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.
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.
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.
Complement System Proteins
Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).
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 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.
A 77-kDa subcomponent of complement C1, encoded by gene C1S, is a SERINE PROTEASE existing as a proenzyme (homodimer) in the intact complement C1 complex. Upon the binding of COMPLEMENT C1Q to antibodies, the activated COMPLEMENT C1R cleaves C1s into two chains, A (heavy) and B (light, the serine protease), linked by disulfide bonds yielding the active C1s. The activated C1s, in turn, cleaves COMPLEMENT C2 and COMPLEMENT C4 to form C4b2a (CLASSICAL C3 CONVERTASE).
Complement Membrane Attack Complex
A product of COMPLEMENT ACTIVATION cascade, regardless of the pathways, that forms transmembrane channels causing disruption of the target CELL MEMBRANE and cell lysis. It is formed by the sequential assembly of terminal complement components (COMPLEMENT C5B; COMPLEMENT C6; COMPLEMENT C7; COMPLEMENT C8; and COMPLEMENT C9) into the target membrane. The resultant C5b-8-poly-C9 is the "membrane attack complex" or MAC.
A 80-kDa subcomponent of complement C1, existing as a SERINE PROTEASE proenzyme in the intact complement C1 complex. When COMPLEMENT C1Q is bound to antibodies, the changed tertiary structure causes autolytic activation of complement C1r which is cleaved into two chains, A (heavy) and B (light, the serine protease), connected by disulfide bonds. The activated C1r serine protease, in turn, activates COMPLEMENT C1S proenzyme by cleaving the Arg426-Ile427 bond. No fragment is released when either C1r or C1s is cleaved.
Complement Inactivator Proteins
Serum proteins that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host. The complement system is tightly regulated by inactivators that accelerate the decay of intermediates and certain cell surface receptors.
A 93-kDa serum glycoprotein encoded by C7 gene. It is a polypeptide chain with 28 disulfide bridges. In the formation of MEMBRANE ATTACK COMPLEX; C7 is the next component to bind the C5b-6 complex forming a trimolecular complex C5b-7 which is lipophilic, resembles an integral membrane protein, and serves as an anchor for the late complement components, C8 and C9.
Complement C3-C5 Convertases
Serine proteases that cleave COMPLEMENT C3 into COMPLEMENT C3A and COMPLEMENT C3B, or cleave COMPLEMENT C5 into COMPLEMENT C5A and COMPLEMENT C5B. These include the different forms of C3/C5 convertases in the classical and the alternative pathways of COMPLEMENT ACTIVATION. Both cleavages take place at the C-terminal of an ARGININE residue.
Complement Factor B
Complement Pathway, Alternative
Complement activation initiated by the interaction of microbial ANTIGENS with COMPLEMENT C3B. When COMPLEMENT FACTOR B binds to the membrane-bound C3b, COMPLEMENT FACTOR D cleaves it to form alternative C3 CONVERTASE (C3BBB) which, stabilized by COMPLEMENT FACTOR P, is able to cleave multiple COMPLEMENT C3 to form alternative C5 CONVERTASE (C3BBB3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.
Complement Pathway, Classical
Complement activation initiated by the binding of COMPLEMENT C1 to ANTIGEN-ANTIBODY COMPLEXES at the COMPLEMENT C1Q subunit. This leads to the sequential activation of COMPLEMENT C1R and COMPLEMENT C1S subunits. Activated C1s cleaves COMPLEMENT C4 and COMPLEMENT C2 forming the membrane-bound classical C3 CONVERTASE (C4B2A) and the subsequent C5 CONVERTASE (C4B2A3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.
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.
Receptors, Complement 3b
Molecular sites on or in some B-lymphocytes and macrophages that recognize and combine with COMPLEMENT C3B. The primary structure of these receptors reveal that they contain transmembrane and cytoplasmic domains, with their extracellular portion composed entirely of thirty short consensus repeats each having 60 to 70 amino acids.
Complement Factor H
An important soluble regulator of the alternative pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It is a 139-kDa glycoprotein expressed by the liver and secreted into the blood. It binds to COMPLEMENT C3B and makes iC3b (inactivated complement 3b) susceptible to cleavage by COMPLEMENT FACTOR I. Complement factor H also inhibits the association of C3b with COMPLEMENT FACTOR B to form the C3bB proenzyme, and promotes the dissociation of Bb from the C3bBb complex (COMPLEMENT C3 CONVERTASE, ALTERNATIVE PATHWAY).
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.
Receptor, Anaphylatoxin C5a
Complement Activating Enzymes
Complement Inactivating Agents
Complement Hemolytic Activity Assay
A screening assay for circulating COMPLEMENT PROTEINS. Diluted SERUM samples are added to antibody-coated ERYTHROCYTES and the percentage of cell lysis is measured. The values are expressed by the so called CH50, in HEMOLYTIC COMPLEMENT units per milliliter, which is the dilution of serum required to lyse 50 percent of the erythrocytes in the assay.
Complement C1 Inactivator Proteins
Receptors, Complement 3d
Molecular sites on or in B-lymphocytes, follicular dendritic cells, lymphoid cells, and epithelial cells that recognize and combine with COMPLEMENT C3D. Human complement receptor 2 (CR2) serves as a receptor for both C3dg and the gp350/220 glycoprotein of HERPESVIRUS 4, HUMAN, and binds the monoclonal antibody OKB7, which blocks binding of both ligands to the receptor.
Serum peptides derived from certain cleaved COMPLEMENT PROTEINS during COMPLEMENT ACTIVATION. They induce smooth MUSCLE CONTRACTION; mast cell HISTAMINE RELEASE; PLATELET AGGREGATION; and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from the strongest to the weakest is C5a, C3a, C4a, and C5a des-arginine.
Complement Fixation Tests
Serologic tests based on inactivation of complement by the antigen-antibody complex (stage 1). Binding of free complement can be visualized by addition of a second antigen-antibody system such as red cells and appropriate red cell antibody (hemolysin) requiring complement for its completion (stage 2). Failure of the red cells to lyse indicates that a specific antigen-antibody reaction has taken place in stage 1. If red cells lyse, free complement is present indicating no antigen-antibody reaction occurred in stage 1.
Complement Factor D
Complement Factor I
A plasma serine proteinase that cleaves the alpha-chains of C3b and C4b in the presence of the cofactors COMPLEMENT FACTOR H and C4-binding protein, respectively. It is a 66-kDa glycoprotein that converts C3b to inactivated C3b (iC3b) followed by the release of two fragments, C3c (150-kDa) and C3dg (41-kDa). It was formerly called KAF, C3bINF, or enzyme 3b inactivator.
Complement C4b-Binding Protein
Complement C3b Inactivator Proteins
Endogenous proteins that inhibit or inactivate COMPLEMENT C3B. They include COMPLEMENT FACTOR H and COMPLEMENT FACTOR I (C3b/C4b inactivator). They cleave or promote the cleavage of C3b into inactive fragments, and thus are important in the down-regulation of COMPLEMENT ACTIVATION and its cytolytic sequence.
Complement C3-C5 Convertases, Classical Pathway
An adrenal microsomal cytochrome P450 enzyme that catalyzes the 21-hydroxylation of steroids in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP21 gene, converts progesterones to precursors of adrenal steroid hormones (CORTICOSTERONE; HYDROCORTISONE). Defects in CYP21 cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL).
Complement C3-C5 Convertases, Alternative Pathway
Complement C1 Inhibitor Protein
An endogenous 105-kDa plasma glycoprotein produced primarily by the LIVER and MONOCYTES. It inhibits a broad spectrum of proteases, including the COMPLEMENT C1R and the COMPLEMENT C1S proteases of the CLASSICAL COMPLEMENT PATHWAY, and the MANNOSE-BINDING PROTEIN-ASSOCIATED SERINE PROTEASES. C1-INH-deficient individuals suffer from HEREDITARY ANGIOEDEMA TYPES I AND II.
Complement C3 Convertase, Alternative Pathway
Complement C5 Convertase, Classical Pathway
Molecular Sequence Data
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Complement C3 Convertase, Classical Pathway
Lupus Erythematosus, Systemic
A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.
Complement C5 Convertase, Alternative Pathway
Amino Acid Sequence
Complement Pathway, Mannose-Binding Lectin
Complement activation triggered by the interaction of microbial POLYSACCHARIDES with serum MANNOSE-BINDING LECTIN resulting in the activation of MANNOSE-BINDING PROTEIN-ASSOCIATED SERINE PROTEASES. As in the classical pathway, MASPs cleave COMPLEMENT C4 and COMPLEMENT C2 to form C3 CONVERTASE (C4B2A) and the subsequent C5 CONVERTASE (C4B2A3B) leading to cleavage of COMPLEMENT C5 and assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.
A 53-kDa protein that is a positive regulator of the alternate pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It stabilizes the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb) and protects it from rapid inactivation, thus facilitating the cascade of COMPLEMENT ACTIVATION and the formation of MEMBRANE ATTACK COMPLEX. Individuals with mutation in the PFC gene exhibit properdin deficiency and have a high susceptibility to infections.
Complement C5a, des-Arginine
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.
Genetic Complementation Test
Enzyme-Linked Immunosorbent Assay
An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.
Major Histocompatibility Complex
The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) TRANSPLANTATION ANTIGENS, genes which control the structure of the IMMUNE RESPONSE-ASSOCIATED ANTIGENS, HUMAN; the IMMUNE RESPONSE GENES which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)
Disease Models, Animal
Blood Bactericidal Activity
The natural bactericidal property of BLOOD due to normally occurring antibacterial substances such as beta lysin, leukin, etc. This activity needs to be distinguished from the bactericidal activity contained in a patient's serum as a result of antimicrobial therapy, which is measured by a SERUM BACTERICIDAL TEST.
Differentiation antigens residing on mammalian leukocytes. CD stands for cluster of differentiation, which refers to groups of monoclonal antibodies that show similar reactivity with certain subpopulations of antigens of a particular lineage or differentiation stage. The subpopulations of antigens are also known by the same CD designation.
Electrophoresis, Polyacrylamide Gel
Complement C3 Nephritic Factor
An IgG autoantibody against the ALTERNATIVE PATHWAY C3 CONVERTASE, found in serum of patients with MESANGIOCAPILLARY GLOMERULONEPHRITIS. The binding of this autoantibody to C3bBb stabilizes the enzyme thus reduces the actions of C3b inactivators (COMPLEMENT FACTOR H; COMPLEMENT FACTOR I). This abnormally stabilized enzyme induces a continuous COMPLEMENT ACTIVATION and generation of C3b thereby promoting the assembly of MEMBRANE ATTACK COMPLEX and cytolysis.
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 deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
Surface Plasmon Resonance
A biosensing technique in which biomolecules capable of binding to specific analytes or ligands are first immobilized on one side of a metallic film. Light is then focused on the opposite side of the film to excite the surface plasmons, that is, the oscillations of free electrons propagating along the film's surface. The refractive index of light reflecting off this surface is measured. When the immobilized biomolecules are bound by their ligands, an alteration in surface plasmons on the opposite side of the film is created which is directly proportional to the change in bound, or adsorbed, mass. Binding is measured by changes in the refractive index. The technique is used to study biomolecular interactions, such as antigen-antibody binding.
Glomerulonephritis associated with autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Lupus nephritis is histologically classified into 6 classes: class I - normal glomeruli, class II - pure mesangial alterations, class III - focal segmental glomerulonephritis, class IV - diffuse glomerulonephritis, class V - diffuse membranous glomerulonephritis, and class VI - advanced sclerosing glomerulonephritis (The World Health Organization classification 1982).
Autoantibodies directed against various nuclear antigens including DNA, RNA, histones, acidic nuclear proteins, or complexes of these molecular elements. Antinuclear antibodies are found in systemic autoimmune diseases including systemic lupus erythematosus, Sjogren's syndrome, scleroderma, polymyositis, and mixed connective tissue disease.
Sequence Homology, Amino Acid
Polymerase Chain Reaction
In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.
Gene Expression Regulation
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.
Mannose-Binding Protein-Associated Serine Proteases
Serum serine proteases which participate in COMPLEMENT ACTIVATION. They are activated when complexed with the MANNOSE-BINDING LECTIN, therefore also known as Mannose-binding protein-Associated Serine Proteases (MASPs). They cleave COMPLEMENT C4 and COMPLEMENT C2 to form C4b2a, the CLASSICAL PATHWAY C3 CONVERTASE.
Adrenal Hyperplasia, Congenital
A group of inherited disorders of the ADRENAL GLANDS, caused by enzyme defects in the synthesis of cortisol (HYDROCORTISONE) and/or ALDOSTERONE leading to accumulation of precursors for ANDROGENS. Depending on the hormone imbalance, congenital adrenal hyperplasia can be classified as salt-wasting, hypertensive, virilizing, or feminizing. Defects in STEROID 21-HYDROXYLASE; STEROID 11-BETA-HYDROXYLASE; STEROID 17-ALPHA-HYDROXYLASE; 3-beta-hydroxysteroid dehydrogenase (3-HYDROXYSTEROID DEHYDROGENASES); TESTOSTERONE 5-ALPHA-REDUCTASE; or steroidogenic acute regulatory protein; among others, underlie these disorders.
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.
Protein Structure, Tertiary
The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.
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.
Sequence Homology, Nucleic Acid
Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
A class of C-type lectins that target the carbohydrate structures found on invading pathogens. Binding of collectins to microorganisms results in their agglutination and enhanced clearance. Collectins form trimers that may assemble into larger oligomers. Each collectin polypeptide chain consists of four regions: a relatively short N-terminal region, a collagen-like region, an alpha-helical coiled-coil region, and carbohydrate-binding region.
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)
Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.
Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.
Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
A mass spectrometric technique that is used for the analysis of large biomolecules. Analyte molecules are embedded in an excess matrix of small organic molecules that show a high resonant absorption at the laser wavelength used. The matrix absorbs the laser energy, thus inducing a soft disintegration of the sample-matrix mixture into free (gas phase) matrix and analyte molecules and molecular ions. In general, only molecular ions of the analyte molecules are produced, and almost no fragmentation occurs. This makes the method well suited for molecular weight determinations and mixture analysis.
Reverse Transcriptase Polymerase Chain Reaction
Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.
Polymorphism, Restriction Fragment Length
Immune Adherence Reaction
A method for the detection of very small quantities of antibody in which the antigen-antibody-complement complex adheres to indicator cells, usually primate erythrocytes or nonprimate blood platelets. The reaction is dependent on the number of bound C3 molecules on the C3b receptor sites of the indicator cell.
A species of gram-negative, facultatively anaerobic, rod-shaped bacteria (GRAM-NEGATIVE FACULTATIVELY ANAEROBIC RODS) commonly found in the lower part of the intestine of warm-blooded animals. It is usually nonpathogenic, but some strains are known to produce DIARRHEA and pyogenic infections. Pathogenic strains (virotypes) are classified by their specific pathogenic mechanisms such as toxins (ENTEROTOXIGENIC ESCHERICHIA COLI), etc.
A technique that combines protein electrophoresis and double immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct elliptical precipitin arc results for each protein detectable by the antisera.
A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.
Fluorescent Antibody Technique
Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.
The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).
Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
Genetic Predisposition to Disease
A condition characterized by the recurrence of HEMOGLOBINURIA caused by intravascular HEMOLYSIS. In cases occurring upon cold exposure (paroxysmal cold hemoglobinuria), usually after infections, there is a circulating antibody which is also a cold hemolysin. In cases occurring during or after sleep (paroxysmal nocturnal hemoglobinuria), the clonal hematopoietic stem cells exhibit a global deficiency of cell membrane proteins.
Polymorphism, Single Nucleotide
Immune Complex Diseases
Group of diseases mediated by the deposition of large soluble complexes of antigen and antibody with resultant damage to tissue. Besides SERUM SICKNESS and the ARTHUS REACTION, evidence supports a pathogenic role for immune complexes in many other IMMUNE SYSTEM DISEASES including GLOMERULONEPHRITIS, systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC) and POLYARTERITIS NODOSA.
Complement activation and expression of membrane regulators in the middle ear mucosa in otitis media with effusion. (1/69)The aetiopathogenesis of chronic otitis media with effusion (OME) in children is not yet fully understood. OME is characterized by metaplasia of the epithelium and accumulation of sticky, glue-like effusion in the middle ear containing different mediators of inflammation, including activation fragments of the complement system. Here we examined whether the fluid phase complement activation is reflected in the middle ear mucosa and how the mucosa is protected against the cytolytic activity of complement. Mucosal biopsies from 18 middle ears of children with a history of chronic OME were taken. The biopsies were analysed by immunofluorescence microscopy after staining for complement fragments iC3b/C3c, C3d and C9, and regulators membrane cofactor protein (MCP; CD46), decay-accelerating factor (DAF; CD55) and protectin (CD59). There was a strong staining for iC3b/C3c, and a weaker one for C3d and C9 on the surface of the middle ear epithelial cells of OME patients but not in controls without OME. MCP was expressed on the hyperplastic three to four outer cell layers of the epithelium, while CD59 was expressed throughout the middle ear mucosa. The results suggest a strong ongoing complement activation and consequent inflammation in the middle ear cavity. Unrestricted complement damage of the epithelial lining is prevented by the strong expression of MCP and CD59. (+info)
Linkage analysis of systemic lupus erythematosus induced in diabetes-prone nonobese diabetic mice by Mycobacterium bovis. (2/69)Systemic lupus erythematosus induced by Mycobacterium bovis in diabetes-prone nonobese diabetic mice was mapped in a backcross to the BALB/c strain. The subphenotypes-hemolytic anemia, antinuclear autoantibodies, and glomerular immune complex deposition-did not cosegregate, and linkage analysis for each trait was performed independently. Hemolytic anemia mapped to two loci: Bah1 at the MHC on chromosome 17 and Bah2 on distal chromosome 16. Antinuclear autoantibodies mapped to three loci: Bana1 at the MHC on chromosome 17, Bana2 on chromosome 10, and Bana3 on distal chromosome 1. Glomerular immune complex deposition did not show significant linkage to any genomic region. Mapping of autoantibodies (Coombs' or antinuclear autoantibodies) identified two loci: Babs1 at the MHC and Babs2 on distal chromosome 1. It has previously been reported that genes conferring susceptibility to different autoimmune diseases map nonrandomly to defined regions of the genome. One possible explanation for this clustering is that some alleles at loci within these regions confer susceptibility to multiple autoimmune diseases-the "common gene" hypothesis. With the exception of the H2, this study failed to provide direct support for the common gene hypothesis, because the loci identified as conferring susceptibility to systemic lupus erythematosus did not colocalize with those previously implicated in diabetes. However, three of the four regions identified had been previously implicated in other autoimmune diseases. (+info)
Immunological and clinical follow up of hepatitis C virus associated cryoglobulinaemic vasculitis. (3/69)OBJECTIVE: To study immunological markers and compare these markers with standard measures for the clinical and immunological follow up of vasculitis activity in hepatitis C virus (HCV) associated cryoglobulinaemic vasculitis (CV). METHODS: Serial serum samples from eight patients with newly diagnosed HCV associated CV were followed during interferon alpha treatment induced remission of the CV. Vasculitis activity and disease extent were evaluated with the Birmingham vasculitis activity score (BVAS) and disease extent index (DEI). Cryoglobulinaemia, complement levels (C3c, C4, and CH50), rheumatoid factor (RF), autoantibodies such as antinuclear antibodies, soluble interleukin 2 receptor (sIL2r), soluble intercellular adhesion molecule-1 (sICAM-1), and soluble CD30 (sCD30) were determined. RESULTS: All patients achieved either complete or partial remission of their CV during interferon alpha treatment. There was a significant reduction in vasculitis activity and disease extent (BVAS, DEI), cryoglobulinaemia, RF, sIL2r, sICAM-1, and sCD30. Complement C3c levels increased significantly during this period. Erythrocyte sedimentation rate and levels of complement C4 and CH50 did not change significantly. Both clinical measures (BVAS and DEI) correlated significantly only with C3c and sCD30. CONCLUSIONS: Although this study was of only a small group of patients, it shows that BVAS and DEI as clinical measures and C3c and sCD30 as immunological markers may be useful in the follow up of disease activity of HCV associated CV. The data indicate that activity of the humoral (cryoglobulinaemia, RF, autoantibodies) and cellular (sIL2r, sICAM-1, sCD30) immune response and endothelial damage (sICAM-1) are found in HCV associated CV. (+info)
Complement activation in patients with rheumatoid arthritis mediated in part by C-reactive protein. (4/69)OBJECTIVE: Complement activation in patients with rheumatoid arthritis (RA) is considered to be triggered by immune complexes. Recently, it was shown that C-reactive protein (CRP) can activate the complement system in vivo. We therefore hypothesized that part of the complement activation in RA is due to CRP. The aim of this study was to investigate CRP-mediated complement activation in RA, and to assess its correlation with disease activity. METHODS: Complexes between CRP and the activated complement components C3d (C3d-CRP) and C4d (C4d-CRP), which reflect CRP-mediated complement activation, as well as the overall levels of activated C3 and C4 were measured in the plasma of 107 patients with active RA and 177 patients with inactive RA. Inactive RA was defined according to the American College of Rheumatology criteria for clinical remission. Disease activity was assessed by the modified Disease Activity Score (DAS28). RESULTS: Plasma levels of C3d-CRP and C4d-CRP were increased in the majority of the patients, and were significantly higher in patients with active disease versus those with inactive RA (P < 0.001). In patients with active RA, the plasma concentrations of C3d-CRP and C4d-CRP correlated significantly with the DAS28 (Spearman's rho 0.61 and 0.55, respectively; P < 0.001), whereas these correlations were less pronounced in patients with inactive RA (Spearman's rho 0.28 [P < 0.001] and 0.25 [P = 0.001], respectively). Levels of activated C3 and C4 were also increased in the majority of the patients, particularly in patients with active RA. CONCLUSION: Part of the activation of complement in RA is mediated by CRP and is correlated with disease activity. We suggest that this activation is involved in the pathogenesis of RA. (+info)
Kinetic analysis of the interactions of complement receptor 2 (CR2, CD21) with its ligands C3d, iC3b, and the EBV glycoprotein gp350/220. (5/69)The molecular mechanisms involved in the interaction of complement receptor 2 (CR2) with its natural ligands iC3b and C3d are still not well understood. In addition, studies regarding the binding site(s) of the receptor on C3 as well as the affinities of the C3 fragments for CR2 have produced contradictory results. In the present study, we have used surface plasmon resonance technology to study the interaction of CR2 with its ligands C3d, iC3b, and the EBV surface glycoprotein gp350/220. We measured the kinetics of binding of the receptor to its ligands, examined the influence of ionic contacts on these interactions, and assessed whether immobilized and soluble iC3b bound with similar kinetics to CR2. Our results indicate that 1) gp350 binding to CR2 follows a simple 1:1 interaction, whereas that of the C3 fragments is more complex and involves more than one intramolecular component; 2) kinetic differences exist between the binding of C3d and iC3b to CR2, which may be due to an additional binding site found on the C3c region of iC3b; and 3) iC3b binds to CR2 with different kinetics, depending on whether the iC3b is in solution or immobilized on the surface. These findings suggest that binding of CR2 to iC3b and C3d is more complex than previously thought. (+info)
Detection of immune deposits in skin lesions of patients with Wegener's granulomatosis. (6/69)BACKGROUND: Wegener's granulomatosis (WG) is considered a pauci-immune systemic vasculitis based on the absence of immune deposits in renal biopsies of patients with active disease. In animal models of antineutrophil cytoplasmic antibody (ANCA) associated glomerulonephritis, immune deposits along the glomerular capillary wall are present at early stages of lesion development. These deposits are degraded rapidly, resulting in "pauci-immune" lesions. OBJECTIVE: To test the hypothesis that immune deposits can also be detected in early lesions of patients with WG, thereby initiating an inflammatory reaction that, in time, is augmented in the presence of ANCA, resulting in pauci-immune lesions later on. METHODS: The presence of immune deposits in skin biopsies taken within 48 hours of lesion development was investigated. Direct immunofluorescence was used to examine 32 skin biopsies for the presence of immune deposits (IgG, IgA, IgM, C3c). When possible, a comparison was made between the immunofluorescence findings in renal and skin biopsies taken at the same time. RESULTS: Four of 11 biopsies taken at initial presentation and four of 21 biopsies taken at the onset of a relapse of WG showed IgG and/or IgA containing immune deposits in the subepidermal blood vessels. All nine renal biopsies showed pauci-immune glomerulonephritis, irrespective of the presence (n=5) or absence (n=4) of immune deposits in the skin biopsy. CONCLUSION: A substantial number of skin biopsies showed immune deposits during active disease. These results could support the hypothesis that immune complexes may trigger vasculitic lesions in WG. (+info)
Human alpha galactosidase and alpha 1,2 fucosyltransferase concordantly inhibit xenoreactivity of NIH 3T3 cells with human serum. (7/69)AIM: To study the influence of the expression of human alpha galactosidase and alpha1,2 fucosyltransferase on Gal alpha 1,3 Gal and consequent xenoreactivity in NIH3T3 cells. METHODS: The expression levels of G antigen and H antigen and binding of human natural antibodies (IgG and IgM) and complement (C3c) to NIH3T3 cells were analyzed by flow cytometry. Western blot was employed to further determine the expression of glycoproteins of G antigen. Cytolysis assay with normal human serum was performed by MTT assay. RESULTS: Western blot showed that glycoproteins with molecular weight of 107 kDa, 98 kDa, 88 kDa, 56 kDa, 40 kDa, and 37 kDa were inhibited and even abrogated totally in alpha galactosidase transfectants and alpha 1,2 fucosyltransferase transfectants. The combined transfection of the two enzymes led to a much stronger inhibition of the glycoproteins. The binding of GS-IB4 was decreased by 57.4 % in alpha galactosidase transfectants, 28.8 % in alpha 1,2 fucosyltransferase transfectants, and 72.1 % in combined transfectants, respectively. In contrast, UEA-1 binding was increased about 6.7-fold, 6.0-fold, and 8.0-fold respectively. The xenoreactivity with human IgG was also reduced by 61.4 %, 67.0 %, and 73.4 %, respectively in the three kinds of transfectants. The resistance to cytolysis mediated by human serum was enhanced by 42.4 % in alpha galactosidase transfectants, 51.9 % in alpha 1,2 fucosyltranferase, and even 65.5 % in the combined transfectants. CONCLUSION: Although alpha galactosidase and alpha 1,2 fucosyltransferase had different biochemical properties, they could inhibit the expression of Gal alpha 1,3 Gal synergistically, leading to stronger resistance of xenograft against cytolysis. (+info)
Progesterone and RU486 regulation of uterine complement C3 after prior induction with estradiol. (8/69)Previous results demonstrated that progesterone (P4) given simultaneously with estradiol (E2) prevented stimulation by E2 of complement C3 expression in the immature rat uterus. Northern blot analysis revealed that simultaneous administration of P4 was able to prevent the E2-stimulated increase in C3 mRNA concentration in the luminal epithelial cells. The purpose of the present investigation was to determine whether progesterone modulates C3 expression after the gene has been induced by prior administration of E2 and also to determine the reversibility of this effect by the concomitant administration of RU38486, 17 beta-hydroxy-11 beta-[4-dimethylaminophenyl]estra-4,9,-dien-3-one (RU486). This regulation was studied by examination of protein synthesis as well as mRNA concentrations. Immature 21-day-old female rats were treated with E2 for 2 days (1 microgram/day), followed 24 h later by P4 (500 micrograms) or vehicle. Uteri were removed 6, 9, and 18 h after progesterone treatment and the radiolabeled secreted proteins were analyzed by SDS-PAGE and immunoprecipitation using a goat anti-rat C3 antibody. In animals treated with vehicle, E2-stimulated C3 synthesis remained elevated at 6 and 9 h and returned to control values by 18 h. In contrast, the administration of P4 resulted in a decrease in C3 synthesis at 6 and 9 h with the greatest decrease observed at 9 h. Similar results were obtained when C3 mRNA concentrations were examined. E2-stimulated C3 mRNA concentrations were decreased in rats treated with progesterone compared to those treated with vehicle alone.2 (+info)
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Alpha galactosidase A Antibody 66121-1-Ig | Proteintech
Alpha galactosidase A Antibody 66121-1-Ig has been identified with IF, IHC, WB, ELISA. 66121-1-Ig detected 49 kDa band in HeLa cells with 1:500-1:2000 dilution...
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Alpha galactosidase A Antibody 19877-1-AP has been identified with IF, WB, ELISA. 19877-1-AP detected 49 kDa band in HEK-293 cells with 1:500-1:3000 dilution...
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Utilization of complement-coated IgA1 antibodies to enhance uptake of antigens by antigen presenting cells :: MEDICA, MUSC...
Both complement and Fc regions of IgA 1 have been shown to enhance the uptake of antigens by antigen presenting cells (Fang, et. aI., 1998, Foged, et. aI., 2005, Perrin-Cocon, et. aI., 2004). However, the utilization of complement and IgA1 antibodies in enhancing the uptake of antigens by dendritic cells has not been examined to date. The aims of this research included attaching complement to antidansyl IgA 1 antibodies followed by induction, activation, and examination of dendritic cells incubated with the antigen-antibody immune complexes to determine potential interactive relationships. Complement was linked to the Fc region of anti-dansyl IgA 1 antibodies using a procedure to activate complement while the IgA 1 was bound to a dansylated Sepharose 4B affinity column. The eluted complement-coated IgA 1 antibodies were mixed with dansylated albumin to form the complement-coated IgA1-immune complexes. Then, the immune complexes were incubated with PBMCderived dendritic cells to induce maturation ...
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Reaction of Bovine Conglutinin in Human in Vitro Phagocytic Systems<...
TY - JOUR. T1 - Reaction of Bovine Conglutinin in Human in Vitro Phagocytic Systems. AU - Kronvall, Göran. AU - Dossett, John. AU - Quie, Paul G.. AU - Williams, Ralph C.. PY - 1970/1/1. Y1 - 1970/1/1. N2 - Bovine conglutinin, a naturally occurring anti-C3 factor, was studied in quantitative human in vitro phagocytosis systems. Striking antiopsonic effect was noted when conglutinin was added to phagocytic systems with gram-negative and gram-positive organisms dependent on heat-labile opsonic factors. In noncomplement-dependent test systems using isolated hyperimmune γG opsonins, no blocking by conglutinin was noted.. AB - Bovine conglutinin, a naturally occurring anti-C3 factor, was studied in quantitative human in vitro phagocytosis systems. Striking antiopsonic effect was noted when conglutinin was added to phagocytic systems with gram-negative and gram-positive organisms dependent on heat-labile opsonic factors. In noncomplement-dependent test systems using isolated hyperimmune γG ...
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1. Disease Pathway - SES.2
Fabry Disease is a disease due to deficiency in alpha galactosidase A. The role of the enzyme is to break down a complex and almost unpronounceable molecule called Globotriaosyl-ceramide into galactose and another smaller molecule. If that doesnt happen Globotriaosyl-ceramide builds up in the cells and that build up over the years eventually results in cell dysfunction, cell death and damage to the organs that are involved.. ...
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The results of this study are consistent with the following conclusions. First, unconjugated β-galactosidase is rapidly cleared from blood in vivo (Table 2), owing to rapid uptake of the unconjugated enzyme by liver and spleen (Figs. 2 and 3). Second, once inside cells, β-galactosidase is rapidly degraded in vivo such that 99% of the organ enzyme activity is lost at 4 h after an intravenous injection (Table 1). Third, the 116-kDa β-galactosidase (Fig. 1B) can be conjugated to the 8D3 TfRmAb without loss of enzyme activity (Fig. 1C). Fourth, there is minimal brain uptake of the unconjugated β-galactosidase, but there is a 10-fold increase in brain uptake of enzyme following conjugation to the 8D3 TfRmAb (Table 1; Figs. 2 and 3).. The β-galactosidase is rapidly removed from the blood due to the avid uptake of the enzyme by liver and spleen (Figs. 2 and 3), which confirms the earlier observation of Onodera et al. (1983). The blood concentration of the β-galactosidase-TfRmAb is 5- to 10-fold ...
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β-galactosidase expressing plasmid encapsulating liposomes
Page contains details about β-galactosidase expressing plasmid encapsulating liposomes . It has composition images, properties, Characterization methods, synthesis, applications and reference articles : nano.nature.com
생쥐 자궁의 β-Galactosidase의 발현 ( Expression of β-Galactosidase in Mouse Uterus )
본 웹사이트에 게시된 이메일 주소가 전자우편 수집 프로그램이나 그 밖의 기술적 장치를 이용하여 무단으로 수집되는 것을 거부하며, 이를 위반시 정보통신망법에 의해 형사처벌됨을 유념하시기 바랍니다. [게시일 2003년 4월 2일 ...
Download PDF Early embryonic somatic movements in birds and in mammals other than man by George Ellett Coghill Ebook
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Molecular Cloning, also known as Maniatis, has served as the foundation of technical expertise in labs worldwide for 30 years. No other manual has been so popular, or so influential.
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β重型海洋性貧血４一般所說的重症海洋性貧血就是指「β重型海洋性貧血「３是β血紅蛋白鏈合成嚴重的不足》剛出生時３患有β重型海洋性貧血的寶寶在外觀上跟正常者沒有任何差別》但是漸漸地到了三到六個月大時３這時候因為β血紅蛋白鏈不夠３沒有辦法合成「成人血紅素「情況產生３因此會有臉色蒼白 食慾 活力變差...等貧血的症狀產生》一旦寶寶發病３後果嚴重３必須每隔二至三週輸血一次》長期的輸血會造成體內鐵質的沉積３導致體內器官逐漸喪失功能３最後常因心臟衰竭而在孩童時即死亡》另一方面３由於長期輸血３容易引起病毒的感染３例如B型 C型肝炎３和愛滋病等》真正要根治這種疾病３需要骨髓移植》我國目前在骨髓移植的成功率大約在60%３其餘40%的失敗者可能因併發症死亡３或者回復原來長期輸血打排鐵劑的狀況》 ...
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賽馬會理大真人圖書網絡》（真人圖書網）乃科研項目，由大學及社區夥伴合作營運，旨在探討如何支援學界及公衆深入瞭解各類真實故事，促進社會聯繫及共融。計劃包括多類活動，例如研讀網上資訊、出席工作坊、撰寫讀後感等等。此研究通過香港理工大學研究委員會人類實驗對象操守小組委員會審核（編號：HSEARS20180302004）。基本資料政策如下： a) 計劃所收集個人資料將會絕對保密及用作： 確認閣下的身份、處理閣下的申請、回答閣下的查詢 、發送與本計劃有關的活動資訊 、與行政及學術有關的用途；b) 本計劃絕不會向外披露閣下任何個人資料，也會採取適當的步驟以防止閣下提供的個人資料被不當使用、遺失，未經授權存取、披露或更改破壞。任何人違反條例，均會受到法律追究或處分；c) ...
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reacts with native and denatured-reduced E. coli β-galactosidase(116 kD); may be usedfor detection of β-galactosidase expressed by E. colilacZ gene encoded in many cloned gene sequences,and serves as an indicator for fusion proteins encodedby an inserted DNA ...
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In the early years of my parents marriage, my mother went on a quest to find the perfect lemon meringue pie recipe. It was my fathers favourite dessert and he told her he hadnt had a good slice since hed moved away from home. Hed never found any that could measure up to his mothers…
Fabry disease - SNPedia
Fabry disease is a rare enzyme deficiency known as a lysosomal storage disease. Wikipedia The enzyme involved, alpha galactosidase A, is coded by the GLA gene. OMIM Although Fabry disease has been considered an X-linked recessive condition, female carriers of a single mutated GLA gene may have significant symptoms. Enzyme replacement therapy is helpful, although it is currently extremely expensive, and production problems have led to shortages of the drug.  ...
m-Fluorotyrosine substitution in β-galactosidase; Evidence for the existence of a catalytically active tyrosine<...
TY - JOUR. T1 - m-Fluorotyrosine substitution in β-galactosidase; Evidence for the existence of a catalytically active tyrosine. AU - Ring, M.. AU - Armitage, I. M.. AU - Huber, R. E.. N1 - Funding Information: This work was supported by the National Council (Canada) and the Alberta Heritage Copyright: Copyright 2014 Elsevier B.V., All rights reserved.. PY - 1985/9/16. Y1 - 1985/9/16. N2 - The pH profiles of β-galactosidase, having tyr replaced by m-fluorotyrosine, were compared to those of normal enzyme. The inflection point on the alkaline side was lowered about 1.5 pH units in the fluoro-enzyme, corresponding to the difference in the phenolic pKa values of m-fluorotyrosine and tyr. When glycosidic bond breakage was rate-limiting, the Vm at pH 7.0 was higher for the fluoro-enzyme. When hydrolysis was rate-limiting or when acceptors which made transgalactosylis rate-limiting were used, the Vm was lower for the fluoro-enzyme. This shows that a tyr in β-galactosidase is a general-acid catalyst ...
fibrin split products | Tabers Medical Dictionary
fibrin split products answers are found in the Tabers Medical Dictionary powered by Unbound Medicine. Available for iPhone, iPad, Android, and Web.
Whole‐Mount Histochemical Detection of β‐Galactosidase Activity - Current Protocols
This unit describes fixation and staining for b‐galactosidase activity; it has been successfully used on vertebrate embryos and tissue explants
Colony Lift Colorimetric Assay for -Galactosidase Activity
Molecular Cloning, also known as Maniatis, has served as the foundation of technical expertise in labs worldwide for 30 years. No other manual has been so popular, or so influential.
anti-SCIN antibody [N3C2], Internal | GeneTex
SCIN antibody [N3C2], Internal (scinderin) for ICC/IF, WB. Anti-SCIN pAb (GTX112591) is tested in Human samples. 100% Ab-Assurance.
1(3)01 | Academic and Research journal of the NAS of Ukraine
https://doi.org/10.15407/scin1.03.020. F. F Sizov1, O. V. Bekhtir1, Ye. O. Bilevych1, A. G. Golenkov1, E. Yu. Gordienko3, M. T. Grinchenko2, J. V. Gumenjuk-Sichevska1, S. E. Dukhnin2, V. V. Zabudsky1, P. V. Zavadsky1, I. I. Ilnitsky1, S. L. Kravchenko1, V. M. Krajovyi1, V. P. Reva2, S. V. Korinets2, L. O. Pisarenko2, Yu. V. Fomenko3, A. V. Shevchyk1, G. V. Shustakova3 ...
5-Bromo-4-chloro-3-indoxyl-α-D-fucopyranoside - Creative Enzymes
Several types of assays can be performed measuring galactosidase activity in yeast using 5-Bromo-4-chloro-3-indoxyl-α-D-fucopyranoside as subtrate.
O-Nitrophenyl-β-D-Galactopyranoside (ONPG) Test | Microbe Notes
O-Nitrophenyl-β-D-Galactopyranoside (ONPG) Test. The objective of ONPG is to determine the ability of an organism to produce β-galactosidase.
Complement component 3
Factor I can cleave C3b into C3c and C3d, the latter of which plays a role in enhancing B cell responses. In the alternative ... Complement component 3, often simply called C3, is a protein of the immune system. It plays a central role in the complement ... "Entrez Gene: C3 complement component 3". Sahu A, Lambris JD (Apr 2001). "Structure and biology of complement protein C3, a ... Next, C3b is broken down progressively to first iC3b, then C3c + C3dg, and then finally C3d. Factor I is the protease cleaves ...
List of MeSH codes (D12.776.124)
... complement c3c MeSH D12.776.124.486.274.250.260.750 - complement c3d MeSH D12.776.124.486.274.350 - complement c4 MeSH D12.776. ... complement c1 MeSH D12.776.124.486.274.050.270 - complement c1q MeSH D12.776.124.486.274.050.280 - complement c1r MeSH D12.776. ... complement c2 MeSH D12.776.124.486.274.150.500 - complement c2a MeSH D12.776.124.486.274.150.750 - complement c2b MeSH D12.776. ... complement c5b MeSH D12.776.124.486.274.550 - complement c6 MeSH D12.776.124.486.274.650 - complement c7 MeSH D12.776.124.486. ...
"Complement Activation in Inflammatory Skin Diseases". Frontiers in Immunology. 9: 639. doi:10.3389/fimmu.2018.00639. ISSN 1664- ... linear IgG and/or C3c deposits (in an n- serrated pattern) by direct immunofluorescence microscopy (DIF) on a skin biopsy ...
Specific Protein Portfolio
Detection of surface bound complement at increasing serum anticoagulant concentrations
Surface mediated immune complement activation can be detected by a variety of antibody utilizing methods such as ELISA, ... fondaparinux and sodium citrate affected the binding of anti-complement factor 3c (anti-C3c) on a model complement activator ... Surface mediated immune complement activation can be detected by a variety of antibody utilizing methods such as ELISA, ... Detection of surface bound complement at increasing serum anticoagulant concentrations Colloids Surf B Biointerfaces. 2008 Apr ...
Others - Creative BioMart
Public Access Database for Medical Device Registration
Therefore, C3c is a stable complement biomarker which will appear in the fluid phase only, without interference of other C3 ... Complement Poster Nov 30, 2018 11:40:00 AM Have you already requested a copy of the Hycult Biotech Complement Poster? Read more ... C3c as a stable complement biomarker Feb 23, 2015 12:01:24 PM ... Mouse Classical Complement Pathway Assay (HIT420) Mouse Lectin ... The activation of the lectin complement pathways in mice can now be measured with the new Hycult Biotech Assays HIT420 and ...
SMART: C345C domain annotation
Staphylococcal Complement Inhibitor (SCIN) in complex with Human Complement C3c. 3ohx. Molecular Basis for Complement ... Staphylococcal Complement Inhibitor (SCIN) in complex with Human Complement Component C3c. 3l5n. Staphylococcal Complement ... Structure of complement C5 in complex with SSL7. 3km9. Structure of complement C5 in complex with the C-terminal beta-grasp ... Structure of Complement C5 in Complex with CVF. 3t4a. Structure of a truncated form of Staphylococcal Complement Inhibitor B ...
Code System Concept
abebio - Elisa china
Anti-C3c (Alpha Chain) Fragment 2 Rabbit Polyclonal IgG Antibody (Cy5.5-conjugated) - Creative Biolabs
Anti-Mouse C3b/iC3b/C3c Monoclonal Antibody (clone 3/26) -100 µg - Creative Biolabs
Anti-Mouse C3b/iC3b/C3c Monoclonal Antibody (clone 3/26) -100 µg is available from creative biolabs. ... Monoclonal antibody 3/26 recognizes the C3 fragments C3b, iC3b and C3c activated by mouse complement proteins. The complement ... The monoclonal antibody 3/26 recognizes mouse complement protein activated C3 fragments C3b, iC3b, and C3c. The complement ... C3b attaches to immune complexes and is further cleaved into iC3b, C3c, C3dg and C3f. The activation products of the complement ...
Tests impacted by Roche reagent shortage
BN ProSpec System
American Society of Nephrology | Kidney Week - Abstract Details (2022)
This study will evaluate the safety and efficacy of complement protein C3 inhibitor pegcetacoplan in treating C3G and IC-MPGN. ... Inclusion criteria include 2+ staining for C3c, global glomerulosclerosis ,50%, urine protein-to-creatinine ratio (uPCR) ≥1000 ... This study will evaluate the safety and efficacy of complement protein C3 inhibitor pegcetacoplan in treating C3G and IC-MPGN. ... This study will evaluate the safety and efficacy of complement protein C3 inhibitor pegcetacoplan in treating C3G and IC-MPGN. ...
Products Archive - Nordic MUbio
Human C3c from Active Bioscience
Human C3c Complement C3c, Complement Component C3c, C3c. ... Complement C3c, Complement Component C3c, C3c.. Source: Human ... Description of Human C3c. Human Complement component C3c (hC3c) derived from human plasma consist of 3 peptides with a total ... The three peptides (C3c Beta chain (23-667), C3c alpha chain fragment 1 (749-954) and C3c alpha chain fragment 2 (1321-1663)) ... To buy Human C3c please click on the Shopping List Symbol right from the indicated price. This will add the product to your ...
Assessing complement blockade in patients with paroxysmal nocturnal hemoglobinuria receiving eculizumab | Blood | American...
C3d deposition on red blood cells was quantified using flow cytometry (monoclonal anti-human C3d, clone A702; anti-human C3c, ... complement hemolytic activity assay, complement system proteins, eculizumab, paroxysmal nocturnal hemoglobinuria, hemolysis ... complement hemolytic activity assay, complement system proteins, eculizumab, paroxysmal nocturnal hemoglobinuria, hemolysis ... Residual complement activity is complement mediated using this assay as shown with plasma from a PNH patient receiving ...
C3c as a fluid phase marker for inflammation-generation and characterization of monoclonal antibodies against neoepitopes on...
XIth European meeting on Complement in Human Disease - Varighed: 24. aug. 2010 → …. Konferencens nummer: 11. ... Skjødt, M-O., Brandt, J., & Vitved, L. (2007). C3c as a fluid phase marker for inflammation-generation and characterization of ... Skjødt, M-O, Brandt, J & Vitved, L 2007, C3c as a fluid phase marker for inflammation-generation and characterization of ... C3c as a fluid phase marker for inflammation-generation and characterization of monoclonal antibodies against neoepitopes on ...
Pesquisa | Portal Regional da BVS
C3c, MBL, and factor B have been documented in the subepithelial immune deposits. However, the changing of complement ... Here we examined the plasma and urinary complement profile of patients with primary FSGS, aiming to investigate the complement ... Complement activation profile of patients with primary focal segmental glomerulosclerosis. Huang, Jing; Cui, Zhao; Gu, Qiu-Hua ... RESULTS: The plasma complement activation products were elevated both in the patients with and without anti-PLA2R antibodies. ...
LabsMD - Simple and Secure Lab Tests Online
The complement (C3c) should be present in sufficient quantities in the blood. A desirable value is 142 mg/L of blood serum. If ... This is the shortage of a certain complement (C3c) which is a component of blood albumen, having a complex structure, and which ... Indeed, we see again and again, for example, during progressive breast cancer, very high complement (C3c) values of the defense ... These facts are often overlooked, as the necessary determination of the C3c-complement is almost never offered by orthodox ...
Complement C3d Human Enzyme | C3d Protein | ProSpec
Human Complement C3d produced in Human plasma having a molecular mass of 33.8kDa. ... Complement C3, C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1, C3, CPAMD1. ... Human Complement C3d produced in Human plasma having a molecular mass of 33.8kDa. ... as occurs during complement activation) the iC3b, C3dg and C3d fragments would remain covalently attached to that surface.C3d ...
A monoclonal antibody against human complement component C3: the production of C3 by human cells in vitro. - Oxford Stem Cell...
Indirect binding assays indicate that the antibody is directed the C3c portion of C3. The immunoprecipitation technique was ... against the third component of human complement (C3) was produced by fusing P3-X63-Ag8 mouse myeloma cells with spleen cells ... A monoclonal antibody against human complement component C3: the production of C3 by human cells in vitro. ... A monoclonal antibody (WM1) against the third component of human complement (C3) was produced by fusing P3-X63-Ag8 mouse ...
Mikkel-Ole Skjødt - Forskning - Region Hovedstaden
Lectin Pathway Enzyme MASP-2 and Downstream Complement Activation in COVID-19. Publikation: Bidrag til tidsskrift › ... "Novel C3C epitope, antibodies binding thereto, and use thereof".PatentNo:US20130177567 A1,PCT/EP2011/058007 ... Innate immunity;Complement;Coagulation;Development of monoclonal antibodies for IVD and research. ... 1. Activation®ulation of complement driven inflammation&thrombosis. I have discovered a novel plasma protein (MAP-1) that ...
Complement - pediagenosis
... releasing the fragment C3c and leaving membrane bound C3d.. ... Complement. Fifteen or more serum components constitute the ... Complement inhibitors. In order to prevent over-activation of the complement cascade, there are numerous inhibitory mechanisms ... Some of these, like C1q inhibitor, block the activity of complement proteinases. Others cleave active complement components ... CR Complement receptor. Three types of molecule that bind different products of C3 breakdown are found on cell surfaces: CR1 is ...
AIM: To review the differential protein profile in serum of hepatitis - CRISPR gene editing in human embryos wreaks
Interestingly, the levels of alpha-2-HS-glycoprotein and complement component C3c were elevated in the serum of the non- ... The Mann-Whitney check was also performed in the validation stage to evaluate the different degrees of complement component C3c ... Summary: Serum alpha-2-HS-glycoprotein Zarnestra kinase activity assay and complement component C3c may be potential serum ... Validation of proteins linked to the immune response We chosen 3 proteins (alpha-2-HS-glycoprotein, complement component C3c, ...
Autosomal Dominant Polycystic Kidney Disease With Idiopathic Membranous Nephropathy: An Unusual Association? | Granata |...
Serum complement fractions, C3 and C4, were within normal range.. Abdominal ultrasound examination showed both enlarged liver ... direct immunofluorescence on cryostatic slides highlighted granular sub endothelial IgG and C3c (Fig. 1) deposits along ... Serum complement fraction, C3 and C4, were within normal range. Abdominal ultrasound examination showed both enlarged liver and ... glomerular capillary wall, while the other immunoglobulins (IgM, IgA) and complement fractions (C4c, C1q) were normal. ...
Modeling hemolytic-uremic syndrome: In-depth characterization of distinct murine models reflecting different features of human...
- Unlike other C3 fragments, C3c does not bind to other structures, like pathogens, cell surface (receptors) and other plasma proteins. (hycultbiotech.com)
- The netrin (NTR) module is an about 130-residue domain found in the C-terminal parts of netrins, complement proteins C3, C4, and C5, secreted frizzled-related proteins, and type I procollagen C-proteinase enhancer proteins (PCOLCEs), as well as in the N-terminal parts of tissue inhibitors of metalloproteinases (TIMPs). (embl.de)
- Monoclonal antibody 3/26 recognizes the C3 fragments C3b, iC3b and C3c activated by mouse complement proteins. (creative-biolabs.com)
- The Mann-Whitney check was also performed in the validation stage to evaluate the different degrees of complement component C3c and CD5 antigen like proteins. (mycareerpeer.com)
- In the present work we investigated how the common anticoagulants heparin, dalteparin, fondaparinux and sodium citrate affected the binding of anti-complement factor 3c (anti-C3c) on a model complement activator surface, immobilised IgG, after incubation in human blood serum. (nih.gov)
- Increasing amounts of heparin, dalteparin and sodium citrate in normal serum resulted in a decreasing anti-C3c binding. (nih.gov)
- Control C3a-des arg ELISA measurements show that the lowered antibody surface binding was not a result of complement depletion in serum. (nih.gov)
- C3 is the most abundant protein in the complement system, and the serum protein level is about 1.3 mg/ml. (creative-biolabs.com)
- Among these potential candidates, serum levels of alpha-2-HS-glycoprotein, complement component C3c and CD5 antigen-like precursor were further analyzed. (mycareerpeer.com)
- Interestingly, the levels of alpha-2-HS-glycoprotein and complement component C3c were elevated in the serum of the non-responders compared to the responders. (mycareerpeer.com)
- Summary: Serum alpha-2-HS-glycoprotein Zarnestra kinase activity assay and complement component C3c may be potential serum biomarkers in predicting the treatment response of peginterferon alfa-2b in individuals with CHB prior to treatment. (mycareerpeer.com)
- Similarly, the immunonephelometry results showed that serum levels of complement component C3c were significantly elevated in the non-responders when compared. (mycareerpeer.com)
- Serum complement fraction, C3 and C4, were within normal range. (journalmc.org)
- Complement C3c Fragment 2 IgG antibody, Polyclonal, 1 μg/μL. (creative-biolabs.com)
- The three peptides (C3c Beta chain (23-667), C3c alpha chain fragment 1 (749-954) and C3c alpha chain fragment 2 (1321-1663)) are joined together by disulphide bonds. (active-bioscience.de)
- C3 (MW 180 000), the central component of all complement reac- tions, split by its convertase into a small (C3a) and a large (C3b) fragment. (pediagenosis.com)
- Two 'C3b inactivator' enzymes rapidly inactivate C3b, releasing the fragment C3c and leaving membrane bound C3d. (pediagenosis.com)
- The larger fragment generated from the cleavage of COMPLEMENT C3 by C3 CONVERTASE. (bvsalud.org)
Staining on renal biopsy1
- and proportion of participants with decreased C3c staining on renal biopsy from baseline at week 26. (asn-online.org)
- hC3c plays an important role in both complement activation pathways, with different specific proteolytic systems cleaving it to form C3 convertase. (active-bioscience.de)
- 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. (bvsalud.org)
- Surface mediated immune complement activation can be detected by a variety of antibody utilizing methods such as ELISA, fluorescence- or radiolabelling techniques, QCM, and ellipsometry. (nih.gov)
- Monoclonal antibody 3/26 preferably recognizes cleaved C3 fragments C3b, iC3b and C3c. (creative-biolabs.com)
- In this case, the C3dg product is mainly located in the inflammation (C3c is cleared) that the antibody (3/26) cannot recognize. (creative-biolabs.com)
- In such cases primarily the C3dg product resides at the place of inflammation (C3c being cleared) which is not recognized by antibody 3/26. (creative-biolabs.com)
- A monoclonal antibody against human complement component C3: the production of C3 by human cells in vitro. (ox.ac.uk)
- A monoclonal antibody (WM1) against the third component of human complement (C3) was produced by fusing P3-X63-Ag8 mouse myeloma cells with spleen cells from BALB/c mice immunized with purified C3. (ox.ac.uk)
- Indirect binding assays indicate that the antibody is directed the C3c portion of C3. (ox.ac.uk)
- Note that, in the absence of antibody, many of the molecules that activate the complement system are carbohydrate or lipid in nature (e.g. lipopolysaccharides, mannose), suggesting that the system evolved mainly to recognize bacterial surfaces via their non-protein features. (pediagenosis.com)
- A positive direct antiglobulin (DAT or Coombs) test identifies in vivo antibody-coated and complement-coated red cells. (jotscroll.com)
- C3b attaches to immune complexes and is further cleaved into iC3b, C3c, C3dg and C3f. (creative-biolabs.com)
- The long-term processing/activation of C3 is at a low level, which will reduce the detection of C3 fragments C3b, iC3b and C3c. (creative-biolabs.com)
- The chronic processing/activation of C3 is taking place at a lower level, which would reduce detection of the C3 fragments C3b, iC3b, and C3c. (creative-biolabs.com)
- Finally, this iC3b is cleaved with trypsin to yield C3d.If the C3b precursor was attached to a surface (as occurs during complement activation) the iC3b, C3dg and C3d fragments would remain covalently attached to that surface.C3d is able to attach to a surfaceonly during complement activation on a surface. (prospecbio.com)
- Puede ser inactivada (iC3b) o desdoblada por varias proteasas produciéndose fragmentos tales como el COMPLEMENTO C3C, COMPLEMENTO C3B, C3e, C3f y C3g. (bvsalud.org)
- The activation of the lectin complement pathways in mice can now be measured with the new Hycult Biotech Assays HIT420 and HIT421. (hycultbiotech.com)
- The third complement component, C3, is essential to the classical, alternative and lectin pathways of complement activation. (creative-biolabs.com)
- Human Complement component C3c (hC3c) derived from human plasma consist of 3 peptides with a total molecular mass of 138 KDa. (active-bioscience.de)
- Complement component C3c was further validated using immunonephelometry and the BN ProSpec system (Siemens Healthcare Diagnostics Products GmbH, Germany). (mycareerpeer.com)
- Direct Coombs Test can initially be performed with a polyspecific anti-human globulin reagent, which contains anti-IgG and anti-C3d and may also contain antibodies to other C3 determinants (C3dg, C3b, C3c) and other immunoglobulins (Iga, IgM). (jotscroll.com)
- Skjødt, M-O, Brandt, J & Vitved, L 2007, ' C3c as a fluid phase marker for inflammation-generation and characterization of monoclonal antibodies against neoepitopes on activated or inactivated split products of C3 ', Molecular Immunology , bind 44, nr. 16, s. 3917-3918. (sdu.dk)
- Innate immunity;Complement;Coagulation;Development of monoclonal antibodies for IVD and research. (regionh.dk)
- The direct Coombs test was the older term used to describe this test and it is a test used to detect antibodies or complement against red blood cells (RBCs). (jotscroll.com)
- The presence of these antibodies or complement on the red blood cells cause the destruction of the RBCs. (jotscroll.com)
- Complement C3, C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1, C3, CPAMD1. (prospecbio.com)
- Decay-accelerating factor (CD55) is a complement regulatory protein, which is expressed by most cells to protect them from complement-mediated attack. (aai.org)
- Decay accelerating factor (CD55) is a 70-kDa single chain complement regulatory protein, that consists of four extracellular short consensus repeat (SCR) 3 domains, linked to the membrane by a GPI anchor ( 1 ). (aai.org)
- The complement system is an important factor in innate immunity. (creative-biolabs.com)
- The activation products of the complement cascade contain new epitopes that are not present in various natural components. (creative-biolabs.com)
- Activation products of the complement cascade contain neo-epitopes that are not present in the individual native components. (creative-biolabs.com)
- Unwanted complement activation is a major cause of tissue damage in various pathological conditions and contributes to quite a few immune complex diseases. (active-bioscience.de)
- 1. Activation®ulation of complement driven inflammation&thrombosis. (regionh.dk)
- Activation of complement can be started either via adaptive or innate immune recognition. (pediagenosis.com)
- Nevertheless, excessive complement activation can cause unpleasant side-effects (see Fig. 36). (pediagenosis.com)
- The degree of complement activation (C3c-deposition), immune cell invasion (macrophages, T lymphocytes), apoptosis and proliferation were significantly increased in kidneys of mice subjected to the 7 day but not in kidneys of mice subjected to the 3 day regime. (leibniz-hki.de)
- In this study, we show that direct stimulation of CD55 on CD4 + T cells with CD97 can modulate T cell activation but does not interfere with CD55-mediated complement regulation. (aai.org)
- The disadvantage of most complement biomarkers is their short half-life, making reliable sample collection and measurements difficult. (hycultbiotech.com)
- Mouse Classical Complement Pathway Assay (HIT420) Mouse Lectin Complemement Pathway Assay (HIT421) The innate immune system is important in the first defense against foreign pathogens. (hycultbiotech.com)
- Complement 3 glomerulopathy (C3G) and immune complex membranoproliferative glomerulonephritis (IC-MPGN) are rare diseases characterized by excessive deposition of C3 breakdown products in renal glomeruli leading to proteinuria and progressive renal disease. (asn-online.org)
- While intrarenal changes (apoptosis, proliferation, complement deposition, immune cell invasion) mainly contribute to the pathophysiology of the subacute model, prerenal pathomechanisms (hypovolemia) play a predominant role in the acute model. (leibniz-hki.de)
- Therefore, C3c is a stable complement biomarker which will appear in the fluid phase only, without interference of other C3 based products. (hycultbiotech.com)
- Lyophilized human Human C3c although stable at 2-8 C for 3 weeks, should be stored desiccated at -20 C , Reconstituted human hC3c should be stored at 4 C between 2-7 days and in working aliquots below -18 C for future use. (active-bioscience.de)
- Pegcetacoplan is a C3 investigational therapy for diseases related to complement overactivation. (asn-online.org)
- Have you already requested a copy of the Hycult Biotech Complement Poster? (hycultbiotech.com)
- Es un constituyente de la C3 CONVERTASA DE LA VÍA ALTERNATIVA (C3bBb), y de las CONVERTASAS del COMPLEMENTO C3 tanto en la vía clásica (C4b2a3b) como alternativa (C3bB3b). (bvsalud.org)
- To buy Human C3c please click on the Shopping List Symbol right from the indicated price. (active-bioscience.de)
- Human Complement C3d produced in Human plasma having a molecular mass of 33.8kDa. (prospecbio.com)
- It is widely expressed on human cells, including PBLs, and protects them from complement-mediated lysis. (aai.org)
- They are released by bone marrow under the influence of complement through a process called granulopoiesis. (hycultbiotech.com)
- A positive direct antiglobulin test with IgG (with or without complement) and a panagglutinin eluate is consistent with the diagnosis of warm autoimmune hemolytic anemia whereas a direct antiglobulin test positive with complement only, is seen in patients with cold agglutinin disease. (jotscroll.com)
- Recently, an increase in T cell responsiveness in CD55 −/− mice was shown to be mediated by a lack of complement regulation. (aai.org)
- Both CH50 and free eculizumab level markers look promising for the monitoring of complement blockade in patients with PNH receiving eculizumab. (ashpublications.org)
- Mouse Complement Pathway Assays! (hycultbiotech.com)