complement leads to excessive complement activation, as observed in paroxysmal nocturnal hemoglobinuria (PNH) and atypical or familial hemolytic uremic syndrome (HUS). (rupress.org)
  • Carroll MC (2004) The complement system in regulation of adaptive immunity. (els.net)
  • Nevertheless, the function of the complement system is associated with processes of development, degeneration, and regeneration of multiple organs [ 12 - 14 ]. (hindawi.com)