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.
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.
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.
An enzyme that catalyzes the phosphorylation of the guanidine nitrogen of arginine in the presence of ATP and a divalent cation with formation of phosphorylarginine and ADP. EC 2.7.3.3.
The predominant form of mammalian antidiuretic hormone. It is a nonapeptide containing an ARGININE at residue 8 and two disulfide-linked cysteines at residues of 1 and 6. Arg-vasopressin is used to treat DIABETES INSIPIDUS or to improve vasomotor tone and BLOOD PRESSURE.
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.
A synthetic nonsteroidal estrogen used in the treatment of menopausal and postmenopausal disorders. It was also used formerly as a growth promoter in animals. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), diethylstilbestrol has been listed as a known carcinogen. (Merck, 11th ed)
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.
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 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.
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.
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)
An amino acid produced in the urea cycle by the splitting off of urea from arginine.
A derivative of complement C5a, generated when the carboxy-terminal ARGININE is removed by CARBOXYPEPTIDASE B present in normal human serum. C5a des-Arg shows complete loss of spasmogenic activity though it retains some chemotactic ability (CHEMOATTRACTANTS).
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.
The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.
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.
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.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Stents that are covered with materials that are embedded with chemicals that are gradually released into the surrounding milieu.
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).
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.
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 are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.
Proteins that bind to particles and cells to increase susceptibility to PHAGOCYTOSIS, especially ANTIBODIES bound to EPITOPES that attach to FC RECEPTORS. COMPLEMENT C3B may also participate.
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.
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).
A ureahydrolase that catalyzes the hydrolysis of arginine or canavanine to yield L-ornithine (ORNITHINE) and urea. Deficiency of this enzyme causes HYPERARGININEMIA. EC 3.5.3.1.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
A reagent that is highly selective for the modification of arginyl residues. It is used to selectively inhibit various enzymes and acts as an energy transfer inhibitor in photophosphorylation.
Any member of the class of enzymes that catalyze the cleavage of the substrate and the addition of water to the resulting molecules, e.g., ESTERASES, glycosidases (GLYCOSIDE HYDROLASES), lipases, NUCLEOTIDASES, peptidases (PEPTIDE HYDROLASES), and phosphatases (PHOSPHORIC MONOESTER HYDROLASES). EC 3.
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.
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 rate dynamics in chemical or physical systems.
A urea cycle enzyme that catalyzes the formation of orthophosphate and L-citrulline (CITRULLINE) from CARBAMOYL PHOSPHATE and L-ornithine (ORNITHINE). Deficiency of this enzyme may be transmitted as an X-linked trait. EC 2.1.3.3.
Proteins prepared by recombinant DNA technology.
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.
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.
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.
Established cell cultures that have the potential to propagate indefinitely.
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.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
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.
A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.
Elements of limited time intervals, contributing to particular results or situations.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
An enzyme of the urea cycle that catalyzes the formation of argininosuccinic acid from citrulline and aspartic acid in the presence of ATP. Absence or deficiency of this enzyme causes the metabolic disease CITRULLINEMIA in humans. EC 6.3.4.5.
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.
Organic compounds that generally contain an amino (-NH2) and a carboxyl (-COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins.
Non-steroidal compounds with estrogenic activity.
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.
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.
An essential amino acid. It is often added to animal feed.
Antibodies produced by a single clone of cells.
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.
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.
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.
Proteins found in any species of bacterium.
Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.
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.
Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.
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).
Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.
Thickening of the walls of small ARTERIES or ARTERIOLES due to cell proliferation or HYALINE deposition.
Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
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.
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 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.)
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.
Recurrent narrowing or constriction of a coronary artery following surgical procedures performed to alleviate a prior obstruction.
Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
Decarboxylated arginine, isolated from several plant and animal sources, e.g., pollen, ergot, herring sperm, octopus muscle.
Transport proteins that carry specific substances in the blood or across cell membranes.
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.
Addition of methyl groups. In histo-chemistry methylation is used to esterify carboxyl groups and remove sulfate groups by treating tissue sections with hot methanol in the presence of hydrochloric acid. (From Stedman, 25th ed)
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.
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.
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.
An enzyme of the urea cycle which splits argininosuccinate to fumarate plus arginine. Its absence leads to the metabolic disease ARGININOSUCCINIC ACIDURIA in man. EC 4.3.2.1.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
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.
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).
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.
A class of enzymes that transfers phosphate groups and has a carboxyl group as an acceptor. EC 2.7.2.
A nonapeptide that contains the ring of OXYTOCIN and the side chain of ARG-VASOPRESSIN with the latter determining the specific recognition of hormone receptors. Vasotocin is the non-mammalian vasopressin-like hormone or antidiuretic hormone regulating water and salt metabolism.
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
Electropositive chemical elements characterized by ductility, malleability, luster, and conductance of heat and electricity. They can replace the hydrogen of an acid and form bases with hydroxyl radicals. (Grant & Hackh's Chemical Dictionary, 5th ed)
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).
Genetically engineered MUTAGENESIS at a specific site in the DNA molecule that introduces a base substitution, or an insertion or deletion.
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.
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).
The sum of the weight of all the atoms in a molecule.
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.
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.
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.
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.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
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.
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.
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.
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.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
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.
The relationship between the dose of an administered drug and the response of the organism to the drug.
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.
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.
An individual in which both alleles at a given locus are identical.
A macrolide compound obtained from Streptomyces hygroscopicus that acts by selectively blocking the transcriptional activation of cytokines thereby inhibiting cytokine production. It is bioactive only when bound to IMMUNOPHILINS. Sirolimus is a potent immunosuppressant and possesses both antifungal and antineoplastic properties.
Specific molecular sites or proteins on or in cells to which VASOPRESSINS bind or interact in order to modify the function of the cells. Two types of vasopressin receptor exist, the V1 receptor in the vascular smooth muscle and the V2 receptor in the kidneys. The V1 receptor can be subdivided into V1a and V1b (formerly V3) receptors.
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).
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.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
Carrier of aroma of butter, vinegar, coffee, and other foods.
Plasmids containing at least one cos (cohesive-end site) of PHAGE LAMBDA. They are used as cloning vehicles.
Glycoproteins found on the membrane or surface of cells.
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
A highly fatal contagious disease of goats and sheep caused by PESTE-DES-PETITS-RUMINANTS VIRUS. The disease may be acute or subacute and is characterized by stomatitis, conjunctivitis, diarrhea, and pneumonia.
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.
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.
Dilation of an occluded coronary artery (or arteries) by means of a balloon catheter to restore myocardial blood supply.
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.
Cyclohexane ring substituted by one or more ketones in any position.
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.
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.
Biologically active substances whose activities affect or play a role in the functioning of the immune system.
The naturally occurring or experimentally induced replacement of one or more AMINO ACIDS in a protein with another. If a functionally equivalent amino acid is substituted, the protein may retain wild-type activity. Substitution may also diminish, enhance, or eliminate protein function. Experimentally induced substitution is often used to study enzyme activities and binding site properties.
Amino acid transporter systems capable of transporting basic amino acids (AMINO ACIDS, BASIC).
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.
Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.
Use of restriction endonucleases to analyze and generate a physical map of genomes, genes, or other segments of DNA.
A non-essential amino acid present abundantly throughout the body and is involved in many metabolic processes. It is synthesized from GLUTAMIC ACID and AMMONIA. It is the principal carrier of NITROGEN in the body and is an important energy source for many cells.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
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 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.
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.
Devices that provide support for tubular structures that are being anastomosed or for body cavities during skin grafting.
The arrangement of two or more amino acid or base sequences from an organism or organisms in such a way as to align areas of the sequences sharing common properties. The degree of relatedness or homology between the sequences is predicted computationally or statistically based on weights assigned to the elements aligned between the sequences. This in turn can serve as a potential indicator of the genetic relatedness between the organisms.
A mitochondrial matrix enzyme that catalyzes the synthesis of L-GLUTAMATE to N-acetyl-L-glutamate in the presence of ACETYL-COA.
A compound formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids.
The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.
A characteristic feature of enzyme activity in relation to the kind of substrate on which the enzyme or catalytic molecule reacts.
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.
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)

Requirements for C5a receptor-mediated IL-4 and IL-13 production and leukotriene C4 generation in human basophils. (1/45)

Anaphylatoxin derived from the fifth complement component (C5a) in the presence of IL-3 induces continuous leukotriene C4 generation and IL-4 and IL-13 expression in human basophils for a period of 16-18 h. This indicates that the G protein-coupled C5a receptor (C5aR) can induce long-lasting cellular responses. Using anti-N-terminal C5aR Abs, C-terminal C5a hexapeptide analogs, and pertussis toxin, we demonstrate that the putative activation site of the C5aR is both necessary and sufficient for these late cellular responses. Furthermore, continuous pertussis toxin-sensitive G protein-coupled receptor activation and receptor-ligand interaction is ongoing and required during the entire period of product release. However, the late basophil responses have a more stringent requirement for optimal receptor activation. Leukotriene C4 generation appears to be influenced mostly by the way the receptor is activated, because the most active hexapeptide is a superagonist for this response. By contrast, C5adesarg, lacking the C-terminal arginine, induces minimal lipid mediator formation but is fully active to induce IL-4 production and is even a superagonist for IL-13 release. Nevertheless, IL-4/IL-13 synthesis in response to C5adesarg could be blocked by both C-terminal antagonistic peptide as well as anti-N-terminal C5aR Abs, indicating only minor differences of ligand-receptor interactions between C5a and C5adesarg. Taken together, our data demonstrate that long-lasting and continuous signaling occurs through a limited activation domain of the C5aR, which can differentially promote separate basophil functions.  (+info)

Altered expression of CD88 and associated impairment of complement 5a-induced neutrophil responses in human immunodeficiency virus type 1-infected patients with and without pulmonary tuberculosis. (2/45)

The effect of infection with human immunodeficiency virus type 1 (HIV patient group), infection with Mycobacterium tuberculosis (TB patient group), and coinfection with both of these organisms (HIV/TB patient group) on the expression of CD88 on polymorphonuclear leukocytes (PMNL) was determined by using a receptor-specific monoclonal antibody and flow cytometry. A significant reduction in the fluorescence intensity of CD88 on PMNL was observed in the HIV and HIV/TB groups, compared with both the healthy donor (HD) and TB groups. Furthermore, when degranulation of PMNL was induced by ligation of CD88 by complement 5a (C5a), a large proportion of patients in the HIV and the HIV/TB groups was found to have reciprocal degranulation responses. Patients in the 2 HIV groups also were found to have significantly reduced C5a-induced chemotactic responses and significantly elevated peripheral levels of C5a des Arg, compared with the HD and TB groups. These differences may contribute to the increased susceptibility of HIV-1-infected individuals to secondary microbial infections.  (+info)

C5a and C5a(desArg) enhance the susceptibility of monocyte-derived macrophages to HIV infection. (3/45)

Mononuclear phagocytes, which include circulating blood monocytes and differentiated tissue macrophages, are believed to play a central role in the sexual transmission of HIV infection. The ability of HIV to productively infect these cells may be influenced by action of exogenous or host-derived substances at the site of viral entry. Given the potent capacities of inflammatory mediators to stimulate anaphylatoxic and immunomodulatory functions in mucosa, the effects of complement-derived anaphylatoxins on the susceptibility of monocytes and monocyte-derived macrophages (MDM) to HIV-1 infection were examined. In our in vitro system, the susceptibility to infection was up to 40 times increased in MDM that had been exposed to C5a or C5a(desArg), but not to C3a or C3a(desArg), for 2 days before adding of virus. By contrast, the treatment with complement anaphylatoxins did not affect HIV replication in fresh monocytes. Stimulatory effect of C5a and its desArg derivative on HIV infection correlated with the increase of TNF-alpha and IL-6 secretion from MDM. All these functional effects of C5a and C5a(desArg) were reversible by treatment of cells with the mAb that functionally blocks C5aR. Taken together, these results indicate that C5a and C5a(desArg) may increase the susceptibility of MDM to HIV infection through stimulation of TNF-alpha and IL-6 secretion from these cells.  (+info)

Contribution of anaphylatoxin C5a to late airway responses after repeated exposure of antigen to allergic rats. (4/45)

We attempted to elucidate the contribution of complement to allergic asthma. Rat sensitized to OVA received repeated intratracheal exposures to OVA for up to 3 consecutive days, and pulmonary resistance was then estimated for up to 6 h after the last exposure. Whereas the immediate airway response (IAR) in terms of R(L) tended to decrease in proportion to the number of OVA exposures, late airway response (LAR) became prominent only after three. Although premedication with two kinds of complement inhibitors, soluble complement receptor type 1 (sCR1) or nafamostat mesylate, resulted in inhibition of the IAR after either a single or a double exposure, the LAR was inhibited after the triple. Premedication with a C5a receptor antagonist (C5aRA) before every exposure to OVA also inhibited the LAR after three. Repeated OVA exposure resulted in eosinophil and neutrophil infiltration into the bronchial submucosa which was suppressed by premedication with sCR1 or C5aRA. Up-regulation of C5aR mRNA was shown in lungs after triple OVA exposure, but almost no up-regulation of C3aR. Pretreatment with sCR1 or C5aRA suppressed the up-regulation of C5aR expression as well as cytokine messages in the lungs. The suppression of LAR by pretreatment with sCR1 was reversed by intratracheal instillation of rat C5a desArg the action of which was inhibited by C5aRA. In contrast, rat C3a desArg or cytokine-induced neutrophil chemoattractant-1 induced cellular infiltration into the bronchial submucosa by costimulation with OVA, but these had no influence on the LAR. These differences might be explained by the fact that costimulation with OVA and C5a synergistically potentiated IAR, whereas that with OVA and either C3a or cytokine-induced neutrophil chemoattractant-1 did not. C5a generated by Ag-Ab complexes helps in the production of cytokines and contributes to the LAR after repeated exposure to Ag.  (+info)

The orphan receptor C5L2 has high affinity binding sites for complement fragments C5a and C5a des-Arg(74). (5/45)

The substantial variations in the responses of cells to the anaphylatoxin C5a and its desarginated form, C5adR(74), suggest that more than one type of cell surface receptor for these ligands might exist. However, only a single receptor for C5a and C5adR(74), CD88, has been characterized to date. Here we report that the orphan receptor C5L2/gpr77, which shares 35% amino acid identity with CD88, binds C5a with high affinity but has a 10-fold higher affinity for C5adR(74) than CD88. C5L2 also has a moderate affinity for anaphylatoxin C3a, but cross-competition studies suggest that C3a binds to a distinct site from C5a. C4a was able to displace C3a, suggesting that C5L2, like the C3a receptor, may have a low binding affinity for this anaphylatoxin. Unlike CD88 and C3a receptor, C5L2 transfected into RBL-2H3 cells does not support degranulation or increases in intracellular [Ca(2+)] and is not rapidly internalized in response to ligand binding. However, ligation of C5L2 by anaphylatoxin did potentiate the degranulation response to cross-linkage of the high affinity IgE receptor by a pertussis toxin-sensitive mechanism. These results suggest that C5L2 is an anaphylatoxin-binding protein with unique ligand binding and signaling properties.  (+info)

A functional C5a anaphylatoxin receptor in a teleost species. (6/45)

The anaphylatoxins are potent, complement-derived low m.w. proteins that bind to specific seven-transmembrane receptors to elicit and amplify a variety of inflammatory reactions. C5a is the most potent of these phlogistic peptides and is a strong chemoattractant for neutrophils and macrophages/monocytes. Although lower vertebrates possess complement systems that are believed to function similarly to those of mammals, anaphylatoxin receptors have not previously been characterized in any nonmammalian vertebrate. To study the functions of C5a in teleost fish, we generated recombinant C5a of the rainbow trout, Oncorhynchus mykiss (tC5a), and used fluoresceinated tC5a (tC5aF) and flow cytometry to identify the C5a receptor (C5aR) on trout leukocytes. Granulocytes/Macrophages present in cell suspensions of the head kidney (HKL), the main hemopoietic organ in teleosts, showed a univariate type of receptor expression, whereas those from the peripheral blood demonstrated either a low or high level of expression. The binding of tC5aF was inhibited by excess amounts of unlabeled tC5a or tC5a(desArg), demonstrating that sites other than the C-terminal of tC5a interact with the C5aR. Both tC5a and tC5a(desArg) were able to induce chemotactic responses in granulocytes in a concentration-dependent manner, but the desArg derivative was at least 10-fold less active. Homologous desensitization occurred after HKL were exposed to continuous or high concentrations of tC5a, with a loss of tC5aF binding and an 80% reduction in chemotactic responses toward tC5a. Pertussis toxin reduced the migration of HKL toward tC5a by 40%, suggesting only a partial involvement of pertussis toxin-sensitive G(i) proteins in tC5a-mediated chemotaxis.  (+info)

The role of the N-terminal domain of the complement fragment receptor C5L2 in ligand binding. (7/45)

C5L2 is a new cellular receptor found to interact with the human anaphylatoxins complement factor C5a and its C-terminal cleavage product C5a des Arg. The classical human C5a receptor (C5aR) preferentially binds C5a, with a 10-100-fold lower affinity for C5a des Arg. In contrast, C5L2 binds both ligands with nearly equal affinity. C5aR presents acidic and tyrosine residues in its N terminus that interact with the core of C5a while a hydrophobic pocket formed by the transmembrane helices interacts with residues in the C terminus of C5a. Here, we have investigated the molecular basis for the increased affinity of C5L2 for C5a des Arg. Rat and mouse C5L2 preferentially bound C5a des Arg, whereas rodent C5aR showed much higher affinity for intact C5a. Effective peptidic and non-peptidic ligands for the transmembrane hydrophobic pocket of C5aR were poor inhibitors of ligand binding to C5L2. An antibody raised against the N terminus of human C5L2 did not affect the binding of C5a to C5L2 but did inhibit C5a des Arg binding. A chimeric C5L2, containing the N terminus of C5aR, had little effect on the affinity for C5a des Arg. Mutation of acidic and tyrosine residues in the N terminus of human C5L2 revealed that 3 residues were critical for C5a des Arg binding but had little involvement in C5a binding. C5L2 thus appears to bind C5a and C5a des Arg by different mechanisms, and, unlike C5aR, C5L2 uses critical residues in its N-terminal domain for binding only to C5a des Arg.  (+info)

Complement C5a receptors in the pituitary gland: expression and function. (8/45)

 (+info)

C5a / C5a des Arg antibody [2942] (complement component 5) for IA, WB. Anti-C5a / C5a des Arg mAb (GTX11877) is tested in Human samples. 100% Ab-Assurance.
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Using polyacrylamide-gel isoelectric focusing followed by immunoblotting, genetic polymorphism of plasma vitamin D-binding protein (Gc) was examined in Asian sheep. The Gc polymorphism was revealed in the Khalkhas sheep of Mongolia, consisting of F, S and W variants, and the Yunnan native sheep of China, consisting of F and S variants. In particular, W was a new variant. The V variant detected in European sheep up to now was not observed in these sheep. The Bhyanglung, Baruwal, Kagi and Lampuchhre sheep of Nepal and local sheep of Bangladesh and Vietnam were monomorphic for the S variant. Family data and population genetic data supported the hypothesis that these variants were controlled by codominant alleles. In these Asian sheep, distribution of the |TEX|$Gc^s$|/TEX| allele was predominant (0.9571-1) and was seen as well in European sheep (Suffolk, Corriedale, Cheviot and Finnish Landrace) raised in Japan. |TEX|$Gc^w$|/TEX| allele was detected only in the Khalkhas sheep with the low frequency of 0
SWISS-MODEL Template Library (SMTL) entry for 1kxp.1. CRYSTAL STRUCTURE OF HUMAN VITAMIN D-BINDING PROTEIN IN COMPLEX WITH SKELETAL ACTIN
title: Relationship between vitamin D-binding protein polymorphisms and blood vitamin D level in Korean patients with COPD., doi: 10.2147/COPD.S96985, category: Article
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The discovery of biologically impactful and personalized melanoma prognostic markers complementing currently established, yet clinically less specific, histopathologic indicators is one of the key objectives of current melanoma research. Recent studies suggest that germline genetic variants may modulate cutaneous melanoma clinical endpoints, thereby representing potentially personalized and easily accessible prognostic biomarkers (7-12). However, while the majority of currently published studies on germline associations with prognosis still require independent validation in larger cohorts, the biologic and functional uncertainty of most prognostic variants further limits their clinical consideration. With the exception of few melanoma etiology related SNPs [e.g., MC1R (9), vitamin D-binding protein (11)], in general, almost exclusively, the genetic variants identified to date for associations with melanoma risk (i.e., GWAS loci) or prognosis (reviewed in ref. 8), map to noncoding regions with ...
TY - JOUR. T1 - Genetic variation in the Vitamin D Receptor (VDR) and the vitamin D-binding protein (GC) and risk for colorectal cancer. T2 - Results from the colon cancer family registry. AU - Poynter, Jenny N.. AU - Jacobs, Elizabeth T.. AU - Figueiredo, Jane C.. AU - Lee, Won H.. AU - Conti, David V.. AU - Campbell, Peter T.. AU - Levine, A. Joan. AU - Limburg, Paul. AU - Le Marchand, Loic. AU - Cotterchio, Michelle. AU - Newcomb, Polly A.. AU - Potter, John D.. AU - Jenkins, Mark A.. AU - Hopper, John L.. AU - Duggan, David J.. AU - Baron, John A.. AU - Haile, Robert W.. PY - 2010/2. Y1 - 2010/2. N2 - Epidemiologic evidence supports a role for vitamin D in colorectal cancer (CRC) risk. Variants in vitamin D-related genes might modify the association between vitamin D levels and CRC risk. In this analysis, we did a comprehensive evaluation of common variants in the vitamin D receptor (VDR) and the vitamin D-binding protein (GC; group-specific component) genes using a population-based ...
TY - JOUR. T1 - Critically ill children have low Vitamin D-binding protein, influencing bioavailability of Vitamin D. AU - Madden, Kate. AU - Feldman, Henry A.. AU - Chun, Rene F.. AU - Smith, Ellen M.. AU - Sullivan, Ryan M.. AU - Agan, Anna A.. AU - Keisling, Shannon M.. AU - Panoskaltsis-Mortari, Angela. AU - Randolph, Adrienne G.. PY - 2015/11. Y1 - 2015/11. N2 - Rationale: Vitamin D deficiency, often defined by total serum 25-hydroxyvitamin D (25[OH]D) ,20 ng/ml, is common in critically ill patients, with associations with increasedmortality andmorbidity in the intensive care unit. Correction of vitamin D deficiency in critical illness has been recommended, and ongoing clinical trials are investigating the effect of repletion on patient outcome. The biologically active amount of 25(OH)D depends on the concentration and protein isoformof vitamin D-binding protein (VDBP), which is also an acutephase reactant affected by inflammation and injury. Objectives: We performed a secondary analysis of ...
Relationship between vitamin D-binding protein polymorphisms and blood vitamin D level in Korean patients with COPD Youngmok Park,1 Young Sam Kim,1 Young Ae Kang,1 Ju Hye Shin,1 Yeon Mok Oh,2 Joon Beom Seo,3 Ji Ye Jung,1 Sang Do Lee2 On behalf of the KOLD study 1Division of Pulmonology, Department of Internal Medicine, Severance Hospital, Institute of Chest Diseases, Yonsei University College of Medicine, 2Department of Pulmonary and Critical Care Medicine, Clinical Research Center for Chronic Obstructive Airway Diseases, 3Department of Radiology and Research Institute of Radiology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea Background: In chronic obstructive pulmonary disease (COPD), the blood vitamin D3 level is generally low, and genetic polymorphisms of vitamin D-binding protein encoded by the GC gene are associated with COPD development. In this study, we examined the relationship between GC polymorphisms and plasma vitamin D3 level in Korean patients
1 reviews. Compare Complement C5a desArg ELISA Kits from leading suppliers on Biocompare. View specifications, prices, citations, reviews, and more.
استاندارد رمزنگاری داده (DES) یك الگوریتمی ریاضی است كه برای رمزنگاری و رمزگشایی اطلاعات كدشده باینری به كار می رود. رمزنگاری داده ها را تبدیل به داده...
The objectives are to define the complete structure of the human receptor for complement fragments C3b/C4b and its functional role in immune and inflammatory re...
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An emerging hypothesis suggests that vitamin D metabolites suppress the development of prostate cancer. In a recent epidemiological study, elevated levels of 1,25-dihydroxyvitamin D (1,25-D) in blood were associated with a greatly reduced risk, particularly in older men. We conducted a nested case-control study to evaluate the relationship between plasma levels of the two major vitamin D metabolites, 1,25-D and 25-hydroxyvitamin D (25-D), and subsequent diagnosis of prostate cancer. We also measured vitamin D-binding protein to investigate the influence of free metabolite levels on risk. Plasma samples from 14,916 participants in the Physicians Health Study were collected and frozen in 1982-1983. This analysis included 232 cases diagnosed up to 1992 and 414 age-matched control participants. Vitamin D metabolite and vitamin D-binding protein assays were conducted without knowledge of case-control status. Median levels of 25-D, 1,25-D, and vitamin D-binding protein were indistinguishable between ...
1869 Highly activated macrophages are tumoricidal. Inflammation-derived macrophage activation is the principal macrophage activation process that requires serum vitamin D-binding protein (known as Gc protein) and participation of B and T lymphocytes. A trisaccharide composed of N-acetylgalactosamine with dibranched galactose and sialic acid termini at 420 threonine residue of Gc protein is hydrolyzed by the inducible ß-galactosidase (Bgl) of inflammation-primed B cells and the Neu-1 sialidase of T cells to yield the macrophage activating factor (MAF). Thus, Gc protein is the precursor for the principal MAF. However, the MAF precursor activity of Gc protein of cancer patients was lost or reduced because Gc protein is deglycosylated by serum α-N-acetylgalactosaminidase (Nagalase) secreted from cancerous cells but not from healthy cells. Thus, serum Nagalase activity is proportional to tumor burden and serves as a prognostic index. Exogenously given macrophage activating factor can bypass ...
Dr. Hirsch has been a longtime friend and supporter in numerous ways of the String Academy. He served on the SAW Board of Directors for many years and was also a collaborative sonata pianist for students at the school. The award has been presented annually since 1991 by the String Academy to an outstanding individual who has made a significant contribution to the Milwaukee arts community.. Erwin was born in Austria in 1920. After studying in Oxford, England, he came to the U.S. where he joined his parents and sister in Boston. He graduated from Harvard College in 1942 and from Harvard Medical School in 1946. Pursuing hematology research, he devised a method that for the first time successfully transfused blood platelets, today a routine procedure. Dr. Hirsch was called into the Army Medical Corps to serve during the Korean War from 1952-1954. After eight years of private practice in Providence, RI, he followed his increasing interest in medical education at Princeton Hospital in NJ. Called to ...
TY - JOUR. T1 - An anti-inflammatory function for the complement anaphylatoxin C5a-binding protein, C5L2. AU - Gerard, Norma P.. AU - Lu, Bao. AU - Liu, Pixu. AU - Craig, Stewart. AU - Fujiwara, Yuko. AU - Okinaga, Shoji. AU - Gerard, Craig. PY - 2005/12/2. Y1 - 2005/12/2. N2 - C5L2 is an enigmatic serpentine receptor that is co-expressed with the C5a receptor on many cells including polymorphonuclear neutrophils. The apparent absence of coupling of C5L2 with G proteins suggests that this receptor may modulate the biological activity of C5a, perhaps by acting as a decoy receptor. Alternatively, C5L2 may affect C5a function through formation of a heteromeric complex with the C5aR, or it may utilize a G protein-independent signaling pathway. Here we show that in mice bearing a targeted deletion of C5L2, the biological activity of C5a/C5adesArg is enhanced both in vivo and in vitro. The biological role of C5L2 thus appears to be limiting to the pro-inflammatory response to the anaphylatoxin. ...
Now, they may soon add a new risk factor to the list: activation of the complement system. The complement system is usually implicated in immune responses, but now theres a role for it in cardiovascular disease. In a new research report appearing in the January 2011 print issue of the FASEB Journal (http://www.fasebj.org), scientists from Europe and the United States show that anaphylatoxin C5a, a protein released when complement is activated, contributes to atherosclerotic disease. C5a causes plaques to break free from where they would be anchored to ultimately cause blockages elsewhere in the body. This new discovery not only shows that C5a is a new marker for identifying risk for heart attack and stroke, but it also establishes C5a as a new therapeutic target for preventing these problems.. Given the huge impact of cardiovascular disease in general, and atherosclerosis in particular, on public health, we feel that unraveling mechanisms involved in the development and progression of the ...
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Black Americans had lower levels of total 25-hydroxyvitamin D and vitamin D-binding protein than whites, but similar levels of bioavailable 25-hydroxyvitamin D, and higher bone density.
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The normal range of human serum albumin in adults (, 3 y.o.) is 3.5 to 5 g/dL. For children less than three years of age, the normal range is broader, 2.9-5.5 g/dL.[9] Low albumin (hypoalbuminemia) may be caused by liver disease, nephrotic syndrome, burns, protein-losing enteropathy, malabsorption, malnutrition, late pregnancy, artefact, genetic variations and malignancy. High albumin (hyperalbuminemia) is almost always caused by dehydration. In some cases of retinol (Vitamin A) deficiency, the albumin level can be elevated to high-normal values (e.g., 4.9 g/dL). This is because retinol causes cells to swell with water (this is also the reason too much Vitamin A is toxic).[10] This swelling also likely occurs during treatment with 13-cis retinoic acid (isotretnoin), a pharmaceutical for treating severe acne, amongst other conditions. In lab experiments it has been shown that all-trans retinoic acid down regulates human albumin production.[11] ...
Rahier, Jacques ; Guiot, Yves ; Sempoux, Christine. Diabète de type 2 et déficit des cellules B.. In: Journées annuelles de diabétologie de lHôtel-Dieu, , p. 19-27 (2004 ...
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... complement c5a MeSH D12.776.124.486.274.024.270.255 - complement c5a, des-arginine MeSH D12.776.124.486.274.050 - complement c1 ... complement c5a, des-arginine MeSH D12.776.124.486.274.450.625 - complement c5b MeSH D12.776.124.486.274.550 - complement c6 ... complement c4b MeSH D12.776.124.486.274.450 - complement c5 MeSH D12.776.124.486.274.450.250 - complement c5a 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. ...
C3a has a regulatory process and a structure homologous to complement component C5a, with which it shares 36% of its sequence ... C3a, like other anaphylatoxins, has a C-terminal arginine residue. Serum carboxypeptidase B, a protease, cleaves the arginine ... C3a desarginine). C3a is an effector of the complement system with a range of functions including T cell activation and ... 12th European Meeting on Complement in Human Disease12th European Meeting on CHD12th European Meeting on Complement in Human ...
C5a is rapidly metabolised by a serum enzyme carboxypeptidase B to a 72 amino acid form C5a des-Arg without C terminal arginine ... C5a des-Arg is a much less potent anaphylatoxin. Both C5a and C5a des-Arg can trigger mast cell degranulation, releasing ... C5a is a protein fragment released from cleavage of complement component C5 by protease C5-convertase into C5a and C5b ... C5a, the other cleavage product of C5, acts as a highly inflammatory peptide, encouraging complement activation, formation of ...
Similarly again, C5b is bound and C5a is released. C5b recruits C6, C7, C8 and multiple C9s. C5, C6, C7, C8 and C9 form the ... Kigerl KA, de Rivero Vaccari JP, Dietrich WD, Popovich PG, Keane RW (August 2014). "Pattern recognition receptors and central ... Complement receptors, collectins, ficolins, pentraxins such as serum amyloid and C-reactive protein, lipid transferases, ... Dardick C, Schwessinger B, Ronald P (August 2012). "Non-arginine-aspartate (non-RD) kinases are associated with innate immune ...
January 2011). "The C5a receptor impairs IL-12-dependent clearance of Porphyromonas gingivalis and is required for induction of ... Nelson KE, Fleischmann RD, DeBoy RT, Paulsen IT, Fouts DE, Eisen JA, et al. (September 2003). "Complete genome sequence of the ... Other studies have found that P. gingivalis can subvert the complement pathway through C5αR and C3αR, which modulates the ... It contains the enzyme peptidyl-arginine deiminase, which is involved in citrullination. Patients with rheumatoid arthritis ...
Nguyen VC, Tosi M, Gross MS, Cohen-Haguenauer O, Jegou-Foubert C, de Tand MF, Meo T, Frézal J (April 1988). "Assignment of the ... Skoog MT, Mehdi S, Wiseman JS, Bey P (June 1989). "The specificity of two proteinases that cleave adjacent to arginine, C1 ... Complement component 1s (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 ...
In vitro and in vivo studies have suggested that human complement component C5a plays a key role in neutrophil injury in the ... Complement C5 / analogs & derivatives * Complement C5 / immunology* * Complement C5a * Complement C5a, des-Arginine ... In vitro and in vivo studies have suggested that human complement component C5a plays a key role in neutrophil injury in the ... We then administered the anti-C5a des arg antibody to septic primates (Macaca fascicularis). Three groups of primates, control ...
C5a and its derivative C5a(desArg), which results from the removal of the C-terminal arginine by ubiquitous carboxypeptidases. ... In this paper we describe the purification of milligram amounts of bovine C5a(desArg) by a simplif … ... Complement activation generates two potent inflammatory mediators from C5, ... Complement Activation * Complement C5a / analysis* * Complement C5a, des-Arginine / analysis* * Electrophoresis, Polyacrylamide ...
... complement C3a: C3a without the COOH-terminal arginine at the 77-position; also known as the acylation-stimulating protein or ... C3a des arg, C4a des arg, C5a des arg, C1rC1s-C1-inhibitor complex, and terminal C complex (C5b-9). ". ... complement C3a, des-Arg-(77); C3a des-Arg; C3a des-Arg(77); C3a des-Arg77; complement 3a, des-Arg-; complement 3a, des-arginine ... Complement System Proteins: 21537*Complement C3: 812*Complement C3a: 43*des-Arg-(77) complement C3a: 14 ...
The order of anaphylatoxin activity from the strongest to the weakest is C5a, C3a, C4a, and C5a des-arginine. ... Complement induction in spinal cord microglia results in anaphylatoxin C5a-mediated pain hypersensitivity. J Neurosci. 2007 Aug ... Human C3a and C3a desArg anaphylatoxins have conserved structures, in contrast to C5a and C5a desArg. Protein Sci. 2013 Feb; 22 ... Serum peptides derived from certain cleaved COMPLEMENT PROTEINS during COMPLEMENT ACTIVATION. They induce smooth MUSCLE ...
... complement c5a MeSH D12.776.124.486.274.024.270.255 - complement c5a, des-arginine MeSH D12.776.124.486.274.050 - complement c1 ... complement c5a, des-arginine MeSH D12.776.124.486.274.450.625 - complement c5b MeSH D12.776.124.486.274.550 - complement c6 ... complement c4b MeSH D12.776.124.486.274.450 - complement c5 MeSH D12.776.124.486.274.450.250 - complement c5a 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. ...
C3a has a regulatory process and a structure homologous to complement component C5a, with which it shares 36% of its sequence ... C3a, like other anaphylatoxins, has a C-terminal arginine residue. Serum carboxypeptidase B, a protease, cleaves the arginine ... C3a desarginine). C3a is an effector of the complement system with a range of functions including T cell activation and ... 12th European Meeting on Complement in Human Disease12th European Meeting on CHD12th European Meeting on Complement in Human ...
3171 (1968)), who have demonstrated a des-R form of complement component C5a and fibrinopeptide B, which are known substrates ... arginine ("R"), to generate degradation products des-R F1.2 or des-R F2. This is postulated based on the work of Chenowith and ... Des-R-PF2-OVA designates a conjugate of ovalbumin with a synthetic peptide emulating the carboxyl terminal of des-R F1.2. ... To produce monoclonal antibodies to the degradation fragments des-R F1.2 and des-R F2, the preferred sequence is Ser-Asp-Arg- ...
des-Arginine Complement C5a Chemical Compounds * Mast Cells Medicine & Life Sciences * Skin Chemical Compounds ... Inflammatory properties of human C5a and C5a des Arg/ in mast cell-depleted human skin. / Swerlick, Robert A.; Yancey, Kim B.; ... Swerlick, R. A., Yancey, K. B., & Lawley, T. J. (1989). Inflammatory properties of human C5a and C5a des Arg/ in mast cell- ... Swerlick, Robert A. ; Yancey, Kim B. ; Lawley, Thomas J. / Inflammatory properties of human C5a and C5a des Arg/ in mast cell- ...
... carboxypeptidase N that removes the carboxy-terminal arginine from C5a forming C5a-des-Arg derivative. C5a-des-Arg exhibits ... 0007] Mature C5 is cleaved into the C5a and C5b fragments during activation of the complement pathways. C5a is cleaved from the ... generation of the terminal complement complex C5b-9. Both C5a and C5b-9 cause the terminal complement-mediated events that are ... Approximately 20% of the 11 kDa mass of C5a is attributed to carbohydrate. [0008] C5a is another anaphylatoxin. C5b combines ...
C3a is considered an anaphylatoxin along with COMPLEMENT C4A; COMPLEMENT C5A; and COMPLEMENT C5A, DES-ARGININE.. MSH ... Uitgebreide planning van de gezondheidszorg medical and nursing care program designed for a particular patient providing for ... The smaller fragment generated from the cleavage of complement C3 by C3 CONVERTASE. C3a, a 77-amino acid peptide, is a mediator ...
... falciparum during pregnancy increases levels of these angiopoietins and complement C5a while reducing nitric oxide ... Rodrigues-Duarte, L., de Moraes, L. V., Barboza, R., Marinho, C. R., Franke-Fayard, B., Janse, C. J., et al. (2012). Distinct ... 2018). Malaria in pregnancy alters l-arginine bioavailability and placental vascular development. Sci. Transl. Med. 10:eaan6007 ... Instituto Gulbenkian de Ciência, Oeiras, Portugal. Infections that reach the placenta via maternal blood can target the fetal- ...
des-Arginine Complement C5a Neutrophil Infiltration Bronchoalveolar Lavage Fluid Tobacco Products Respiratory System ... De Blasio, F., Daughton, D. M., Thompson, A. B., Robbins, R. A., Spurzem, J. R., Sisson, J. H., Von Essen, S. G., Romberger, D. ... Paul, S., Said, S. I., Thompson, A. B., Volle, D. J., Agrawal, D. K., Foda, H. & de la Rocha, S., Jul 1989, In : Journal of ... De Blasio, F., Pezza, A. & Rennard, S. I., Dec 1 1992, In : Archivio Monaldi per le malattie del torace. 47, 1-6, p. 17-29 13 p ...
Antibodies, Monoclonal, Antibody Specificity, Complement Activation, Complement C5a, des-Arginine, immunology, isolation & ... Surprisingly high levels of anaphylatoxin C5a des Arg are extractable from psoriatic scales.. 1993 K Bergh et al. Archives of ...
Complement C5a, des-Arginine. *Vitamin D-Binding Protein. *Complement C5a. Grant support. *HL-01542/HL/NHLBI NIH HHS/United ... C5a des Arg over a wide concentration range. The effect was most pronounced at nonchemotactic doses of C5a (0.01 nM) and C5a ... Finally, radioiodinated C5a or C5a des Arg formed a 1:1 complex with purified Gc-globulin when analyzed by gel filtration ... Gc-globulin (vitamin D-binding protein) enhances the neutrophil chemotactic activity of C5a and C5a des Arg.. Kew RR1, Webster ...
In this study we explored the potential mechanisms involved in C5a-mediated neuroprotection. We found that C5a neuroprotects in ... The study suggests that C5a may protect against glutamate-induced apoptosis in neurons through MAPK-mediated regulation of ... Also, hrC5a-mediated responses appeared to be receptor-mediated because pretreatment of cultures with the specific C5a receptor ... vitro through inhibition of apoptotic death because pretreatment with human recombinant (hr)C5a prevented nuclear DNA ...
The order of anaphylatoxin activity from the strongest to the weakest is C5a, C3a, C4a, and C5a des-arginine. ... Serum peptides derived from certain cleaved COMPLEMENT PROTEINS during COMPLEMENT ACTIVATION. They induce smooth MUSCLE ... The order of anaphylatoxin activity from the strongest to the weakest is C5a, C3a, C4a, and C5a des-arginine.. ... Serum peptides derived from certain cleaved COMPLEMENT PROTEINS during COMPLEMENT ACTIVATION. They induce smooth MUSCLE ...
The complement cleavage product C5a is a potent agonist of different leukocyte types and also has anaphylatoxic properties ... C5a is very rapidly degraded by serum carboxypeptidase N which cleaves the functionally important carboxy-terminal arginine, ... The complement cleavage product C5a is a potent agonist of different leukocyte types and also has anaphylatoxic properties ... C5a is very rapidly degraded by serum carboxypeptidase N which cleaves the functionally important carboxy-terminal arginine, ...
Complement C3a, Complement C5, Complement C5a, des-Arginine,... ... 1987 R A De La Cadena et al. Journal of Laboratory and Clinical ... Adult, Aged, Antigen-Antibody Complex, analysis, Cell Aggregation, Complement C3, analogs & derivatives, ...
With respect to the complement system, C3a, C4a, and C5a, all have C-terminal arginine residues (Pasupuleti et al., 2007). ... whereas cleaved des-arg9-bradykinin, which can be produced from bradykinin by proteolytic removal of the C-terminal arginine, ... Thus, proteolytic cleavage of the C-terminal arginines of both C3a and C5a by cell surface or secreted CPD may play a critical ... and complement fragments C3a, C4a, and C5a (Skidgel, 1988; Skidgel, 1996). With respect to the former, CPD has been suggested ...
DE-alpha-MSH use alpha-MSH de-Arginine Complement 5a use Complement C5a, des-Arginine ... De Toni-Debre-Fanconi Syndrome use Fanconi Syndrome ... De Langes Syndrome use De Lange Syndrome de Meleda, Mal use ... De Quervains Disease use De Quervain Disease ... de Pointes, Torsade use Torsades de Pointes de Pointes, ... De Quervains Disease use De Quervain Disease ... De Quervain Disease De Quervain Stenosing Tenosynovitis use De ...
de Diego, I., Veillard, F., Sztukowska, M. N., Guevara, T., Potempa, B., Pomowski, A., et al. (2014). Structure and mechanism ... Hajishengallis, G., Abe, T., Maekawa, T., Hajishengallis, E., and Lambris, J. D. (2013). Role of complement in host-microbe ... These proteinases are commonly known as gingipains, namely gingipain R and K, that cleave after arginine and lysine, ... by interfering cross-talk between C5a receptor and toll-like receptor signaling to prevent bacterial clearance. In vitro ...
Ebanks RO, Isenman DE (1995) Evidence for the involvement of arginine 462 and the flanking sequence of human C4 beta‐chain in ... or the disordered C5a loop (red dashed line, residues 744-750). (D) Close‐up of the suggested C5-Bb interface with C5a in red ... Bestebroer J, Aerts PC, Rooijakkers SH, Pandey MK, Kohl J, van Strijp JA, de Haas CJ (2010) Functional basis for complement ... Complement activation and the structure of the C5-CVF complex. (A) The three activation pathways of complement (left) induce ...
Complement 5a. Complement C5a. Complement 5a, des-Arginine. Complement C5a, des-Arginine. ... Complement Inactivators. Complement Inactivator Proteins. DNA-Binding Protein, Cyclic AMP-Responsive. Cyclic AMP Response ... Complement 1s. Complement C1s. Glyceraldehyde 3 Phosphate-Dehydrogenase (NADP+)(Phosphorylating). Glyceraldehyde-3-Phosphate ... Complement. Complement System Proteins. Complement 1. Complement C1. Complement 1 Inactivators. Complement C1 Inactivator ...
Arginine at this position in C5a1 is 4.3 Å away from the backbone of PMX53. Lysine or arginine at position 6.55 forms a salt ... C5a1, C5a2, complement peptide receptors; CCK1, CCK2, cholecystokinin receptors; DOR, KOR, MOR, NOP, opioid receptors; ETA, ETB ... Laboratoire de Physique et Chimie des Nano-Objets, CNRS UMR5215-INSA, Université de Toulouse III, Toulouse, France (V.G., D.F.) ... Laboratoire de Physique et Chimie des Nano-Objets, CNRS UMR5215-INSA, Université de Toulouse III, Toulouse, France (V.G., D.F.) ...
39] S. M. Drouin, J. Kildsgaard, J. Haviland et al., "Expression of the complement anaphylatoxin C3a and C5a receptors on ... 1) Universite de Montreal, Laboratoire dimmunologie moleculaire, Departement de microbiologie, Infectiologie et Immunologie, ... Poly-L-Arginine Induces Apoptosis of NCI-H292 Cells via ERK1/2 Signaling Pathway.. ... C5a, in allergic asthma [36-38], we wondered if March1 could modulate the complement receptor (C5aR; CD88) expression in lung ...
Chemotactic factor for tumor cells derived from the C5a fragment of complement component C5. ... Dec 1, 1978·Archives internationales de physiologie et de biochimie·M De WolfW Dierick ... Analysis of transient and reversible effects of poly-L-arginine on the in vivo nasal absorption of FITC-dextran in rats. ... Oct 1, 1979·Proceedings of the National Academy of Sciences of the United States of America·I GresserE De Maeyer ...
Cahiers de Nutrition et de Diététique (Followers: 5) Canadian Food Studies / La Revue canadienne des études sur lalimentation ... Chemical synthesis and characterisation of the complement C5 inhibitory. peptide zilucoplan*Abstract: Abstract The complement ... Arginine methylation: the promise of a silver bullet for. brain tumours*Abstract: Abstract Despite intense research efforts ... describe an approach for the chemical synthesis of zilucoplan and validate that the synthesised compound blocks LPS-induced C5a ...
... complement-C1q-tumor-necrosis- XP008274125.1 gene:103353115 transcript:XP008274125.1 DBNLINE,295, ... serine-arginine-repetitive-mat XP008274479.1 gene:103353337 transcript:XP008274479.1 DBNLINE,514, ... C5a-anaphylatoxin-chemotactic- XP008274122.1 gene:103353113 transcript:XP008274122.1 DBNLINE,293, ... phosphopantothenoylcysteine-de XP008275051.1 gene:103353717 transcript:XP008275051.1 DBNLINE,876, ...
Thrombin-activatable procarboxypeptidase B regulates activated complement C5a in vivo BLOOD Nishimura, T., Myles, T., Piliposky ... Arginine methylation is a common post-translation modification found in many proteins. Protein-arginine methyltransferase I ( ... and sputum culture results.A de novo diagnosis of cystic fibrosis (CF) was established in 10 patients (20%). Patients with CF ... Protein-arginine methyltransferase I, the predominant protein-arginine methyltransferase in cells, interacts with and is ...
TNF receptor: Adalimumab fake TNF receptor: Etanercept Complement: C_a for anaphylaxis (histamine release , edema , hypotension ... ARGININE(R), LYSINE(K)) Negatively charged amino acids: Negative experience to be burned by Acid: Aspartic acid and glutamic ... de-prESsed Heart is Sick from Too Much Blood. Heart = CHF Sick = Sickle Cell Too Much Blood = Polycythemia Pharmacology: ... C5a, IL8, LTB4, Kallikrein IL8: 8 looks like multilobed nucleus of neutrophil = PMN chemotaxis LTB4s B also looks like ...
tartarato de varenicline vs bupropion. Gene therapy model for stromal precursor cells of hematopoietic microenvironment. ... The presence of multiple arginines in individual methylated proteins also raises the question of whether overall methylation or ... and to a lesser degree with C5a. ... Myeloperoxidase directs properdin-mediated complement ...
De Jager, S. C., Van Middelaar, B. J., Smeets, M. B., . . . De Kleijn, D. P. (2014), Leucocyte expression of complement C5a ... Craig, M., Sadik, A. Y., Golubeva, Y. A., Tidhar, A., & Slauch, J. M. (2013), Twin-arginine translocation system (tat) mutants ... van der Veen EL, Suurs FV, Cleeren F, Bormans G, Elsinga PH, Hospers GAP, Lub-de Hooge MN, de Vries EGE, de Vries EFJ, Antunes ... Suurs FV, Lorenczewski G, Stienen S, Friedrich M, de Vries EGE, de Groot DJA, Lub-de Hooge MN., The Biodistribution of a CD3 ...
INSTITUTO DE CIENCIAS BÁSICAS Y PRECLÍNICAS "VICTORIA DE GIRÓN" DEPARTAMENTO DE HISTOLOGÍA ... BMC Complement Altern Med. The positive effects of Ginsenoside Rg1 upon the hematopoietic microenvironment in a D-Galactose- ... L-ARGININE, BUT NOT L-NAME PROTECTS AGAINST LIVER INJURY INDUCED BY EXPERIMENTAL ISCHEMIA-REPERFUSION Tdmu:Source. ... Treatment of Paraquat-Induced Lung Injury With an Anti-C5a Antibody: Potential Clinical Application Pubmed:29293144. ...
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Previous studies have shown that complement C5a is present venex $300 tablet pc and injurious in the brains of foetal mice ... determination of 2 isomers of eicosatrienoic acid of rat liver The hemocytes and plasma proteomes were compared by 2-DE between ... vessel the relaxation caused by thrombin was abolished by antithrombin III and the tripeptide D-phenylalanine-proline-arginine- ...
Coleman, DE, Berghuis, AM, Lee, E, Linder, ME, Gilman, AG and Sprang, SR (1994). Structures of active conformations of Gi alpha ... Lee, CH, Katz, A and Simon, MI (1995). Multiple regions of G alpha 16 contribute to the specificity of activation by the C5a ... Ho, MK, Yung, LY and Wong, YH (1999). Disruption of receptor-mediated activation of G protein by mutating a conserved arginine ... These GPCRs included Gi-coupled adenosine A1 receptor (A1R), complement C5aR receptor, formyl peptide receptor (fMLPR), and the ...
Our results suggest that an increase in C3a and C5a levels during saturation diving correlates with decompression stress and ... Paired sera from 60 patients with respiratory infection who had tested positive for M pneumoniae by complement fixation test ... argF extracellularly produced a large amount of D-ornithine when cultivated in a CGXII medium containing 1 mM L-arginine. ... EN DE FR IT ES PT JP Currency: USD USD EUR CAD GBP CHF AUD JPY BRL MXN NZD ...
  • 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)
  • Surprisingly high levels of anaphylatoxin C5a des Arg are extractable from psoriatic scales. (naver.com)
  • Complement anaphylatoxin C5a neuroprotects through mitogen-activated protein kinase-dependent inhibition of caspase 3. (semanticscholar.org)
  • We previously reported that pretreatment of murine cortico-hippocampal neuronal cultures with the complement-derived anaphylatoxin C5a, protects against glutamate neurotoxicity. (semanticscholar.org)
  • Pangburn and Rawal, 2002 ) to form a C5 convertase (C3bBb3b or C4b2a3b), which cleaves C5 to generate the large fragment C5b and the anaphylatoxin C5a ( Figure 1A ). (embopress.org)
  • The present invention refers to muteins of the C5a anaphylatoxin (C5a) which are C5a receptor antagonists, to nucleic acid molecules comprising a nucleotide sequence encoding such muteins of C5a anaphylatoxin, to host cells containing a nucleic acid molecule comprising a nucleotide sequence encoding such muteins of the C5a anaphylatoxin as well as to a pharmaceutical composition comprising a mutein of the C5a anaphylatoxin acting as a C5a receptor antagonists. (freepatentsonline.com)
  • Human C3a anaphylatoxin (C3a), a C3 split fragment produced during the activation of the complement system, is one of the complement molecules that have been reported to serve non-immune roles. (spandidos-publications.com)
  • Infiltrating leukocytes are known to be recruited by the downstream products of complement activation, especially the soluble anaphylatoxin C5a, with subsequent enlistment of other components of the membrane attack complex [ 5 , 6 ]. (biomedcentral.com)
  • AF was cultured and analyzed for C3a and C5a by enzyme-linked immunosorbent assay kits. (bvsalud.org)
  • Bajic G, Yatime L, Klos A, Andersen GR. Human C3a and C3a desArg anaphylatoxins have conserved structures, in contrast to C5a and C5a desArg. (harvard.edu)
  • Gutzmer R, Köther B, Zwirner J, Dijkstra D, Purwar R, Wittmann M, Werfel T. Human plasmacytoid dendritic cells express receptors for anaphylatoxins C3a and C5a and are chemoattracted to C3a and C5a. (harvard.edu)
  • Like other anaphylatoxins, C3a is regulated by cleavage of its carboxy-terminal arginine, which results in a molecule with lowered inflammatory function (C3a desarginine). (wikipedia.org)
  • Anaphylatoxins are small complement peptides that induce proinflammatory responses in tissues. (wikipedia.org)
  • Certain signals, including substance P, the complement anaphylatoxins C3a and C5a, and endothelin 1, induced human MCs rapidly to secrete small and relatively spherical granule structures, a pattern consistent with the secretion of individual granules. (jci.org)
  • Mass spectrometric analyses identified the cleavage products as C3a and C5a, displaying identical molecular weights as the native anaphylatoxins C3a and C5a. (jimmunol.org)
  • CARDIOPULMONARY bypass (CPB) promotes significant activation of the complement cascade, resulting in the production of both C3a and C5a anaphylatoxins, [1,2] which in turn act as potent stimulators of polymorphonuclear leukocytes (PMNs). (asahq.org)
  • Serum peptides derived from certain cleaved COMPLEMENT PROTEINS during COMPLEMENT ACTIVATION. (harvard.edu)
  • This enhancing activity was not due to a nonspecific effect of anionic proteins since other purified serum proteins, of similar size and charge as Gc-globulin (alpha 1 acid glycoprotein, alpha 2 HS glycoprotein, alpha 2 histidine-rich glycoprotein), could not increase the chemotactic activity of C5a des Arg. (nih.gov)
  • Complement acts as a danger‐sensing system in the innate immune system, and its activation initiates a strong inflammatory response and cleavage of the proteins C3 and C5 by proteolytic enzymes, the convertases. (embopress.org)
  • Activation of the proteolytic complement cascade triggers cleavage of the homologous 185-200 kDa proteins C3, C4, and C5 ( Supplementary Figure S1 ). (embopress.org)
  • Both in patients with AMD and in a recently described mouse model of AMD, early subretinal pigmented epithelium deposition of complement components C3 and C5 occurs, suggesting a contributing role for these inflammatory proteins in the development of AMD. (pnas.org)
  • Two of these proteins, CD55 and CD59, are complement regulatory proteins. (cancertherapyadvisor.com)
  • The loss of complement regulatory proteins renders PNH erythrocytes susceptible to both intravascular and extravascular hemolysis, but it is the intravascular hemolysis that contributes to much of the morbidity and mortality from the disease. (cancertherapyadvisor.com)
  • We investigated the possibility that the multifunctional serum protein Gc-globulin (vitamin D-binding protein) may also enhance the neutrophil chemotactic activity of complement-derived peptides. (nih.gov)
  • References (14) and (15) disclose that peptides containing 6 to 15 contiguous arginine residues can increase cellular uptake of conjugated molecules. (justia.com)
  • These references also disclose that the peptoid analogs of 6 to 9 arginine residue peptides display even higher cellular uptake properties. (justia.com)
  • Despite the apparent success in the use of peptide-based molecule transporters, including peptides and peptoids derived from arginine, lysine (see reference (8)), and ornithine (see reference (9)), such molecules are limited by their toxicity, availability, and cost. (justia.com)
  • Septic primates treated with anti-C5a antibodies did not die and did not develop decreased oxygenation (P less than 0.05) or increased extravascular lung water (P less than 0.05). (nih.gov)
  • This study demonstrates that treatment with rabbit anti-human C5a des arg antibodies attenuates ARDS and some of the systemic manifestations of sepsis in nonhuman primates. (nih.gov)
  • In this paper we describe the purification of milligram amounts of bovine C5a(desArg) by a simplified procedure, and the preparation of mouse monoclonal antibodies (MAbs) to C5a/C5a(desArg) which do not recognize native C5. (nih.gov)
  • The classical pathway of complement activation is initiated when the C1 complex, made up of C1r and C1s serine proteases, recognizes the Fc region of IgM or IgG antibodies bound to a pathogen. (wikipedia.org)
  • They are the source of the rheumatoid factors and anticitrullinated protein antibodies, which contribute to immune complex formation and complement activation in the joints. (biomedcentral.com)
  • C3a formation occurs through activation and cleavage of complement component 3 in a reaction catalyzed by C3-convertase. (wikipedia.org)
  • The complement cleavage product C5a is a potent agonist of different leukocyte types and also has anaphylatoxic properties through the release of mediators by basophils and tissue mast cells. (uni-konstanz.de)
  • Complement activation generates two potent inflammatory mediators from C5, C5a and its derivative C5a(desArg), which results from the removal of the C-terminal arginine by ubiquitous carboxypeptidases. (nih.gov)
  • Small amounts (means +/- SEM) of C5a/C5a(desArg) were found in EDTA-plasma (0.58 +/- 0.06 ng.mL-1). (nih.gov)
  • Complement activation occurred during coagulation since the baseline concentration of C5a/C5a(desArg) (15.4 +/- 4.1 ng.mL-1) was higher than in plasma. (nih.gov)
  • Zymosan, a potent activator of the complement cascade, was used to generate C5a/C5a(desArg). (nih.gov)
  • The maximal concentration of C5a/C5a desArg attained in zymosan-activated serum was 4.28 +/- 0.14 micrograms.mL-1. (nih.gov)
  • Normal milk (from healthy, uninflamed mammary glands) contained on average 0.12 ng of C5a/C5a(desArg).mL-1 (range 0.02-0.19 ng.mL-1). (nih.gov)
  • The maximal amount of C5a/C5a(desArg) which was generated in milk with zymosan was 1.1 ng.mL-1 (range 0.68-2.17 ng.mL-1). (nih.gov)
  • In milk from quarters with subclinical infections by coagulase-negative staphylococci, values were 0.18 ng.mL-1 and 2.37 ng.mL-1 for spontaneous and zymosan-generated C5a/C5a(desArg) concentrations, respectively. (nih.gov)
  • In milk from Escherichia coli endotoxin-induced mastitis, C5a/C5a(desArg) concentrations (means of four cows) before and after zymosan activation reached 6.5 ng.mL-1 and 55 ng.mL-1, respectively. (nih.gov)
  • These results indicate that a C5-convertase can operate in normal milk, that only minute amounts of C5a/C5a(desArg) can be generated (less than 1/1,000 of plasma potential), but that much higher concentrations are reached in milk during endotoxin-induced inflammation. (nih.gov)
  • The ELISA made it possible to determine normal ranges of C5a/C5a(desArg) in bovine blood plasma and in milk, and is a valuable tool to define the variations of its concentrations in exudates during inflammatory reactions. (nih.gov)
  • In vitro and in vivo studies have suggested that human complement component C5a plays a key role in neutrophil injury in the adult respiratory distress syndrome (ARDS). (nih.gov)
  • First, using leukocyte aggregometry, we demonstrated that the addition of a recently developed rabbit anti-human polyclonal antibody to C5a des arg to endotoxin-activated plasma prevented leukocyte aggregation in vitro. (nih.gov)
  • The anticoagulant EDTA was more efficient than citrate or heparin in inhibiting in vitro activation of the complement system. (nih.gov)
  • Complement protein C1q modulates neurite outgrowth in vitro and spinal cord axon regeneration in vivo. (semanticscholar.org)
  • Here we provide evidence that bioactive fragments of these complement components (C3a and C5a) are present in drusen of patients with AMD, and that C3a and C5a induce VEGF expression in vitro and in vivo . (pnas.org)
  • The current study reports multiple links for various factors of the coagulation and fibrinolysis cascades with the central complement components C3 and C5 in vitro and ex vivo. (jimmunol.org)
  • RFs efficiently fix and activate complement in vitro by the classic pathway [ 1 ]. (biomedcentral.com)
  • Moreover, no clinical reactions were detectable in mast cell-depleted human skin after intradermal challenge with 50 ng of either C5a or C5a des Arg, despite the fact that biopsies of these sites revealed substantial, neutrophil-rich infiltrates. (elsevier.com)
  • Gc-globulin (vitamin D-binding protein) enhances the neutrophil chemotactic activity of C5a and C5a des Arg. (nih.gov)
  • However, as little as 0.01 nM Gc-globulin greatly enhanced the neutrophil chemotactic activity of C5a and its derivative, C5a des Arg over a wide concentration range. (nih.gov)
  • On binding to a ligand, MBL may activate the lectin pathway of complement via the MBL-associated serine protease 2. (ahajournals.org)
  • C5a is very rapidly degraded by serum carboxypeptidase N which cleaves the functionally important carboxy-terminal arginine, generating C5desarg, a chemotactic agonist with little mast cell-activating ability. (uni-konstanz.de)
  • Serum depleted of Gc-globulin by immunoaffinity chromatography totally lacked chemotactic enhancing activity for C5a des Arg. (nih.gov)
  • Addition of FXa to human serum or plasma activated complement ex vivo, represented by the generation of C3a, C5a, and the terminal complement complex, and decreased complement hemolytic serum activity that defines exact serum concentration that results in complement-mediated lysis of 50% of sensitized sheep erythrocytes. (jimmunol.org)
  • RESULTS: In multivariable analysis, AF level of C3a was the only variable significantly associated with IAI, whereas C5a level in AF and serum C-reactive protein level were not associated with IAI. (bvsalud.org)
  • The serum levels of HMGB1, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), complement 3a (C3a), and complement 5a (C5a) were measured. (bvsalud.org)
  • The complement cascade is a dual-edged sword, causing protection against. (alterauto.fr)
  • The complement cascade is a central component of innate immunity which plays a critical role in brain inflammation. (bvsalud.org)
  • complement fragments (e. g. (parasitol.kr)
  • It has also been reported that arginine-rich fragments of HIV-1 Tat are efficiently internalized by cultured cells. (justia.com)
  • C5a and its degradation product, C5a des Arg, elicit immediate cutaneous inflammatory reactions after intradermal injection. (elsevier.com)
  • This experimental approach in vivo has allowed the independent analysis of the anaphylactogenic and chemoattractant activities of human C5a and C5a des Arg in human skin, demonstrated the importance of dermal mast cells in these clinical responses, and shown that leukocytes can accumulate at these infection sites directly in response to these mediators. (elsevier.com)
  • Furthermore, the multiple pathophysiologic processes, including necrosis, apoptosis, mesenchymal transformation, cellular infiltration, coagulation, and complement activation that contribute to AKI and the multitude of cell types and processes within the innate and adaptive immune response contribute to a nearly infinite combination of events and processes to consider (Figure 1 ). (jci.org)
  • The complement system as well as the coagulation system has fundamental clinical implications in the context of life-threatening tissue injury and inflammation. (jimmunol.org)
  • Furthermore, in plasma from patients with multiple injuries ( n = 12), a very early appearance and correlation of coagulation (thrombin-antithrombin complexes) and the complement activation product C5a was found. (jimmunol.org)
  • Traditionally, the complement and coagulation systems are described as separate cascades. (jimmunol.org)
  • The results show that E. histolytica clearance from the mouse liver is related to a low chemotactic activity of complement, which results in poor inflammatory response and parasite inability to cause tissue damage. (portlandpress.com)
  • C3a is also able to play a role in chemotaxis for mast cells and eosinophils, but C5a is a more potent chemoattractant. (wikipedia.org)
  • More recently, a prospective study revealed that blood levels of L-arginine, a precursor to the potent vasodilator nitric oxide, were reduced in women with placental malaria while levels of dimethylarginine, an inhibitor of nitric oxide biosynthesis, were increased. (frontiersin.org)
  • On a molar basis C5adesarg is only one order of magnitude less potent and about half as efficacious as C5a at inducing basophil degranulation. (uni-konstanz.de)
  • C3a has a regulatory process and a structure homologous to complement component C5a, with which it shares 36% of its sequence identity. (wikipedia.org)
  • We then administered the anti-C5a des arg antibody to septic primates (Macaca fascicularis). (nih.gov)
  • Three groups of primates, control, septic, and anti-C5a antibody treated septic, were studied (n = 4 in each group). (nih.gov)
  • Septic animals not treated with anti-C5a antibody had 75% mortality (3/4), decreased oxygenation, severe pulmonary edema, and profound hypotension. (nih.gov)
  • We also show that genetic ablation of receptors for C3a or C5a reduces VEGF expression, leukocyte recruitment, and CNV formation after laser injury, and that antibody-mediated neutralization of C3a or C5a or pharmacological blockade of their receptors also reduces CNV. (pnas.org)
  • l -NAME, thrombin, and PMA also significantly increased polymorphonuclear leukocyte adherence to the coronary artery endothelium, an effect that was significantly attenuated by the anti-P-selectin monoclonal antibody PB1.3 or by UCN-01, l -arginine, 8-bromo-cGMP or SNP but not by d -arginine or the nonblocking anti-P-selectin monoclonal antibody NBP1.6. (ahajournals.org)
  • Eculizumab is a monoclonal antibody that blocks terminal complement activation and is effective in treating some forms of PNH. (cancertherapyadvisor.com)
  • 15. A method of treating glaucoma, the method comprising administering a therapeutic amount of a complement inhibitor to a patient suffering from glaucoma to thereby treat the glaucoma, wherein the complement inhibitor is an anti-C1s antibody. (patentsencyclopedia.com)
  • A MAb was used to develop a sandwich ELISA which made it possible to quantify levels of C5a/C5adesArg in bovine biological fluids. (nih.gov)
  • The efficacy of C5a and C5adesarg at inducing histamine and LTC4 release by primed basophils was similar. (uni-konstanz.de)
  • Thus, C5adesarg is a stable inducer of release of inflammatory mediators by human basophils, particularly in primed cells, and complement may, therefore, play a role in immediate-type hypersensitivity diseases in allergic late-phase reactions. (uni-konstanz.de)
  • Swerlick, RA , Yancey, KB & Lawley, TJ 1989, ' Inflammatory properties of human C5a and C5a des Arg/ in mast cell-depleted human skin ', Journal of Investigative Dermatology , vol. 93, no. 3, pp. 417-422. (elsevier.com)
  • Complement C3a enhances CXCL12 (SDF-1)-mediated chemotaxis of bone marrow hematopoietic cells independently of C3a receptor. (harvard.edu)
  • The Alternative Receptor for Complement Component 5a, C5aR2, Conveys Neuroprotection in Traumatic Spinal Cord Injury. (semanticscholar.org)
  • A mutein of the invention is a C5a receptor antagonist wherein the amino acid residue naturally occurring at sequence position 69 is mutated. (freepatentsonline.com)
  • Despite the observation that EhROM1 relocalized to the cap during surface receptor capping, EhROM1 knockdown [ROM(KD)] parasites had no gross changes in cap formation or complement resistance. (asm.org)
  • Complement C3a receptor (C3aR) is a key mediator of post-ischemic cerebral injury, and pharmacological antagonism of the C3a receptor is neuroprotective in stroke. (bvsalud.org)
  • C3a is an effector of the complement system with a range of functions including T cell activation and survival, angiogenesis stimulation, chemotaxis, mast cell degranulation, and macrophage activation. (wikipedia.org)
  • These infiltrates were qualitatively and quantitatively identical to C5a or C5a des Arg-induced infiltrates in mast cell replete skin. (elsevier.com)
  • These findings suggest that subclinical IAI or SPTD in the context of cervical insufficiency is related to activation of complement system in AF. (bvsalud.org)
  • They also lack hemolytic complement, C5. (jax.org)
  • It has been shown to have both proinflammatory and anti-inflammatory responses, its activity able to counteract the proinflammatory effects of C5a. (wikipedia.org)
  • Traditionally thought to serve a strictly pro-inflammatory role, recent investigations have shown that C3a can also work against C5a to serve an anti-inflammatory role. (wikipedia.org)
  • 19 However, experimental data and clinical observations suggest that MBL and the lectin pathway of complement may initiate the inflammatory reaction seen in relation to ischemia reperfusion injury. (ahajournals.org)
  • is a split product of complement component 4. (alterauto.fr)
  • Complement component 1s ( EC 3.4.21.42 , C1 esterase , activated complement C1s , complement C overbar 1r , C1s ) is a protein involved in the complement system . (wikipedia.org)
  • Molecular cloning of cDNA for human complement component C1s. (wikipedia.org)
  • Human complement component C1s. (wikipedia.org)
  • The alternative pathway of complement activation is typically always active at low levels in blood plasma through a process called tick-over, in which C3 spontaneously hydrolyzes into its active form, C3(H2O). (wikipedia.org)
  • Here, we discuss the impact of malaria in pregnancy on three pathways that are important regulators of healthy pregnancy outcomes: L-arginine-nitric oxide biogenesis, complement activation, and the heme axis. (edu.au)
  • Nitric oxide plays a key role in placental vascular function, and its synthesis requires l -arginine. (sciencemag.org)
  • The release of C3a and C5a increases vascular permeability and blood flow, thereby promoting further transport of other snake venom components ( Vogel and Fritzinger, 2010 ). (embopress.org)
  • 6 7 l -Arginine/NO can also attenuate monocyte adherence to the vascular endothelium in hypercholesterolemic rabbits. (ahajournals.org)
  • 6 Furthermore, either l -arginine, a precursor of NO, or 8-bromo-cGMP, a stable cGMP analogue, significantly attenuated the l -NAME-induced increase in P-selectin expression. (ahajournals.org)
  • C4b2a is the widely used short‐hand nomenclature for the C4b-C2a complex in the complement field, and similar nomenclature is used for the remaining complexes in the following). (embopress.org)
  • Because NO has been shown to inhibit protein kinase C (PKC) activity, we examined the hypothesis that the NO synthase inhibitor N G -nitro- l -arginine methyl ester ( l -NAME) stimulates P-selectin expression on platelets via PKC activation. (ahajournals.org)
  • Immune phenotypes in the NOD background consist of defects in antigen presentation, T lymphocyte repertoire, NK cell function, macrophage cytokine production, wound healing, and C5 complement. (jax.org)
  • The cytokine storm-activated complement pathways lead to even greater synthesis of cytokines, as well as increased production of adhesion molecules. (umj.com.ua)
  • As a part of the immune system, the complement system is initially involved in host defense against pathogens. (spandidos-publications.com)
  • for example, the complement system was discovered to be involved in the control of tissue morphogenesis, wound healing and synaptic pruning ( 1 ). (spandidos-publications.com)
  • Systemic complement activation is associated with respiratory failure in COVID-19 hospitalized patients. (uio.no)
  • BACKGROUND: We aimed to estimate whether elevated levels of complement C3a and C5a in amniotic fluid (AF) are independently associated with increased risks of intra-amniotic infection and/or inflammation (IAI) and spontaneous preterm delivery (SPTD) in women with cervical insufficiency or a short cervix (≤ 25 mm). (bvsalud.org)
  • These statistical methods, available to the research community, assist in the design and interpretation of P. A striking finding is the fact that the production of oxidants following stimulation with the complement factors C3a-C5a and aggregated IgG is appreciably lower than following stimulation with PMA or zymosan. (faintpower.tk)