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.

Deficiency of human complement protein C4 due to identical frameshift mutations in the C4A and C4B genes. (1/96)

The complement protein C4, encoded by two genes (C4A and C4B) on chromosome 6p, is the most polymorphic among the MHC III gene products. We investigated the molecular basis of C4 deficiency in a Finnish woman with systemic lupus erythematosus. C4-specific mRNA was present at low concentrations in C4-deficient (C4D) patient fibroblasts, but no pro-C4 protein was detected. This defect in C4 expression was specific in that synthesis of two other complement proteins was normal. Analysis of genomic DNA showed that the proposita had both deleted and nonexpressed C4 genes. Each of her nonexpressed genes, a C4A null gene inherited from the mother, a C4A null gene, and a C4B null gene inherited from the father, all contained an identical 2-bp insertion (TC) after nucleotide 5880 in exon 29, providing the first confirmatory proof of the C4B pseudogene. This mutation has been previously found only in C4A null genes. Although the exon 29/30 junction is spliced accurately, this frameshift mutation generates a premature stop at codon 3 in exon 30. These truncated C4A and C4B gene products were confirmed through RT-PCR and sequence analysis. Among the possible genetic mechanisms that produce identical mutations is both genes, the most likely is a mutation in C4A followed by a gene conversion to generate the mutated C4B allele.  (+info)

Analysis of human C4A and C4B binding to an immune complex in serum. (2/96)

Previous studies using isolated complement proteins have shown that more C4A than C4B binds to certain types of immune complexes. However, the in vivo binding of the C4 isoforms to an immune complex has not been investigated in detail and may differ from events when measured with the isolated proteins. We report here the binding of C4A and C4B to an immune complex of bovine serum albumin (BSA) anti-BSA as it occurs in serum. We found that when using the isolated C4 proteins more C4A than C4B bound to the complex, but in serum similar amounts of C4A and C4B were found to bind. Furthermore, these results were not explainable by a difference in activity between isoforms. In an attempt to explain these results a number of unexpected observations were noted. First C4A, but not C4B, bound specifically to a yet unidentified 38-kD serum protein. Second, when both covalent and non-covalent binding was assessed, we found that as serum concentration increased there followed a concomitant decrease in covalent binding and C4B was more affected than C4A. The potential biological significance of these findings is discussed.  (+info)

Possible mechanism for in vitro complement activation in blood and plasma samples: futhan/EDTA controls in vitro complement activation. (3/96)

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)

Deficiencies of human complement component C4A and C4B and heterozygosity in length variants of RP-C4-CYP21-TNX (RCCX) modules in caucasians. The load of RCCX genetic diversity on major histocompatibility complex-associated disease. (4/96)

The complement component C4 genes located in the major histocompatibility complex (MHC) class III region exhibit an unusually complex pattern of variations in gene number, gene size, and nucleotide polymorphism. Duplication or deletion of a C4 gene always concurs with its neighboring genes serine/threonine nuclear protein kinase RP, steroid 21-hydroxylase (CYP21), and tenascin (TNX), which together form a genetic unit termed the RCCX module. A detailed molecular genetic analysis of C4A and C4B and RCCX modular arrangements was correlated with immunochemical studies of C4A and C4B protein polymorphism in 150 normal Caucasians. The results show that bimodular RCCX has a frequency of 69%, whereas monomodular and trimodular RCCX structures account for 17.0 and 14.0%, respectively. Three quarters of C4 genes harbor the endogenous retrovirus HERV-K(C4). Partial deficiencies of C4A and C4B, primarily due to gene deletions and homoexpression of C4A proteins, have a combined frequency of 31.6%. This is probably the most common variation of gene dosage and gene size in human genomes. The seven RCCX physical variants create a great repertoire of haplotypes and diploid combinations, and a heterozygosity frequency of 69.4%. This phenomenon promotes the exchange of genetic information among RCCX constituents that is important in homogenizing the structural and functional diversities of C4A and C4B proteins. However, such length variants may cause unequal, interchromosomal crossovers leading to MHC-associated diseases. An analyses of the RCCX structures in 22 salt-losing, congenital adrenal hyperplasia patients revealed a significant increase in the monomodular structure with a long C4 gene linked to the pseudogene CYP21A, and bimodular structures with two CYP21A, which are likely generated by recombinations between heterozygous RCCX length variants.  (+info)

Deficient APC-cofactor activity of protein S Heerlen in degradation of factor Va Leiden: a possible mechanism of synergism between thrombophilic risk factors. (5/96)

In protein S Heerlen, an S-to-P (single-letter amino acid codes) mutation at position 460 results in the loss of glycosylation of N458. This polymorphism has been found to be slightly more prevalent in thrombophilic populations than in normal controls, particularly in cohorts of patients having free protein S deficiency. This suggests that carriers of the Heerlen allele may have an increased risk of thrombosis. We have now characterized the expression in cell cultures of recombinant protein S Heerlen and investigated the anticoagulant functions of the purified recombinant protein in vitro. Protein S Heerlen was synthesized and secreted equally well as wild-type protein S by transiently transfected COS-1 cells. The recombinant protein S Heerlen interacted with conformation-dependent monoclonal antibodies and bound C4b-binding protein to the same extent as wild-type protein S. Protein S Heerlen displayed reduced anticoagulant activity as cofactor to activated protein C (APC) in plasma-based assays, as well as in a factor VIIIa-degradation system. In contrast, protein S Heerlen functioned equally well as an APC cofactor in the degradation of factor Va as wild-type protein S did. However, when recombinant activated factor V Leiden (FVa:Q506) was used as APC substrate, protein S Heerlen was found to be a poor APC cofactor as compared with wild-type protein S. These in vitro results suggest a possible mechanism of synergy between protein S Heerlen and factor V Leiden that might be involved in the pathogenesis of thrombosis in individuals carrying both genetic traits. (Blood. 2000;96:523-531)  (+info)

Lack of evidence of a specific role for C4A gene deficiency in determining disease susceptibility among C4-deficient patients with systemic lupus erythematosus (SLE). (6/96)

The aim of the present study was to investigate the prevalence of C4 and C2 deficiencies and to characterize genomic alterations in C4 genes in a large cohort of 125 unselected patients with SLE. We determined the protein concentration and functional activity of C2 and C4, as well as the C4 phenotype. C4 genotyping included Taq 1 restricted fragment lengh polymorphism (RFLP) analysis and polymerase chain reaction using sequence-specific primers (SSP-PCR). Type I C2 deficiency was diagnosed by PCR. Overall, 79.2% of the patients exhibited abnormalities of the C4 genes including deletion, non-expression, gene conversion and duplication. Among C4-deficient patients (n = 66, 52.8% prevalence), 41.0% of the patients exhibited a C4A deficiency and 59.0% a C4B deficiency. Half of the C4 deficiencies were due to a gene deletion. There was a strong association between C4A and C4B gene deletion and the presence of the DRB1*03 allele. Among the silent C4A genes, only two cases were related to a 2-bp insertion in exon 29 of the C4A gene. A gene conversion was demonstrated in eight patients (6.4%). One patient had a homozygous C4A deficiency. Three (2.4%) patients presented with a heterozygous type I C2 deficiency and none with homozygous deficiency. Our results argue against a specific role for C4A gene deficiency in determining disease susceptibility among patients with SLE that are C4-deficient.  (+info)

Characterization of a de novo conversion in human complement C4 gene producing a C4B5-like protein. (7/96)

Complement C4 is a highly polymorphic protein essential for the activation of the classical complement pathway. Most of the allelic variation of C4 resides in the C4d region. Four polymorphic amino acid residues specify the isotype and an additional four specify the Rodgers and Chido determinants of the protein. Rare C4 allotypes have been postulated to originate from recombination between highly homologous C4 genes through gene conversions. Here we describe the development of a de novo C4 hybrid protein with allotypic and antigenic diversity resulting from nonhomologous intra or interchromosomal recombination of the maternal chromosomes. A conversion was observed between maternal C4A3a and C4B1b genes producing a functional hybrid gene in one of the children. The codons determining the isotype, Asp(1054), Leu(1101), Ser(1102), Ile(1105) and His(1106), were characteristic of C4B gene, whereas the polymorphic sites in exon and intron 28 were indicative of C4A3a sequence. The protein produced by this hybrid gene was electrophoretically similar to C4B5 allotype. It also possesses reversed antigenicity being Rodgers 1, 2, 3 and Chido-1, -2, -3, 4, -5, and -6. Our case describes the development of a rare bimodular C4B-C4B haplotype containing a functional de novo C4 hybrid gene arisen through gene conversion from C4A to C4B. Overall the data supports the hypothesis of gene conversions as an ongoing process increasing allelic diversity in the C4 locus.  (+info)

Determining the one, two, three, or four long and short loci of human complement C4 in a major histocompatibility complex haplotype encoding C4A or C4B proteins. (8/96)

The complex genetics of human complement C4 with unusually frequent variations in the size and number of C4A and C4B, as well as their neighboring genes, in the major histocompatibility complex has been a hurdle for accurate epidemiological studies of diseases associated with C4. A comprehensive series of novel or improved techniques has been developed to determine the total gene number of C4 and the relative dosages of C4A and C4B in a diploid genome. These techniques include (1) definitive genomic restriction-fragment-length polymorphisms (RFLPs) based on the discrete duplication patterns of the RCCX (RP-C4-CYP21-TNX) modules and on the specific nucleotide changes for C4A and C4B isotypes; (2) module-specific PCR to give information on the total number of C4 genes by comparing the relative quantities of RP1- or TNXB-specific fragments with TNXA-RP2 fragments; (3) labeled-primer single-cycle DNA polymerization procedure of amplified C4d genomic DNA for diagnostic RFLP analysis of C4A and C4B; and (4) a highly reproducible long-range-mapping method that employs PmeI-digested genomic DNA for pulsed-field gel electrophoresis, to yield precise information on the number of long and short C4 genes in a haplotype. Applications of these vigorously tested techniques may clarify the roles that human C4A and C4B gene-dosage variations play in infectious and autoimmune diseases.  (+info)

Fluorescein-Conjugated Goat F(ab)|sub|2|/sub| Fragment to Human Complement C3 is the lyophilized powder of fluorescein-5-isothiocyanate (FITC Isomer I)-conjugated goat F(ab)|sub|2|/sub| fragment to human complement C3 and buffer salts.
Human Complement C2 ELISA Kit is a Sandwich (quantitative) ELISA for the measurement of Human Complement C2 in Human Cell culture supernatant, Saliva, Milk, Serum, Plasma, Cerebral Spinal Fluid…
Abcams Complement C4 ELISA Kit (ab108825) suitable for Cell culture supernatant, Saliva, Milk, Urine, Cerebral Spinal Fluid in human. Reliably quantify 0.07…
The Major Histocompatibility Complex (MHC) is a gene-dense region located on the short arm of chromosome 6 (6p21.31). This region contains the highly polymorphic HLA genes as well as many other genes with immunological and non-immunological function. The susceptibility genes of many human disorders have been mapped to genes within the MHC. However, the genes themselves and indeed the locations of the genes, for many of the disorders, remain a mystery. This is a result of the high degree of linkage disequilibrium (LD) that exists between loci within the MHC. The high LD is explained by the genomic structure of the MHC. The MHC contains several blocks of DNA within which recombination is extremely rare, whereas the boundaries of the blocks are defined as hotspots of recombination. Most disease association studies have used the highly polymorphic HLA class I and class II genes which are separated by an, as yet, undefined number of blocks and several hundred kilobases of DNA. The MHC gamma block ...
Aida Ahmadi, University of Calgary. Determination of Total C18O Column Density in Orion KL. The large number of high-energy rotational lines of C18O, available via the Herschel Space Observatory, provides an unprecedented ability to model the total C18O column density in hot cores. Using the emission from all the observed lines (up to J=16-15) we use an automated algorithm to model all transitions simultaneously. Under Local Thermodynamic Equilibrium (LTE) assumptions and knowledge of source size, centroid velocity and line width, the model determines the values for total C18O column densities in 4 separate line-of-sight components of Orion KL known as the Extended Ridge, the Outflow/Plateau, the Compact Ridge, and the Hot Core. These values are determined to be: 2.5 X 10^16, 5.9 X 10^16, 1.8 X 10^16, and 6.0 X 10^16 cm^(-2) respectively. We also explain the difficulties in using the said algorithm to model optically thick molecules such as CO which require non-LTE modeling.. Khulud Almutairi, ...
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Human Complement C4c (C4c) is used as an immunogen and is the inactive form of Human Complement C4. C4c interacts with complement C1 and complement C2 to form complement C3 convertase of the classic activation pathway. Systemic lupus erythematosus is ofte
High-resolution versions of our original photographs are available for purchase for you to use in printed publications or elsewhere. Contact us for further information. Be sure to make a note of the URL of the photos you are interested in. We do not sell these photos for profit, only to cover the maintenance costs of the website.. ...
I was at the cardiologist yesterday, while sitting there A friend I see occasionally has the same card and walked in. Get this, hes 55 and had a quadrupedal by pass which I had heard about some time back. I start asking questions and find out his total C was 120 before the heart trouble and had been for some time. The doctors told him he was fine, but here he is with blocked arterys. He is a Merchant sailor and has worked on fuel barges all his life. First thing hits me is inflammation from the chemicals in the fumes, the next thing I wonder about is why the liver is not in over drive making C, everybody else I know with quads had C well above the 180-190 normal marker. I remember sometime back reading here that there are many people with low to normal C that end up with CVD also. Doctor has the privacy thing going on so I got no where asking him with the exception of different risk factors . Here is an example of the exception to the rule, low C and still has CVD ...
HEERLEN, Netherlands, Aug. 18, 2020 /PRNewswire/ -- Royal DSM, a global science-based company active in Nutrition, Health and Sustainable Living, has repurchased
What a great start of our autumn tour! We had a blast in Solingen and Heerlen. Thanx to all who came to the shows. A very special thanx to our 50 friends from Genk who came by bus. You are amazing!. ...
The human body is a mystery. As much and as fast as were learning, we still know very little. This post is about a recent discovery. I call it a discovery, because Ive lived out what this theory holds to be true, as have a number of patients I work with, and perhaps some of you reading this. RCCX theory is quite complex. The best I can do is share my personal experience with the hope that doing so will help make this information more accessible. ...
Gentaur molecular products has all kinds of products like :search , Ray Biotech \ Recombinant Human Complement C1q Tumor Necrosis Factor-Related Protein 1 \ 228-10151-2 for more molecular products just contact us
Opioid drug users on methadone treatment are routinely offered voluntary screening for HIV, HBV and HCV. Data on uptake and outcome of anti-HIV, anti-HBC, and anti-HCV screening among Opioid DUs receiving methadone were obtained from Amsterdam from 2004 to 2008 and Heerlen from 2003 to 2009. Annual screening uptake for HIV, HBV and HCV varied from 34 to 69%, depending on disease and screening site. Of users screened, 2.5% were HIV-positive in Amsterdam and 11% in Heerlen; 26% were HCV-positive in Amsterdam and 61% in Heerlen. Of those screened for HBV, evidence of current or previous infection (anti-HBC) was found among 33% in Amsterdam and 48% in Heerlen. In Amsterdam, 92% were fully vaccinated for HBV versus 45% in Heerlen.. ...
Complement C6 Antibodies available through Novus Biologicals. Browse our Complement C6 Antibody catalog backed by our Guarantee+.
It is increasingly evident that the brain is not isolated from events in the peripheral immune system and that innate pathways important in host protection can become dysregulated leading to neuropsychiatric changes. For example, increased copy number of the human complement C4A gene is a major risk factor for Schizophrenia; while in the periphery, it is protective against systemic autoimmunity such as lupus. Elevation in peripheral levels of interferon alpha (IFN-a) such as in viral infection, autoimmunity, interferonopathies or treatment with recombinant cytokine are strongly associated with psychiatric symptoms. We propose that blood-brain barrier entry of inflammatory cytokines such as IFN-a can activate multiple cell types in the brain triggering excess pruning of synapses altering neural circuits critical in executive function and cognitive memory.. ...
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Itrary criterion, and other values can not surprisingly be employed, but we look at that it corresponds to sturdy constructive or damaging associations. In terms of percentages, anTable 1. Schematic and illustrative two-way tables with the number of surveys in which each of two species was present or absent. Letters c, d, e, and f represent percentages of web pages at which the two species have been present or absent. Species B Species A Present Absent Total Present c e c+e Species B Species A Present Absent Total Present 15 5 20 Absent 35 45 80 Total 50 50 one hundred Absent d f d+f Total c+d e+f c+d+e+fMeasurement and visualization of species pairwise associationsOur strategy for examining species pairwise association seeks to quantify the strength of association between two individual species with regards to two odds ratios: the odds of your 1st species becoming present when the second one particular is (i.e., P(1 ), where P would be the probability of your very first species getting present ...
Sorry, I dont mean to be a total c**** tease. Because there is no Kogi app. BUT THERE JUST MIGHT BE ONE fairly soon. MIGHT. The thing is, were fairly
To be able to seek, first you have to be aware. Wolfgang Reinhardt has looked at knowledge workers, researchers in particular, and examined how they can be aware in their fields of expertise. Wolfgang graciously sent me a copy of his PhD thesis (Awareness: Support for knowledge workers in research networks) which he will be defending on 5 April at the Open Universiteit Nederland in Heerlen.. Wolfgang describes 10 knowledge worker roles that I think are helpful in understanding how all collaborative workers can share their knowledge.. ...
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.
IVERIC bio, Inc. announced initial topline data confirming that Zimura® met its prespecified primary endpoint in its Phase 2b clinical trial.
The RCCX gene cluster located on chromosome 6 is one of the most complex and intriguing regions of the human genome. Situated in the middle of the MHC region, RCCX genotypes have been extensively studied in association with many complex diseases, yet no published literature exists which links the myriad of comorbidities to RCCX haplotypes.. Furthermore, no existing therapies have been considered …until now…. Scroll down for more info. ...
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.
REIS, E S; BARACHO, G V; LIMA, A S; ISAAC, Lourdes. A stop codon in exon 13 causes the complete lack of human complement component C3 deficiency. Molecular Immunology[S.l: s.n.], 2001 ...
Complement component 4 (C4) gene copy number (GCN) affects the susceptibility to systemic lupus erythematosus (SLE) in different populations, however the possible phenotype significance remains to be determined. This study aimed to associate C4A, C4B and total C4 GCN and SLE, focusing on the clinical phenotype and disease progression. C4, C4A and C4B GCN were determined by real-time PCR in 427 SLE patients and 301 healthy controls, which underwent a detailed clinical evaluation according to a pre-established protocol. The risk of developing SLE was 2.62 times higher in subjects with low total C4 GCN (| 4 copies, OR = 2.62, CI = 1.77 to 3.87, p | 0.001) and 3.59 times higher in subjects with low C4A GCN (| 2 copies; OR = 3.59, CI = 2.15 to 5.99, p | 0.001) compared to those subjects with normal or high GCN of total C4 (≥4) and C4A (≥2), respectively. An increased risk was also observed regarding low C4B GCN, albeit to a lesser degree (OR = 1.46, CI = 1.03 to 2.08, p = 0.03). Furthermore, subjects
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: ...
C3 exhibits two common allotypic variants that may be separated by gel electrophoresis and are called C3 fast (C3 F) and C3 slow (C3 S). C3 F, the less common v
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 ...
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.
Lehner B، Semple JI، Brown SE، وآخرون. (2004). Analysis of a high-throughput yeast two-hybrid system and its use to predict the function of intracellular proteins encoded within the human MHC class III region. Genomics. 83 (1): 153-67. PMID 14667819. doi:10.1016/S0888-7543(03)00235-0. ...
The TNX is currently just under 4%, that was a doubling of rates from 2%. The target on a break is 6%. While that may not sound like much, it is a tripling of the borrowing costs from a little over a year ago. And while it is closer to historic norms in terms of rates, whats different is that the level of debt in the system has grown exponentially and there is a ton of supply still coming on. Most of it was financed short term and that presents a problem going forward. Also, if those targets are achieved, interest rates will break a 28 year downtrend line, portending the possibility of even higher rates. So, its crunch time again. They either try to stop it here again, or they let the markets do what they are going to do ...
The TNX is currently just under 4%, that was a doubling of rates from 2%. The target on a break is 6%. While that may not sound like much, it is a tripling of the borrowing costs from a little over a year ago. And while it is closer to historic norms in terms of rates, whats different is that the level of debt in the system has grown exponentially and there is a ton of supply still coming on. Most of it was financed short term and that presents a problem going forward. Also, if those targets are achieved, interest rates will break a 28 year downtrend line, portending the possibility of even higher rates. So, its crunch time again. They either try to stop it here again, or they let the markets do what they are going to do ...
Free Online Library: Maternal vitamin B deficiency and epigenetic changes of genes involved in the Alzheimers disease pathogenesis.(Research Article, Report) by Biology and Medicine; Science and technology, general Development and progression Genetic aspects Epigenetic inheritance Health aspects Mothers Vitamin B deficiency Complications and side effects
Answer 1 of 3: We will be staying is Sittard in August, and want to travel to Aachen by public transport. Unfortunately, Im having difficulty finding travel info cross-border. Can anyone point me to the correct website? Thanks!
Complement C1r, Human, Activated, Two-Chain Form, CAS 80295-34-7, is a native, activated, C1r complement component. - Find MSDS or SDS, a COA, data sheets and more information.
Complement C9 Polyclonal Antibody from Invitrogen for Western Blot and Immunohistochemistry (Paraffin) applications. This antibody reacts with Human samples. Supplied as 100 µg purified antibody (1 mg/ml) in PBS with 1% BSA and 0.02% sodium azide; pH 7.4.
Complement C6 Polyclonal Antibody from Invitrogen for Western Blot and Immunohistochemistry (Frozen) applications. This antibody reacts with Mouse samples. Supplied as 100 µg purified antibody (0.1 mg/ml) in PBS with 0.1% BSA and 0.02% sodium azide.
Walk-In Labs complement C3 serum test helps determine causes of recurrent infections, autoimmune disorders & more. A cheap, convenient online blood test.
Glutamine is the most abundant amino acid in the body, comprising more than 60% of the free amino acid pool in skeletal muscle and greater than 20% of total c
Rare mutations in the switch III region of Ras can increase its nanoscale clustering, which enhances effector recruitment and downstream signaling.
Content - SummaryComplement C5 (C3 And PZP Like Alpha 2 Macroglobulin Domain Containing Protein 4 or C5) pipeline Target constitutes close to 33 molec
Caroline Herman January 30, 2015 at 9:21 pm # Hi. Im eighteen several years outdated and I am not solely positive but I believe Im homozygous c677t. My physician before didnt definitely know very well what it intended at the time then we moved. Ahead of we moved even though, he begun me on 15mg of Deplin. At first I felt terrific like you claimed, but then every single every so often Ive relapses of worry attacks and serious panic ...
The human body is a mystery. As much and as fast as were learning, we still know very little. This post is about a recent discovery. I call it a discovery, because Ive lived out what this theory holds to be true, as have a number of patients I work with, and perhaps some of you reading this. RCCX theory is quite complex. The best I can do is share my personal experience with the hope that doing so will help make this information more accessible. ...
Complement C3b, Human, is a native C3b complement component. It is a glycoprotein composed of the modified C3-α chain (αʹ) (M.W. 105,000) and the intact C3-β chain (M.W. 75,000). - Find MSDS or SDS, a COA, data sheets and more information.
1 reviews. Compare Complement C5a desArg ELISA Kits from leading suppliers on Biocompare. View specifications, prices, citations, reviews, and more.
This Competitive Intelligence report about Complement C5 Inhibitors 2017 - Biosuperiors & Biosimilars provides a competitor evaluation in the field of mainly...
If an object would be put onto the battlefield or onto the stack under the control of a player who has left the game, that object remains in its current zone. A working-class hero type would go on first, setting up an energetic, bright, and enthralling mood, followed by a princess type, who would deliver a feminine, quiet, adorable, yet intelligent speech. Women showed higher anxiety symptoms than men, while men showed higher depressive symptoms than women. The xps c1s spectra in figure 3.23 (a) demonstrate that the total c1s intensity was almost completely restored by ch4 plasma. The situation ceases, he said, when taxpayers begin handing over funds in april and may. What addresses will host a use to for the destination ip and mac addresses in this communication? Cv of a denier: david bellamy, a botanist, is special professor of geography at the university of nottingham and honorary professor of the university of central queensland. So i taught my patient about this method and provided her ...
Analysis of the class III region of the mouse, using human probes, showed that all human class III genes tested thusfar seem to have homologous counterparts in the mouse genome. Furthermore, the...
DI-fusion, le Dépôt institutionnel numérique de lULB, est loutil de référencementde la production scientifique de lULB.Linterface de recherche DI-fusion permet de consulter les publications des chercheurs de lULB et les thèses qui y ont été défendues.
In a paper published online in Nature Communications, a team of SickKids clinician-scientists led by Drs. Aleixo Muise and Walter Kahr report the discovery of a new hereditary condition: ARPC1B deficiency.
Ganesalingam J, An J, Shaw CE, Shaw G, Lacomis D, Bowser R. Combination of neurofilament heavy chain and complement C3 as CSF biomarkers for ALS ...
Title: Converging Pathways in the Occurrence of Endoplasmic Reticulum (ER) Stress in Huntingtons Disease. VOLUME: 11 ISSUE: 1. Author(s):R. Vidal, B. Caballero, A. Couve and C. Hetz. Affiliation:Institute of Biomedical Sciences, University of Chile. Independencia 1027, Santiago, P.O. BOX 70086, Chile.. Keywords:Huntingtons disease, ER stress, protein misfolding, Unfolded protein response, Huntingtin, endoplasmic reticulum, neurodegenerative disease, cognitive defects, dementia, polyglutamine, spinobulbar muscular atrophy, spinocerebellar ataxias, Machado-Joseph Disease, mutations, protein conformational disorders, aggregation, apoptosis, translocation, homeostasis, PERK signaling, morphogenesis, phenotype, mutant Htt, tunicamycin, vesicular trafficking, autophagy, ERAD, calnexin cycle, chaperones, familial amyotrophic lateral sclerosis, brefeldin A, ER/Golgi trafficking, Parkinsons disease, Synuclein, NMDAR, AMPA receptors, axonal transport, Macroautophagy, autophagosome, Beclin-1, ...
Complement peptide C5a, C4a, and C3a receptors". Pharmacol. Rev. 65 (1): 500-43. doi:10.1124/pr.111.005223. PMID 23383423. ... 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". 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 ...
Complement peptide C5a, C4a, and C3a receptors". Pharmacological Reviews. 65 (1): 500-43. doi:10.1124/pr.111.005223. PMID ... bacteria-induced complement activation also causes the formation of complement component 3a (C3a) by cleavage from complement ... Li R, Coulthard LG, Wu MC, Taylor SM, Woodruff TM (Mar 2013). "C5L2: a controversial receptor of complement anaphylatoxin, C5a ... interaction of bacteria with blood plasma components to activate the complement cascade which then cleave C5a from Complement ...
C4a and C5a) that are produced as part of the activation of the complement system. Complement components C3, C4 and C5 are ... C3, C4A, C4B, C4B-1, C5, FBLN1, FBLN2 Allergy Anaphylatoxin receptors Anaphylaxis Complement system Inflammation Immune system ... coded for by a single exon within the complement protein gene. The C3a, C4a and C5a components are referred to as ... C4a is the least active anaphylatoxin. Although some drugs (morphine, codeine, synthetic ACTH) and some neurotransmitters ( ...
Cite journal requires ,journal= (help) Yu CY (1991). "The complete exon-intron structure of a human complement component C4A ... 1994). "Structure and genetics of the partially duplicated gene RP located immediately upstream of the complement C4A and the ... "Characterisation of the novel gene G11 lying adjacent to the complement C4A gene in the human major histocompatibility complex ... 1996). "Complete sequence of the complement C4 gene from the HLA-A1, B8, C4AQ0, C4B1, DR3 haplotype". Immunogenetics. 43 (4): ...
The C1 complex (complement component 1, C1) is a protein complex involved in the complement system. It is the first component ... Active C1s splits C4 and then C2, producing C4a, C4b, C2a and C2b. The classical pathway C3-convertase (C4bC2b complex) is ... 2001). "The complement system and innate immunity". Immunobiology: The Immune System in Health and Disease. New York: Garland ... The antibodies IgM or certain subclasses of IgG complexed with antigens are able to initiate the complement system: a single ...
Complement peptide C5a, C4a, and C3a receptors". Pharmacological Reviews. 65 (1): 500-43. doi:10.1124/pr.111.005223. PMID ... The receptor binds to complement component C3a, although there is limited evidence that this receptor also binds C4a in lesser ... The C3a receptor also known as complement component 3a receptor 1 (C3AR1) is a G protein-coupled receptor protein involved in ... Sayegh ET, Bloch O, Parsa AT (August 2014). "Complement anaphylatoxins as immune regulators in cancer". Cancer Medicine. 3 (4 ...
... mechanism for this interaction is increased complement factor C3 deposition onto synaptosomes as a consequence of increased C4A ... Genes in the Complement Component 4 (C4) locus of the major histocompatibility complex (MHC), which encode for complement ... Specifically, complement factors C1q and C3 have been found to have a role in microglia-mediated synaptic pruning. Carriers of ... The fact that some of these complement factors are involved in signaling during synaptic pruning also seems to suggest that ...
"Structure and genetics of the partially duplicated gene RP located immediately upstream of the complement C4A and the C4B genes ... Yang Z, Qu X, Yu CY (August 2001). "Features of the two gene pairs RD-SKI2W and DOM3Z-RP1 located between complement component ... are present between complement component genes factor B and C4 in the class III region of the HLA". Genomics. 53 (3): 338-47. ... are present between complement component genes factor B and C4 in the class III region of the HLA". Genomics. 53 (3): 338-47. ...
... in the major histocompatibility complex III close to the Complement component 4 genes C4A and C4B, the Tenascin X gene TNXB and ... In the chicken and quail, there is only a single CYP21 gene, which locus is located between complement component C4 and TNX ... Yu CY (1999). "Molecular genetics of the human MHC complement gene cluster". Experimental and Clinical Immunogenetics. 15 (4): ... "Two genes encoding steroid 21-hydroxylase are located near the genes encoding the fourth component of complement in man". ...
C4a and C2a are released. C4a is an anaphylatoxin. C3 convertases are unstable (half-life 10 - 20 min) - respectively they are ... 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 ...
... complement c4 MeSH D12.776.124.486.274.350.250 - complement c4a MeSH D12.776.124.486.274.350.260 - complement c4b 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 complement system can be activated through three pathways: the classical pathway, the alternative pathway, and the lectin ... the MASP protein functions to cleave the blood protein C4 into C4a and C4b. The C4b fragments can then bind to the surface of ... The subsequent complement cascade catalyzed by C3-convertase results in creating a membrane attack complex, which causes lysis ... In order to activate the complement system when MBL binds to its target (for example, mannose on the surface of a bacterium), ...
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 ...
... histamine-inducers Complement proteins C3a, C4a, and C5a work by triggering histamine release from mast cells and basophil ...
Classical complement pathway C1Q complex - C1R / C1S C4 - C4a C2 Mannan-binding lectin pathway MASP1 / MASP2 Mannan-binding ... system Complement system Classical complement pathway Mannan-binding lectin pathway Alternate complement pathway Complement ... see complement proteins section) Collectins Mannan-binding lectin (MBL) Surfactant protein A (SP-A) Surfactant protein D (SP-D ... Complement receptor of the immunoglobulin family) Anaphylatoxin receptors C3a receptor C5a receptor (CD88) C5AR2 Fc receptor Fc ...
MASP-2 is activated to cleave complement components C4 and C2 into C4a, C4b, C2a, and C2b. MASP1 (protein) Mannan-binding ... MASP-2 is involved in the complement system. MASP-2 is very similar to the C1s molecule, of the classical complement pathway, ... The Ra-reactive factor (RARF) is a complement-dependent bactericidal factor that binds to the Ra and R2 polysaccharides ... Petersen SV, Thiel S, Jensenius JC (2001). "The mannan-binding lectin pathway of complement activation: biology and disease ...
Complement C4-A is a protein that in humans is encoded by the C4A gene. This gene encodes the acidic form of complement factor ... Complement component 4 Complement component 4B HLA A1-B8-DR3-DQ2 haplotype Complement system Complement deficiency ... Media related to C4A at Wikimedia Commons Human C4A genome location and C4A gene details page in the UCSC Genome Browser. Hugli ... "Entrez Gene: C4A complement component 4A (Rodgers blood group)". Dawkins RL, Uko G, Christiansen FT, Kay PH (Sep 1983). "Low C4 ...
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 ...
C1q mediates the classical pathway by activating the C1 complex, which cleaves C4 and C2 into smaller fragments (C4a, C4b, C2a ... 12th European Meeting on Complement in Human Disease12th European Meeting on CHD12th European Meeting on Complement in Human ... C3a is one of the proteins formed by the cleavage of complement component 3; the other is C3b. C3a is a 77 residue ... Anaphylatoxins are small complement peptides that induce proinflammatory responses in tissues. C3a is primarily regarded for ...
Complement receptors, collectins, ficolins, pentraxins such as serum amyloid and C-reactive protein, lipid transferases, ... binding the C4b subunit and releasing C4a into the bloodstream; similarly, binding of C2 causes release of C2b. Together, MBL, ... Once bound to the ligands MBL and Ficolin oligomers recruit MASP1 and MASP2 and initiate the lectin pathway of complement ... "/"self turned nonself" type pathogen pattern are also identified and destroyed (e.g. by complement fixation or other cytotoxic ...
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 ...
C4A-C4A, or C4B-C4B) and 31% trimodular configuration (equally split between LLL as C4A-C4A-C4B or LSS as C4A-C4B-C4B). ... Complement component 4A Complement component 4B HLA A1-B8-DR3-DQ2 haplotype Complement system Complement deficiency Sekar A, ... Law SK, Dodds AW, Porter RR (August 1984). "A comparison of the properties of two classes, C4A and C4B, of the human complement ... Law SK, Dodds AW, Porter RR (August 1984). "A comparison of the properties of two classes, C4A and C4B, of the human complement ...
"Lack of evidence of a specific role for C4A gene deficiency in determining disease susceptibility among C4-deficient patients ... Complement component 4 Complement component 4A HLA A1-B8-DR3-DQ2 haplotype Complement system Complement deficiency ... Complement component 4B (Chido blood group) is a protein that in humans is encoded by the C4B gene. This gene encodes the basic ... "Entrez Gene: Complement component 4B (Chido blood group)". Retrieved 2012-01-27. CS1 maint: discouraged parameter (link) Yu CY ...
MASP-1 and MASP-2 are activated to cleave complement components C4 and C2 into C4a, C4b, C2a, and C2b. In f, two smaller MBL- ... C4a and C2b act as potent cytokines, with C4a causing degranulation of mast cells and basophils and C2b acting to increase ... The lectin pathway or lectin complement pathway is a type of cascade reaction in the complement system, similar in structure to ... Additional resources on Endothelial Injury Syndrome Classical complement pathway Alternative complement pathway Mannan-binding ...
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 ...
The system also complements the school curriculum, where in many cases, students in Years 9 and 10 and 11 are in the same ... Upon reaching a C4a, the student is removed from the classroom and given an after-school School punishment30 mins. If the ...
... (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 ...
C4A(Null), DR3, DQ2.5.[32] The entire haplotype, A1-Cw7-B8-TNFB*1-C4A(Null)-DR3-DQ2, is increased in patients and the genetic ... July 2008). "Autoimmune-associated HLA-B8-DR3 haplotypes in Asian Indians are unique in C4 complement gene copy numbers and HSP ... Closer to DR3, C4A is null in B8-DR3 haplotype. In autoimmune hepatitis[edit]. In 1972, a link between "HLA A1,8" (current:HLA ... Scully LJ, Toze C, Sengar DP, Goldstein R (May 1993). "Early-onset autoimmune hepatitis is associated with a C4A gene deletion ...
Zipfel, P. F., Hallström, T., & Riesbeck, K. (2013). Human complement control and complement evasion by pathogenic microbes- ... C4a ja C4b. C2a ja C4b kombineeruvad ning moodustub C3-konvertaas C4bC2a. Sama konvertaasi moodustumine on omane 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. ...
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. ...
Sengeløv H (1996). "Complement receptors in neutrophils.". Crit. Rev. Immunol. 15 (2): 107-31. PMID 8573284. ... C: C1Q/C1R/C1S - C4 (C4a) - C2. L: MASP1/MASP2 - MBL. A: Faktor B - Faktor D - Faktor P/Properdin ... "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 ... Piştê girêdana MBL, proteîna C4 a nav xwînê tê perçekirin, ji C4ê C4a û C4b çê dibin. C4b jî li rûyê hokara nexweşiyê de tê ... Sîstema temamker an jî sîstema tewawker (bi îngilîzî: complement system)[1] beşek ji sîstema bergiriya giştî ye. Sîstema ...
... 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 ... CFHR5 (Complement Factor H-Related protein 5) is able to bind to act as a cofactor for factor I, has decay accelerating ...
... is a member of the immunoglobulin superfamily, with a structure related to the putative primordial form of the family. As members of the immunoglobulin superfamily play fundamental roles in intercellular recognition involved in various immunologic phenomena, differentiation, and development, basigin is thought also to play a role in intercellular recognition (Miyauchi et al., 1991; Kanekura et al., 1991).[9][10] It has a variety of functions. In addition to its metalloproteinase-inducing ability, basigin also regulates several distinct functions, such as spermatogenesis, expression of the monocarboxylate transporter and the responsiveness of lymphocytes.[6] Basigin is a type I integral membrane receptor that has many ligands, including the cyclophilin (CyP) proteins Cyp-A and CyP-B and certain integrins.[11][12][13] It is expressed by many cell types, including epithelial cells, endothelial cells and leukocytes. The human basigin protein contains 269 amino acids that form two heavily ...
C4 (complement 4) produces a null allele at on locus C4AQ. This locus in part of the HLA A1-B8-DR3-DQ2 haplotype (markers are ... C4A(Null), DR3, DQ2.5. While type 1 diabetes shows an extended association on the HLA A1-B8-DR3-DQ2 haplotype, the association ...
Long PCR detection of the C4A null allele in B8-C4AQ0-C4B1-DR3 Grant SF, Kristjansdottir H, Steinsson K, Blondal T, Yuryev A, ... Determination of the structural basis for selective binding of Epstein-Barr virus to human complement receptor type 2 Martin DR ...
Null alleles of human complement C4. Evidence for pseudogenes at the C4A locus and for gene conversion at the C4B locus. Braun ... Deficiency of human complement protein C4 due to identical frameshift mutations in the C4A and C4B genes. Lokki, M.L., Circolo ... Characterisation of the novel gene G11 lying adjacent to the complement C4A gene in the human major histocompatibility complex. ... Genetic sophistication of human complement components C4A and C4B and RP-C4-CYP21-TNX (RCCX) modules in the major ...
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 ... Patients often ask if there are other medical conditions that may lower or raise the C3a and/or C4a. Both of these complement ... Stricker, R. B., Savely, V.R., Motanya, N.C. & Giglas, B.C. (2009). Complement split products C3a and C4a in chronic Lyme ...
Note: complement C4a, which the study terms "a clinically important biomarker for postexertional malaise in people with ME/CFS ... Postexercise complement C4a level was identified as a clinically important biomarker for postexertional malaise in people with ... However, neither exercise bout altered elastase activity, IL-1beta or complement C4a split product levels in people with ME/CFS ... 1beta and complement C4a levels. Design: Comparative experimental design.. Setting: University.. Subjects: Twenty-two women ...
Trichorhinophalangeal syndrome type I and systemic lupus erythematosus with complement C4A homozygous null alleles in the same ... Trichorhinophalangeal syndrome type I and systemic lupus erythematosus with complement C4A homozygous null alleles in the same ... All living family members in the first and second generation had homozygous C4A null alleles. In three of the adults the two ... like syndrome with complement C4 homozygous null alleles is described. Five family members in three generations were affected ...
C4A kills bacteria and boosts immunity, but too much can damage tissues and trigger allergic reactions. Learn what high levels ... C4A is often elevated in chronic inflammation.. What is C4A?. C4A is part of a "complement" group. The term complement means it ... C4A Test. You can request that your doctor test your C4A. Conventional doctors will look at high or low C4A levels and not ... High & Low C4A Levels (Complement C4A) & Mold Illness. By Joe Cohen, BS ...
Compare C4A ELISA Kits from Abbexa Ltd from leading suppliers on Biocompare. View specifications, prices, citations, reviews, ... Human Complement C4-A ELISA Kit Abbexa Ltd *Detection Target: Complement C4-A ... C4A ELISA Kits from Abbexa Ltd. The ELISA (enzyme-linked immunosorbent assay) is a well-established antibody-based tool for ...
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). ... C3a, C4a, and C5a (CD88) receptors. Receptors for C3a and C5a have been identified; whether a distinct receptor for C4a is ... The complement system exerts many of its effects through complement receptors (CRs). Of the 8 plasma membrane receptors for ...
Complement Component 4a) ELISA Kit OSCAR DIAGNOSTIC SERVICES PVT. LTD.is an India based Company in Delhi. ... Chicken C4a (Complement Component 4a) ELISA Kit » Chicken C4a (Complement Component 4a) ELISA Kit. Chicken C4a (Complement ... Chicken C4a (Complement Component 4a) ELISA Kit. Chicken C4a (Complement Component 4a) ELISA Kit. Chicken C4a (Complement ... Chicken C4a (Complement Component 4a) ELISA Kit. Chicken C4a (Complement Component 4a) ELISA Kit. Chicken C4a (Complement ...
Sim, Edith and Law, Sai-Kit A. (1985) Hydralazine binds covalently to complement component-C4: Different reactivity of C4A AND ... Hydralazine binds covalently to complement component-C4: Different reactivity of C4A AND C4B Gene-Products ...
The fourth component of the human complement system (C4) is coded for by two genes, C4A and C4B, located within the MHC. Null ... Genetic basis of human complement C4A deficiency. Detection of a point mutation leading to nonexpression.. ... Genetic basis of human complement C4A deficiency. Detection of a point mutation leading to nonexpression.. ... In a previous study, evidence was obtained for nonexpressed defective genes at the C4A locus, and for gene conversion at the ...
C4A and C4B) could be markers for RHD in the Brazilian population. Forty-nine patients with chronic RHD were studied. The ... The aim of the present investigation was to determine whether the alleles of the MHC class III complement proteins BF, C2 and ... The aim of the present investigation was to determine whether the alleles of the MHC class III complement proteins BF, C2 and ... The results showed a significantly elevated presence of the C4A*6 rare allele (p = 0.003 RR = 11.85) and a decrease of C4A*3 in ...
... and extracellular presence of activated C1s that independently of microbial triggers can activate the classical complement ... Missense or in-frame insertion/deletion mutations in complement 1 subunits C1r and C1s cause periodontal Ehlers-Danlos Syndrome ... Heterozygous missense or in-frame insertion/deletion mutations in complement 1 subunits C1r and C1s cause periodontal Ehlers- ... C4a was measured in serum and supernatant as a marker for complement 1 activation. (A) After addition of C4 to the supernatant ...
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 ... Ehrlich and Morgan termed this factor complement. The complement system as understood today is a multimolecular system composed ...
B, C and D. Gene copy-number variations of complement C4, C4A and C4B in JDM and controls. The p-values and chi-square values ... Complement C4A deficiency appears to be an important factor for the genetic risk and pathogenesis of JDM, particularly in ... Gene copy-number variations (CNVs) of complement C4 and C4A deficiency in genetic risk and pathogenesis of juvenile ... Gene Copy-Number Variations (CNVs) of Complement C4 and C4A Deficiency in Genetic Risk and Pathogenesis of Juvenile ...
Downregulation of C3 and C4A/B complement factor fragments in plasma from patients with squamous cell carcinoma of the penis ... Downregulation of C3 and C4A/B complement factor fragments in plasma from patients with sq ... and C4a/b (m/z 2021.26) complement proteins. ...
Low copy numbers of complement C4 and homozygous deficiency of C4A may predispose to severe disease and earlier disease onset ... Low copy numbers of complement C4 and homozygous deficiency of C4A may predispose to severe disease and earlier disease onset ... Low copy numbers of complement C4 and homozygous deficiency of C4A may predispose to severe disease and earlier disease onset ... to investigate the independence of complement C4 in association with SLE. Results Homozygous deficiency of the C4A isotype was ...
... and another associated with C4AQ0 without detectable impairment in the complement dependent IC transport mechanism. Individuals ... Complement C4a / analysis* * Complement C4a / genetics * Erythrocytes / immunology * Female * Genetic Predisposition to Disease ... IC levels were measured by complement consumption assay, C3d by a sandwich ELISA, factor B by immunoelectrophoresis, and the ... Results: Family members with homozygous or heterozygous C4AQ0 (47%) showed no impaired complement dependent opsonization of IC ...
Frequency of Common Alleles of C4A, C4B, and C3 Complement Genes in Patients With CVD and Healthy Controls Aged ,60 Years ... In CVD patients the frequency of the C4A*2 allele was relatively low, while that of the C4A*4 allele was relatively high. ... Allotypes of the 2 genes encoding the fourth component of complement, C4, and that encoding the third component of complement, ... C4A, C4B, and C3) encoding proteins of the complement system were determined by electrophoresis and immunofixation. Serum ...
C4a and C5a) that are produced as part of the activation of the complement system. Complement components C3, C4 and C5 are ... C3, C4A, C4B, C4B-1, C5, FBLN1, FBLN2 Allergy Anaphylatoxin receptors Anaphylaxis Complement system Inflammation Immune system ... coded for by a single exon within the complement protein gene. The C3a, C4a and C5a components are referred to as ... C4a is the least active anaphylatoxin. Although some drugs (morphine, codeine, synthetic ACTH) and some neurotransmitters ( ...
Abcams Complement C4 ELISA Kit (ab108825) suitable for Cell culture supernatant, Saliva, Milk, Urine, Cerebral Spinal Fluid in ... Derived from proteolytic degradation of complement C4, C4a anaphylatoxin is a mediator of local inflammatory process. It ... A Complement C4 specific antibody has been precoated onto 96-well plates and blocked. Standards or test samples are added to ... Complement component C4 is expressed at highest levels in the liver, at moderate levels in the adrenal cortex, adrenal medulla ...
Complement peptide C5a, C4a, and C3a receptors". Pharmacol. Rev. 65 (1): 500-43. doi:10.1124/pr.111.005223. PMID 23383423. ... Complement 3 (C3) through its interaction with factors B and D (adipsin) generates C3a. In the human body, C3a is rapidly ...
They noted associations near the C4 gene, which encodes for complement component 4. C4 is part of the complement cascade, an ... Human C4 exists in 2 forms, C4A and C4B. The protein products from these genes vary in structure and in their molecular targets ... When they measured RNA levels in post-mortem human adult brain samples, they found that the different forms predicted C4A and ... Both genes were expressed at higher levels in brain tissues from schizophrenia patients, but expression levels of C4A were 2-3 ...
... far exceeding the classical examples of diseases associated with complement deficiencies. Finally, we discuss complement as a ... In pathology, complement can be a friend or a foe. It acts as a friend in the defense against pathogens, by inducing a direct ... In pathology, complement can be a friend or a foe. It acts as a friend in the defense against pathogens, by inducing ... Inadequate complement activation becomes a disease cause, as in atypical hemolytic uremic syndrome, C3 glomerulopathies, and ...
Complement components. Ex. C3A C4A C5A 27 To keep up with the demand for neutrophils the _______releases more neutrophils into ... Anaphylatoxic agents generated from complement pathway activation. Mechanism of action: Stimulate histamine release and ...
The important activated complement fragments for inflammation are C3a, C4a, and C5a. Activation of these products produces ... Does not affect cutaneous IgA and complement deposition. It may inhibit the alternate pathway of complement and interfere with ... The antibody also marks the antigen with complement, a series of blood proteins. Complement coats antigens recognized by ... Generally levels of serum complement are normal but drop during preactive phases. Serum complement levels, particularly C9m ...
Yu CY (1991). "The complete exon-intron structure of a human complement component C4A gene. DNA sequences, polymorphism, and ... 1994). "Structure and genetics of the partially duplicated gene RP located immediately upstream of the complement C4A and the ... "Characterisation of the novel gene G11 lying adjacent to the complement C4A gene in the human major histocompatibility complex ... 1996). "Complete sequence of the complement C4 gene from the HLA-A1, B8, C4AQ0, C4B1, DR3 haplotype". Immunogenetics. 43 (4): ...
C4a is an anaphylatoxin.. *C4b forms part of C3-convertase, in conjunction with 2a: ... C4d is the degradation product of the activated complement factor C4, a component of the classical complement cascade which is ... Complement receptors. CR1 - CR2 - CR3 - CR4 - CD11b/CD11c/CD18 - Anaphylatoxin (C3a, C5a) ... Categories: Genes on chromosome 6 , Blood , Hematology , Transfusion medicine , Blood antigen systems , Complement system ...
Mouse Monoclonal Anti-Complement C4d Antibody (C4D204) [DyLight 550]. Acute Humoral Rejection Marker. Validated: ICC/IF, IHC-Fr ... C4A. Purity. Protein A purified. Innovators Reward. Test in a species/application not listed above to receive a full credit ... Home » Complement C4d » Complement C4d Antibodies » Complement C4d Antibody (C4D204) [DyLight 550] ... Blogs on Complement C4d. There are no specific blogs for Complement C4d, but you can read our latest blog posts. ...
This gene encodes the acidic form of complement factor 4 part of the classical activation pathway. The protein is expressed as ... Home , Life Science Research , Products , PCR Amplification , PrimePCR™ PCR Primers, Assays, and Arrays , Gene: C4A, Human , ... PrimePCR™ ddPCR™ Expression Probe Assay: C4A, Human. print ddPCR™ probe assay designed for gene expression analysis. Probe ... The trimer provides a surface for interaction between the antigen-antibody complex and other complement components. The alpha ...
  • 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)
  • C4A is an activation protein, which means it also activates the other complement proteins to increase in level [ 1 ]. (selfhacked.com)
  • The aim of the present investigation was to determine whether the alleles of the MHC class III complement proteins BF, C2 and C4 (C4A and C4B) could be markers for RHD in the Brazilian population. (nih.gov)
  • The complement system as understood today is a multimolecular system composed of more than 32 proteins and consisting of serum proteins, serosal proteins, and cell membrane receptors that bind to complement fragments. (medscape.com)
  • The complement system consists of 7 serum and 9 membrane regulatory proteins, 1 serosal regulatory protein, and 8 cell membrane receptors that bind complement fragments. (medscape.com)
  • These two peptides were identified by the proteomic approach based on a MALDI -TOF/TOF as fragments of C3 (m/z 1896.17) and C4a/b (m/z 2021.26) complement proteins . (bvsalud.org)
  • Allele frequencies of 3 genes (C4A, C4B, and C3) encoding proteins of the complement system were determined by electrophoresis and immunofixation. (ahajournals.org)
  • Unfortunately, the lack of coherence in complement proteins nomenclature and the complexity of the enzymatic cascade render complement one of the "most complicated and incomprehensible" parts of immunology and is frequently avoided by students and scientists. (frontiersin.org)
  • C3 and C4, mainly produced by the liver, are the major plasma proteins of the immune system complement pathways. (thermofisher.com)
  • The Classical pathway of activation of the complement system is a group of blood proteins that mediate the specific antibody response. (wikipathways.org)
  • 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)
  • Four of the significant differentially expressed proteins (lipopolysaccharide binding protein, fibrinogen β chain, α‑1 antitrypsin, and complement factor H) were validated by western blotting. (spandidos-publications.com)
  • 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)
  • Kirjavainen V, Jarva H, Biedzka Sarek M, Blom A, Skurnik M, Meri S. Yersinia enterocolitica serum resistance proteins YadA and ail bind the complement regulator C4b-binding protein. (labome.org)
  • The gene variants are a member of the complement system, a cascade of proteins that help antibodies and phagocytic cells remove damaged cells of a person's own body, as well as an infection defense that promotes inflammation and attacks pathogens. (uab.edu)
  • For the complement proteins that are encoded by the genes for C4 and for complement component 3, or C3, both C4 protein and its effector C3 protein were present at greater levels in men than in women in cerebrospinal fluid and blood plasma among adults ages 20-50. (uab.edu)
  • Deposition of complement proteins on the bacteria was monitored by Western blotting. (asm.org)
  • The complement system is a series of proteins that act in a defined sequence (Fig. 1 ) to promote immune clearance by opsonizing or killing microorganisms and augmenting the inflammatory response. (asm.org)
  • The nonactivated complement proteins are indicated above and to the right of the wide arrows, and the arrows pointing from them show the product that is released during activation. (asm.org)
  • To elucidate the molecular basis for complement resistance by BrkA, in this study we have attempted to determine which step in the complement cascade is affected by BrkA by monitoring the deposition of complement proteins on the surface of strains either expressing or not expressing BrkA. (asm.org)
  • Most complement proteins are zymogens which are proteases that become activated when cleaved. (davidson.edu)
  • C3b is a membrane associated protein which binds covalently to other complement proteins already on the pathogen surface. (davidson.edu)
  • The complex of complement proteins on the cell surface after C3b binds forms the C5 convertase. (davidson.edu)
  • After cleavage C5b interacts nonenzymatically with other complement proteins to form the MAC. (davidson.edu)
  • The binding domain of C5b for other complement proteins such as C6 and C7 has been recently characterized and is homologous to a complement binding domain on C3 and C4. (davidson.edu)
  • Other complement proteins such as C6 and C7 interact with C5 at the active site C345C in forming the MAC. (davidson.edu)
  • Results After short-term ERT (4-12 months), the levels of 15 plasma proteins involved in inflammation, oxidative and ischaemic injury, or complement activation were reduced significantly. (bmj.com)
  • Circulating complement proteins in patients with sepsis or systemic inflammatory response syndrome. (springer.com)
  • Furthermore, the structure and functions of several complement proteins as well as the protein-protein interactions that underlie these functions are now being investigated with the aid of cross-disciplinary approaches ranging from mathematics and biophysics to comparative phylogenesis, in silico studies, mimetics and proteomics. (upenn.edu)
  • Our laboratory, extending its research beyond the scope of traditional complement pathobiology, has embraced this global and combinatorial approach to biomedical research and has been actively engaged in defining the function of complement proteins in several biological contexts and pathophysiological states. (upenn.edu)
  • Serum peptides derived from certain cleaved COMPLEMENT PROTEINS during COMPLEMENT ACTIVATION. (harvard.edu)
  • The new approach to targeting complementing proteins fills scientists with hope for a whole range of treatment down the road. (rt.com)
  • The complexity of the complement cascade together with the lack of multiplex tools, makes it difficult to elucidate the key interacting proteins that underlie the pathogenesis of AMD. (arvojournals.org)
  • Our goal was to qualify a multiplex complement panel as a tool for future determination of complement proteins associated with ocular disease in donor eyes. (arvojournals.org)
  • Pooled normal human serum from Quidel (San Diego, CA), and complement proteins from CompTech (Tyler, TX) and Quidel, were used to benchmark the assay and to assess assay specificity, accuracy, linearity and matrix effects. (arvojournals.org)
  • Serum levels of the complement proteins approximated values from the literature and showed corresponding changes upon serum activation. (arvojournals.org)
  • Derived from proteolytic degradation of complement C4, C4a anaphylatoxin is a mediator of local inflammatory process. (abcam.com)
  • C4a is an anaphylatoxin . (thefullwiki.org)
  • 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)
  • 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)
  • The structure of an AT module was determined for the complement-derived anaphylatoxin C3a, and was found to be a compact alpha-helical fold that is stabilised by three disulphide bridges in the pattern Cys1-4, Cys2-5 and Cys3-6 (where Cys is cysteine). (embl.de)
  • Support for a causal role for altered anaphylatoxin production in human disease comes from reports of exaggerated complement production in the lungs of asthmatics as well as the association of asthma with polymorphisms in C3/C3aR genes. (springer.com)
  • The presence of the complement-derived anaphylatoxin peptides, C3a and C5a, in the lung can induce respiratory distress characterized by contraction of the smooth muscle walls in bronchioles and pulmonary arteries and aggregation of platelets and leukocytes in pulmonary vessels. (jimmunol.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)
  • The order of anaphylatoxin activity from the strongest to the weakest is C5a, C3a, C4a, and C5a des-arginine. (harvard.edu)
  • Complement induction in spinal cord microglia results in anaphylatoxin C5a-mediated pain hypersensitivity. (harvard.edu)
  • There are three general pathways by which the body increases C4a: The Alternative Pathway, The Lectin Pathway, and The Classical Pathway. (selfhacked.com)
  • Activation of the complement pathways. (medscape.com)
  • All three pathways merge through at common intersection, complement C3. (sigmaaldrich.com)
  • Its activation is required for both classical and alternative complement activation pathways. (thermofisher.com)
  • Three biochemical pathways activate the complement system: the classical complement pathway , the alternative complement pathway , and the lectin pathway . (wikipedia.org)
  • 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)
  • Alternative complement pathway - The classical and alternative complement pathways. (academic.ru)
  • Herein, we explore our current understanding of the role of complement activation in asthma pathogenesis and highlight the potential of targeting complement pathways for therapeutic drug development. (springer.com)
  • We selected most pathways f11 participated on our site, such as Complement and coagulation cascades, which may be useful for your reference. (creativebiomart.net)
  • Both the classical and alternative pathways of complement activation are represented, although details are given only for the classical pathway. (asm.org)
  • Each of the three pathways of the complement system results in the formation of C3 convertase on the pathogen surface. (davidson.edu)
  • In addition we study the involvement of various complement components with developmental pathways and the role of complement in tissue regeneration, early hematopoietic development and cancer. (upenn.edu)
  • Human MBL also bound to DENV and neutralized infection of all four DENV serotypes through complement activation-dependent and -independent pathways. (asm.org)
  • Here, we show that mannose-binding lectin (MBL), a pattern recognition molecule that initiates the lectin pathway of complement activation, neutralized infection of all four DENV serotypes through complement activation-dependent and -independent pathways. (asm.org)
  • The involvement of three upstream complement pathways in septic shock is more complicated. (hindawi.com)
  • It is unknown whether excessive activation of these three upstream complement pathways may contribute to the detrimental effects in septic shock. (hindawi.com)
  • There are three pathways in the complement system: classical, alternative, and lectin. (hindawi.com)
  • The C3a complement protein level was normal in the AIDS patients, the healthy patients and the chronic Lyme patients. (publichealthalert.org)
  • Note: complement C4a, which the study terms "a clinically important biomarker for postexertional malaise in people with ME/CFS," is a protein encoded by the C4A gene, associated with the classical activation pathway, part of the immune system that can kill pathogens "without antibody participation. (prohealth.com)
  • C1r and C1s have a similar protein domain structure with the N-terminal interaction domain including CUB (complement C1r/C1s, Uegf, Bmp1) and EGF (epidermal growth factor) modules in a CUB1-EGF-CUB2 arrangement, two complement-control-protein modules CCP1 and CCP2, and a serine protease (SP) domain ( Figure 1A , Table 1 ). (frontiersin.org)
  • C4A isotype is responsible for effective binding to form amide bonds with immune aggregates or protein antigens, while C4B isotype catalyzes the transacylation of the thioester carbonyl group to form ester bonds with carbohydrate antigens. (abcam.com)
  • Complement component 4 is a protein involved in the complement system . (thefullwiki.org)
  • 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)
  • The C4 protein derives from the C4A-C4B genes. (cellsciences.com)
  • Seven individual protein spots were identified as either significantly increased (α 2 -macroglobulin, haptoglobin, albumin) or decreased (complement C-4, serum retinol binding protein, apolipoprotein A-1, and two isoforms of apolipoprotein A-IV) with advanced fibrosis. (biomedcentral.com)
  • They compared this with its homologue in the vaccinia virus vaccinia virus complement control protein, or VCP. (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)
  • Meri T, Blom A, Hartmann A, Lenk D, Meri S, Zipfel P. The hyphal and yeast forms of Candida albicans bind the complement regulator C4b-binding protein. (labome.org)
  • C3a, C4a and C5a anaphylatoxins are protein fragments generated enzymatically in serum during activation of complement molecules C3, C4, and C5. (embl.de)
  • A-fragments form distinct structural domains of approximately 76 amino acids, coded for by a single exon within the complement protein gene. (embl.de)
  • 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)
  • Thus, differences in complement protein levels in men and women occur mostly during the reproductive years, ages 20-50. (uab.edu)
  • The researchers say sex differences in complement protein levels may help explain the larger effects of C4 alleles in men, the greater risk of women for lupus and Sjögren's, and the greater vulnerability of men for schizophrenia. (uab.edu)
  • Bordetella pertussis produces a 73-kDa protein, BrkA (Bordetella resistance to killing), which inhibits the bactericidal activity of complement. (asm.org)
  • The complement system consists of a series of plasma protein interactions which mediate direct attack on pathogens (opsonization) and induce inflammation. (davidson.edu)
  • Selberg O, Hecker H, Martin M, Klos A, Bautsch W, Kohl J. Discrimination of sepsis and systemic inflammatory response syndrome by determination of circulating plasma concentrations of procalcitonin, protein complement 3a, and interleukin-6. (springer.com)
  • Our current research efforts focus on the structural-functional aspects of protein-protein interactions and the rational design of small-size complement inhibitors. (upenn.edu)
  • Mannose-binding lectin (MBL) is a key soluble pathogen recognition protein of the innate immune system that binds specific mannose-containing glycans on the surfaces of microbial agents and initiates complement activation via the lectin pathway. (asm.org)
  • Different initiators activate each pathway but all converge to complement protein C3 and are followed by a common cascade (C5-9), resulting in the deposition of a membrane-attack-complex on targets and the release of chemoattractants (C3a and C5a) for inflammatory cells. (hindawi.com)
  • The central elements in the pathogenesis of pEDS seem to be the intracellular activation of C1r and/or C1s, and extracellular presence of activated C1s that independently of microbial triggers can activate the classical complement cascade. (frontiersin.org)
  • The complement system functions as an interactive sequence, with one reaction leading to another in the form of a cascade. (medscape.com)
  • C4 is part of the complement cascade, an immune system pathway that eliminates pathogens and cellular debris. (nih.gov)
  • These findings, along with evidence from other studies, suggested to the researchers that C4 might work with other components of the classical complement cascade to promote synaptic pruning. (nih.gov)
  • The complement system has been considered for a long time as a simple lytic cascade, aimed to kill bacteria infecting the host organism. (frontiersin.org)
  • Complement cascade is activated immediately after encountering the pathogen. (frontiersin.org)
  • C4d is the degradation product of the activated complement factor C4, a component of the classical complement cascade which is typically initiated by binding of antibodies to specific target molecules. (thefullwiki.org)
  • The complement system is a complex cascade involving proteolytic cleavage of serum glycoproteins often activated by cell receptors. (sigmaaldrich.com)
  • Ischaemic infarction may also cause initiation of the complement cascade. (sigmaaldrich.com)
  • The complement system is a biochemical cascade that helps, or complements, the ability of antibodies to clear pathogens from an organism. (wikipathways.org)
  • 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)
  • The mouse monoclonal antibody recognizes human Complement component 4 c (C4c), a component in the complement cascade and a degradation product of C4b which is cleaved by C4b/C3b inactivator to yield C4d and C4c. (cellsciences.com)
  • In this study we characterized the step in the complement cascade where BrkA acts, using three strains: a wild-type strain, a strain containing an insertional disruption of brkA , and a strain containing two copies of the brkA locus. (asm.org)
  • The complement cascade. (asm.org)
  • Prior studies showed that MBL-dependent activation of the complement cascade neutralized insect cell-derived West Nile virus (WNV) in cell culture and restricted pathogenesis in mice. (asm.org)
  • The predominant networks were related to oxidative stress, the inflammatory response, and the complement cascade. (hindawi.com)
  • Basic and clinical studies suggest that activation of complements in the common cascade, for example, complement component 3 (C3) and C5, is involved in the development of septic shock. (hindawi.com)
  • Genetic dysregulation of the complement cascade has been linked to an increased risk for the development of age related macular degeneration (AMD). (arvojournals.org)
  • These genes code for complement 1 subunits C1r and C1s, serine proteases that play a key role in the innate immune response. (frontiersin.org)
  • Microarray profiling of blood RNA revealed upregulation of type I interferon-stimulated genes and lower abundance of transcripts for T-cell and chemokine function genes in JDM, but this was less prominent among C4A-deficient or DR3-positive patients. (cdc.gov)
  • Objectives Low copy numbers and deletion of complement C4 genes are potent risk factors for systemic lupus erythematosus (SLE). (uni-kiel.de)
  • Conclusions Our findings confirm the important role of complement C4 genes in the development of SLE. (uni-kiel.de)
  • Previously we have found a highly significant association between the morbidity and mortality of myocardial infarction and C4B*Q0, the silent allele of 1 of the 2 genes encoding C4, a component of the complement system. (ahajournals.org)
  • 1994). "Structure and genetics of the partially duplicated gene RP located immediately upstream of the complement C4A and the C4B genes in the HLA class III region. (wikipedia.org)
  • We further identify changes in gene expression within the prenatal brain that potentially mediate risk for neuropsychiatric traits, including increased expression of C4A in association with genetic risk for schizophrenia, increased expression of LRRC57 in association with genetic risk for bipolar disorder, and altered expression of multiple genes within the chromosome 17q21 inversion in association with variants influencing the personality trait of neuroticism. (nih.gov)
  • The genes which are now known to be important in predisposing towards lupus are the DR genes, the complement genes, the X chromosome and race. (lupusuk.org.uk)
  • The fourth component of complement (C4) is encoded by two closely linked genes (C4A and C4B) within the MHC. (jci.org)
  • Volanakis JE (1995) Transcriptional regulation of complement genes. (els.net)
  • this study reveals that alleles at this locus associate with schizophrenia in proportion to their tendency to generate greater expression of complement component 4 ( C4A ) genes and that C4 promotes the elimination of synpases. (nature.com)
  • Genes differentially expressed include lower expression of AQP5, VEGF and RAD51C and higher expression of hemoglobin B, and complement factors CFD and C4A in tumors from African Americans. (aacrjournals.org)
  • A Complement C4 specific antibody has been precoated onto 96-well plates and blocked. (abcam.com)
  • Standards or test samples are added to the wells and subsequently a Complement C4 specific biotinylated detection antibody is added and then followed by washing with wash buffer. (abcam.com)
  • However, it should be kept in mind that apart from the classical antibody-mediated route of complement activation, C4 can also be activated via an alternative, antibody-independent mechanism, the 'mannan-binding lectin' pathway. (thefullwiki.org)
  • There are currently no images for Complement C4d Antibody (NBP2-34581R). (novusbio.com)
  • There are currently no images for Complement Component C1r Antibody (AF1807). (novusbio.com)
  • 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)
  • The following product was used in this experiment: Complement Polyclonal Antibody from Thermo Fisher Scientific, catalog # RAHU-C. (thermofisher.com)
  • The classical complement pathway typically requires antigen-antibody complexes for activation (specific immune response), whereas the alternative pathway can be activated by spontaneous C3 hydrolysis, foreign material, pathogens, or damaged cells. (wikipedia.org)
  • The trimer provides a surface for interaction between the antigen-antibody complex and other complement components. (bio-rad.com)
  • complement - Ehrlich term for the thermolabile substance, normally present in serum, that is destructive to certain bacteria and other cells sensitized by a specific c. fixing antibody. (academic.ru)
  • lectin pathway - a pathway of complement activation initiated in the absence of antibody by the binding of mannose binding lectin (MBL) to carbohydrates on the surface of microorganisms. (academic.ru)
  • Complement receptors and Fc receptors, expressed on effector cells, have a synergistic role in antibody‐mediated immune modulation and antigen clearance. (els.net)
  • Antigen-antibody complexes on the surface of a microorganism can activate the classical pathway of complement, a part of the acquired immune system (Fig. 1 ), by providing a binding site for C1. (asm.org)
  • Complement, a phylogenetically conserved arm of innate immunity, functions together with the adaptive immune response by serving as an important inflammatory mediator of antigen-antibody interactions. (upenn.edu)
  • The alternative complement pathway provides innate protection against microbial agents in the absence of specific antibody. (quidel.com)
  • In JDM, C4A-deficient subjects had higher levels of E-C4d (p=0.0003) and higher frequency of elevated levels of multiple serum muscle enzymes at diagnosis (p=0.0025). (cdc.gov)
  • Measurements of serum complement components C3 and C4 are useful in the diagnosis and monitoring of immune complex disease. (thermofisher.com)
  • Reduced levels of components of the classic pathway (Complements C1, C2, C4, C3) are common after such activation, Systemic lupus erythematosus, acute serum sickness and conditions associated with circulating immune complexes. (cellsciences.com)
  • Activation of human serum complement with allergens. (springer.com)
  • Although often overlooked as a defense of the respiratory tract, complement levels in this location are normally 10 to 20% of that found in serum and increase during inflammation ( 21 ). (asm.org)
  • The MicroVue C4a Enzyme Immunoassay measures the amount of C4a present in human serum, plasma and other biological or experimental samples. (quidel.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)
  • Baumann U and Schmidt RE (2001) The role of Fc receptors and complement in autoimmunity. (els.net)
  • Ravetch JV and Clynes RA (1998) Divergent roles for Fc receptors and complement in vivo. (els.net)
  • Complement factors and their receptors. (springer.com)
  • Complement receptors C5aR1 and C5aR2 act differentially during the early immune response after bone fracture but are similarly involved in bone repair. (upenn.edu)
  • Complement-activation fragment C4a mediates effector functions by binding as untethered agonist to protease-activated receptors 1 and 4. (upenn.edu)
  • Non-enzymatic component of C3 and C5 convertases and thus essential for the propagation of the classical complement pathway. (abcam.com)
  • Complement component C4 is expressed at highest levels in the liver, at moderate levels in the adrenal cortex, adrenal medulla, thyroid gland,and the kidney, and at lowest levels in the heart, ovary, small intestine, thymus, pancreas and spleen. (abcam.com)
  • They noted associations near the C4 gene, which encodes for complement component 4. (nih.gov)
  • Schizophrenia risk from complex variation of complement component 4. (nih.gov)
  • The complete exon-intron structure of a human complement component C4A gene. (wikipedia.org)
  • Detects human Complement Component C1r in direct ELISAs and Western blots. (novusbio.com)
  • In direct ELISAs, less than 1% cross-reactivity with recombinant human Complement Component C1s is observed. (novusbio.com)
  • Complement component C3 plays a central role in the activation of complement system. (thermofisher.com)
  • In 1899, Paul Ehrlich renamed the heat-sensitive component "complement. (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)
  • The fourth component of complement (C4) is crucial to the activation of the classical complement pathway, a key defense against invading microorganisms. (nih.gov)
  • The identified alleles are complement component 4A and 4B, known as C4A and C4B. (uab.edu)
  • The complement system is a key component of the innate immune system that is involved in eliminating unwanted self and nonself material via cellular and humoral mechanisms. (els.net)
  • That is what led them to a specific region containing the gene called complement component 4(C4) - a well-known gene with regard to its role in the immune system and brain development. (rt.com)
  • BF, C2, C4A and C4B allotypes were determined by standard technologies including Western blots for C2 and C4 variants with monoclonal and policlonal antibodies. (nih.gov)
  • After generation of pathogen-specific antibodies, complement contributes in the clearance of immune complexes and pathogen elimination. (frontiersin.org)
  • 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)
  • Monitoring patients with the C1q assay, which detects antibodies that fix complement, offers a minimally invasive means of identifying patients at risk for transplant glomerulopathy and graft loss. (labome.org)
  • 05). The results of our study suggest that anti-beta2GPI antibodies may play a role in GMT formation, and this process might involve complement activation. (labome.org)
  • The C3a, C4a, and C5a components are referred to as anaphylatoxins, causing smooth muscle contraction, histamine release from mast cells, and enhanced vessel permeability [ 2 , 3 ]. (selfhacked.com)
  • Recently, there has been a resurgence of interest in the role of the innate immune mediators of the complement pathway in asthma pathogenesis, particularly the anaphylatoxins (C3a, C5a). (springer.com)
  • Upon activation of the complement system, cleavage of the third and fifth components of the complement system (C3 and C5, respectively) generates the peptides C3a and C5a, both of which are potent anaphylatoxins (reviewed in Ref. 3 ). (jimmunol.org)
  • Elevated plasma levels of the anaphylatoxins C3a and C4a are associated with a fatal outcome in sepsis. (springer.com)
  • Along the way, 70- to 80-residue pro-inflammatory anaphylatoxins C3a, C4a, and C5a are also produced. (aspetjournals.org)
  • Your search returned 3 C4A ELISA ELISA Kit across 1 supplier. (biocompare.com)
  • Gene copy-number variations (CNVs) of complement C4 and C4A deficiency in genetic risk and pathogenesis of juvenile dermatomyositis. (cdc.gov)
  • Complement C4A deficiency appears to be an important factor for the genetic risk and pathogenesis of JDM, particularly in patients with a DR3-positive background. (cdc.gov)
  • Low copy numbers of complement C4 and homozygous deficiency of C4A may predispose to severe disease and earlier disease onset in patients with systemic lupus erythematosus. (uni-kiel.de)
  • Systemic lupus erythematosus is often associated with congenital complement C4 deficiency. (cellsciences.com)
  • Although the risk of lupus in patients with complement deficiency is high, C1q deficiency and C2 deficiency is extremely rare, with less than 100 patients with each being described in the world literature. (lupusuk.org.uk)
  • In addition, any patients with C4a deficiency are likely to have both copies of C4b, so true C4 deficiency is extremely rare. (lupusuk.org.uk)
  • Linton S (2001) Animal models of inherited complement deficiency. (els.net)
  • O'Neil KM (2000) Complement deficiency. (els.net)
  • 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)
  • IC levels were measured by complement consumption assay, C3d by a sandwich ELISA, factor B by immunoelectrophoresis, and the alternative pathway function by a hemolytic assay. (nih.gov)
  • Interestingly, B. pertussis does not activate the alternative pathway of complement ( 7 ). (asm.org)
  • The large fragment formed when COMPLEMENT C4 is cleaved by COMPLEMENT C1S. (labome.org)
  • Trichorhinophalangeal syndrome type I and systemic lupus erythematosus with complement C4A homozygous null alleles in the same family. (bmj.com)
  • A three generation family from northern Sweden with both trichorhinophalangeal syndrome type I (TRP I) and systemic lupus erythematosus (SLE)-like syndrome with complement C4 homozygous null alleles is described. (bmj.com)
  • All living family members in the first and second generation had homozygous C4A null alleles. (bmj.com)
  • The association of homozygous deletion of C4A and SLE is accompanied by the presence of HLA-DRB1*0301 without a proven pathophysiological mechanism. (uni-kiel.de)
  • Family members with homozygous or heterozygous C4AQ0 (47%) showed no impaired complement dependent opsonization of IC and binding to erythrocytes. (nih.gov)
  • Patients with homozygous complement deficiencies have a very high frequency of lupus. (lupusuk.org.uk)
  • 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)
  • While complement is an important defense system against bacterial infection, earlier clinical observations suggest that activation of complement factors is associated with detrimental effects in septic shock, such as multiorgan damages and poor outcome [ 5 - 8 ]. (hindawi.com)
  • Complements C3a and C4b are opsonins that bridge phagocytes to microorganisms. (sigmaaldrich.com)
  • The complement system helps defend the host by initiating inflammatory and immunological responses and by promoting the cell lysis and death of invading microorganisms (reviewed in Ref. 2 ). (jimmunol.org)
  • The systemic inflammatory response of the body to invading microorganisms, called sepsis, leads to profound activation of the complement (C3 and C4) system. (springer.com)
  • C4A is often elevated in chronic inflammation. (selfhacked.com)
  • C4a activates Neutrophils, which increases inflammation and free radicals [ 4 ]. (selfhacked.com)
  • Nowadays, this vision has changed and it is well accepted that complement is a complex innate immune surveillance system, playing a key role in host homeostasis, inflammation, and in the defense against pathogens. (frontiersin.org)
  • In an era that nurtures the integrated study of biological systems as the prevalent concept in contemporary scientific thinking, complement research is being revisited and our current knowledge of this innate immune system is enriched by findings that point to novel functions that do not strictly correlate with immunological defense and surveillance, immune modulation or inflammation. (upenn.edu)
  • Complement C5a-Induced Changes in Neutrophil Morphology During Inflammation. (upenn.edu)
  • The connections among oxidative stress, inflammation, and the complement system described in our study seem to indicate a pivotal axis in breast cancer chemoresistance. (hindawi.com)
  • Nevertheless, it can be also an enemy, when pathogens hijack complement regulators to protect themselves from the immune system. (frontiersin.org)
  • 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)
  • The complement system is part of the body's immune system to fight pathogens and remove cell debris. (uab.edu)
  • Complement is also part of the innate immune defenses and provides a defense against pathogens that have not previously infected the host by recognizing repeating structures such as lipopolysaccharide (LPS) found on the surface of bacteria. (asm.org)
  • Complement resistance is common among respiratory pathogens. (asm.org)
  • Complement system represents a major part of the innate immunity. (frontiersin.org)
  • After that, for a long time, complement system has been considered as a supportive part of the innate immunity and received relatively little attention from the immunologists. (frontiersin.org)
  • Ehrlich introduced the term "complement" as part of his larger theory of the immune system. (wikipedia.org)
  • This revealed that the acute phase response, LXR/RXR and FXR/RXR activation, the complement system and the intrinsic prothrombin activation pathway were significantly changed. (spandidos-publications.com)
  • Experimental infection of wild-type (WT) and C3 −/− mice demonstrated for the first time that the complement system protects naive mice against invasive mucosal S. suis infection. (asm.org)
  • The complement system is involved in innate and adaptive immune responses. (asm.org)
  • Disease is amplified by activation of the complement system and secretion of inflammatory cytokines. (childrenshospital.org)
  • What are the cell sources and regulation of the complement system in the brain? (childrenshospital.org)
  • Complement system - This article is about an aspect of the immune system. (academic.ru)
  • One potential mechanism by which the lung can protect itself from infection is through in situ activation of the complement system (reviewed in Ref. 1 ). (jimmunol.org)
  • Crawford K and Alper CA (2000) Genetics of the complement system. (els.net)
  • 1998) The Human Complement System in Health and Disease New York, NY: Marcel Dekker, Inc. (els.net)
  • We used complement system product C4a and elastase activity as indicators of immune system activity. (meresearch.org.uk)
  • Immune system function was assessed measuring complement system C4a products and elastase activity. (meresearch.org.uk)
  • The change in the complement system following submaximal exercise might be able to explain part of the change in patient's pain thresholds, providing evidence for a potential link between immune system alteration and dysfunctional endogenous pain modulation. (meresearch.org.uk)
  • However, the role of the complement system is questionable. (meresearch.org.uk)
  • Using complement as a model system we apply ideas and methods embodied in engineering, computer science, physics, chemistry, and other fields to address today's challenges in biomedical research. (upenn.edu)
  • The complement system has been long appreciated as a major effector arm of the innate immune response. (upenn.edu)
  • During complement activation, C4 is cleaved by the serine protease C1s to C4a (9 kDa) and C4b (190 kDa). (leebio.com)
  • 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)
  • 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)
  • 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)
  • It inhibits complement activation at the yeast surface and, in addition, mediates adhesion of C. albicans to host endothelial cells. (labome.org)
  • Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. (novusbio.com)
  • 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)
  • C4c interacts with complement C1 and complement C2 to form complement C3 convertase of the classic activation pathway. (cellsciences.com)
  • Abcam's Complement C4 Human in vitro ELISA (Enzyme-Linked Immunosorbent Assay) kit is designed for the quantitative measurement of Complement C4 levels in urine, milk, saliva, CSF and cell culture supernatants. (abcam.com)
  • Human C4 exists in 2 forms, C4A and C4B . (nih.gov)
  • When they measured RNA levels in post-mortem human adult brain samples, they found that the different forms predicted C4A and C4B expression levels in the brain. (nih.gov)
  • Human Complement C4c (C4c) is used as an immunogen and is the inactive form of Human Complement C4. (cellsciences.com)
  • 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)
  • Variola virus immune evasion design: expression of a highly efficient inhibitor of human complement. (umn.edu)
  • Binding of C4bp could help Y. enterocolitica to evade complement-mediated clearance in the human host. (labome.org)
  • Human C3a and C4a (but not C5a) were antimicrobial, in. (lu.se)
  • Human C3a and C4a (but not C5a) were antimicrobial, in concert with the separate evolutionary development of the chemotactic C5a. (lu.se)
  • Overexpression of schizophrenia susceptibility factor human complement C4A promotes excessive synaptic loss and behavioral changes in mice. (harvard.edu)
  • Safety and Efficacy of the Complement Inhibitor AMY-101 in a Natural Model of Periodontitis in Non-human Primates. (upenn.edu)
  • Potent Cyclic Antagonists of the Complement C5a Receptor on Human Polymorphonuclear Leukocytes. (aspetjournals.org)
  • We qualified a multiplex complement panel for use in ocular tissues and provide the first report for levels of C5, C3, FD, FB, FP, FI, FH, MBL in donor human eyes. (arvojournals.org)
  • They discovered that the more strongly a variation correlated with the predicted expression of C4A , the more strongly it associated with schizophrenia. (nih.gov)
  • Does "too much" expression of C4A promote loss of synapses leading to schizophrenia? (childrenshospital.org)
  • Now complement gene variants apparently play a contributing role in the diseases systemic lupus erythematosus, Sjögren's syndrome and schizophrenia. (uab.edu)
  • Recent investigations have shed light on the role of lectin complement pathway in septic shock. (hindawi.com)
  • This gene encodes the acidic form of complement factor 4 part of the classical activation pathway. (bio-rad.com)
  • Consequently, the production of the inflammatory mediators C3a, C4a, and C5a is also decreased. (umn.edu)
  • Dr. Stricker and I recently published a study in the Scandinavian Journal of Immunology comparing C3a and C4a levels of chronic Lyme patients to those of healthy controls, AIDS patients and patients with systemic lupus. (publichealthalert.org)
  • Complement was discovered at the end of the nineteenth century and described as a "factor" or "principle" capable to induce bacterial lysis. (frontiersin.org)
  • Complement factors C3a, C5a and C4 can induce vasodilatation, increased capillary permeability, and expression of leukocyte adhesion molecules. (sigmaaldrich.com)
  • Complements C3a and C4a promote phagocyte chemotaxis. (sigmaaldrich.com)
  • Complement C3a enhances CXCL12 (SDF-1)-mediated chemotaxis of bone marrow hematopoietic cells independently of C3a receptor. (harvard.edu)
  • Complement activation was monitored by enzyme-linked immunosorbent assay (ELISA) or Western blotting. (asm.org)
  • Null alleles at either locus (C4AQ0 or C4BQ0) are relatively common, occurring at the C4A locus in approximately 10% of normal individuals and at the C4B locus in approximately 16% of normal individuals. (jci.org)
  • This review discusses recent advances in the understanding of the role of complement in physiology and pathology. (frontiersin.org)
  • OBJECTIVE The aim of this study was to investigate whether or not the inherited polymorphism of complement C4 is associated with genetic susceptibility to microvascular complications in IDDM as previously reported. (diabetesjournals.org)
  • Our results do not support an association of the inherited polymorphism of complement C4 with genetic susceptibility to microvascular complications in patients with IDDM. (diabetesjournals.org)
  • The classical complement pathway plays a major role in innate immunity against infection. (novusbio.com)
  • Many people who believe they have histamine intolerance have high C4a because this activates mast cells. (selfhacked.com)
  • In the alternate pathway complement C3 undergoes spontaneous cleavage resulting in complement B binding to C3b. (sigmaaldrich.com)
  • These studies show that BrkA inhibits the classical pathway of complement activation and prevents accumulation of deposited C4. (asm.org)
  • Schneider PM and Rittner C (1997) Complement genetics. (els.net)
  • Proceedings of the Complement Genetics Workshop and Conference, Mainz 15: 201-296. (els.net)
  • Complement activation and polymorphonuclear neutrophil leukocyte elastase in sepsis: correlation with severity of disease. (springer.com)
  • C4a levels were also elevated in the AIDS and systemic lupus groups, but not in the healthy controls. (publichealthalert.org)
  • To investigate the association of C4AQ0 with increased incidence of systemic lupus erythematosus (SLE) or positive serology (28%) in an extended Icelandic family, and whether this can be explained by impaired complement function in handling immune complexes (IC). (nih.gov)
  • Inadequate complement activation becomes a disease cause, as in atypical hemolytic uremic syndrome, C3 glomerulopathies, and systemic lupus erythematosus. (frontiersin.org)
  • We assess gene copy-number variations (CNVs) for complement C4 and its isotypes, C4A and C4B, in genetic risks and pathogenesis of JDM. (cdc.gov)
  • Complement has a central role in the pathogenesis of lupus. (lupusuk.org.uk)
  • Complement is also important in the clearance of immune complexes which themselves are thought to be involved in the pathogenesis of disease. (lupusuk.org.uk)
  • Our studies suggest that allelic variation of MBL in humans may impact complement-dependent control of DENV pathogenesis. (asm.org)
  • Age-related macular degeneration and cancer will be described as examples showing that complement contributes to a large variety of conditions, far exceeding the classical examples of diseases associated with complement deficiencies. (frontiersin.org)
  • Higher plasma levels of complement C3a, C4a and C5a increase the risk of subretinal fibrosis in neovascular age-related macular degeneration. (qub.ac.uk)
  • The two isotypes of C4, C4A and C4B, have very different in vitro activities. (nih.gov)
  • The present study aimed at examining whether two different types of exercise results in changes in health status, circulating elastase activity, interleukin (IL)-1beta and complement C4a levels. (prohealth.com)
  • Submaximal exercise as well as self-paced, physiologically limited exercise triggers postexertional malaise in people with ME/CFS, but neither type of exercise alters acute circulating levels of IL-1beta, complement C4a split product or elastase activity. (prohealth.com)
  • This hypothesis is based on the observation that complement components are important in the clearance of material from apoptotic or necrotic cells. (lupusuk.org.uk)
  • C5b begins the assembly of complement components by binding C6 and C7 to its C5-C345C domain, creating a C5b-7 complex which remains loosely associated with C3b (Dalmasso, 1998). (davidson.edu)
  • In this respect, recent evidence produced by our laboratory (and others) suggests that complement components can modulate diverse biological processes by closely interacting with other intra- and intercellular networks. (upenn.edu)
  • Using a panel of naïve sera from mouse strains deficient in different complement components, we showed that inhibition of infection by insect cell- and mammalian cell-derived DENV was primarily dependent on the lectin pathway. (asm.org)
  • whether a distinct receptor for C4a is present is unclear (see Table 1). (medscape.com)
  • The C3a receptor binds C3a and C4a. (medscape.com)
  • It functions as a complement receptor. (wikipedia.org)
  • Heterozygous missense or in-frame insertion/deletion mutations in complement 1 subunits C1r and C1s cause periodontal Ehlers-Danlos Syndrome (pEDS), a specific EDS subtype characterized by early severe periodontal destruction and connective tissue abnormalities like easy bruising, pretibial haemosiderotic plaques, and joint hypermobility. (frontiersin.org)